Well, the 5 year ban on funding dedicated to inspection of horse slaughter facilities hasended. The question now is whether the industry has been effectively killed, or if there is still a large enough market to find the funding and overcome the opposition.
Full disclosure: I have no problem with horse slaughter, and I also really like horses. The animals are subject to the same humane end as beef and poultry, and any objection to the consumption of horse products by those who enjoy other animal products is hypocritical. You may now choose to read or ignore the rest of this post if you wish, knowing that I’ll speak with this bias. I will however, make my points respectfully, and fully welcome reasoned and intelligent debate from anyone who disagrees.
Psych Your Mind has a great post discussing how we meat eaters manage to both love animals and eat them. A lot of it boils down to our separation of cow and steak, and how we perceive livestock animals as opposed to pets. Horses are unique in that they fall into both the work and companion categories, and it’s amazing to see how they can switch back and forth. This is similar to the many free chickens you find on Craigslist that no longer lay eggs, but “make great pets!”. The original owners clearly want them for production, but want no part in their non-economic use.
Google scholar shows a host of articles looking at the impacts of the ban that I’m not going to detail here. However I would really like to hear from readers in the comments, specifically readers opposed to horse slaughter and consumption! It’s difficult to find arguments not rooted in a religious, animal rights, or sentimental background, and I’m really interested to hear if there is empirical evidence that supports a slaughter ban. Whether it be based on export economics, public health (I have heard of food-borne illness concerns with horse meat), or potential detriment to other industries, I want to hear about it! So please feel free to comment and let me know where you stand on the issue!
Just a short one here today. Not too much interesting going on in a study that supports the null, but the methods are great.
This study looked at the affect that one or two rectal palpations to determine pregnancy had on embryo viability. I can see why there would be a question, it seems like a highly invasive procedure when you’re shoulder deep in cow rectum and feeling for an amnion several layers of membranes away. But we tend to anthropomorphize, and many dairy cattle require minimal restraint for the procedure. Nonetheless, it does seem likely that there could be a negative effect on the embryo, especially when rupturing or crushing the amnion via rectal palpation has been a historical method of terminating an unwanted pregnancy in cows (before we started using PGF2α) (Romano, 2011).
The study did a great job of identifying factors that have created conflicting results in the past. Whether that was sampling bias, uncontrolled treatments (multiple people and techniques for palpation), or a lack of a true control. They took the time to show how each one of those shortcomings was corrected in this study, and I think they did a great job designing the experiment.
In the end it was surprising to see that there was no difference between the cows subjected to rectal palpation once or twice compared to the control. I didn’t expect to see a significant difference, but potentially a small one. The authors did warn that because this experiment was so controlled, the results may not be similar to every situation. Inexperienced personnel or different techniques could change the pregnancy rates in practice (the study employed a single veterinarian with >25 years experience). One difference they took time to note was the much lower pregnancy rate in dairy cows as opposed to primiparous heifers. The exact etiology of this is unknown, but is commonly found in dairy. The authors mention it as it played a role in their analysis of the two farms involved (other factors affecting rates between the farms were geographic area, rate of twinning, and breed of cattle).
Not especially exciting, but it’s always great seeing researchers identify a conflicted area and tackle it with strict methods/controls and a large sample size.
Romano JE, Thompson JA, Kraemer DC, Westhusin ME, Tomaszweski MA, & Forrest DW (2011). Effects of early pregnancy diagnosis by palpation per rectum on pregnancy loss in dairy cattle. Journal of the American Veterinary Medical Association, 239 (5), 668-73 PMID: 21879969
It’s funny how reading these articles is incredibly relieving for me. They confirm that I actually did learn and do remember principals and details from my classes. Today’s article comes from Veterinary Research, and discusses the mechanisms and variables involved in the emergence of a virus.
” A viral emergence is generally defined as the appearance of a new pathogen for a host, such as human immunodeficiency virus (HIV)-1 for humans in the twentieth century. Viral re-emergence often refers to the reappearance of a viral pathogen after a period of absence, such as the periodic human influenza epidemics or pandemics.” (Domingo, 2010)
There’s a huge amount of information on viral evolution and mutation, a concept that (like everything else you haven’t specifically studied) I had greatly oversimplified. It was incredibly fascinating to read how viruses can recombine and splice gene segments from other unrelated infections, and the various pathways new genes can be created or introduced that allow viruses to jump host species. I’m not going to try to summarize all of those, the article explains them much better than I could, but there’s still a few broad topics in the paper worth discussing.
The concept of viral quasispecies is something I’ve never heard about. I’ve discussed viral serovars on here before, but I believe that term specifically refers to antigen variation. Quasispecies refers to groups of virus that are labeled and operate as one species (for example, Influenza H1N1) but contain different genomes. For example, if I get the flu this winter, the virus I am exposed to may contain several quasispecies, that are the same virus, but contain different genes. Now any deleterious mutations or reassortments will probably be wiped out by my immune system, but the ones with a fitness advantage will reproduce and take over. Here’s the extra interesting part, even if I had been infected with just one quasispecies, I could still shed several while I’m infected. There is so much mutation and variation in viral reproduction that I would be generating new ones as a single host.
Quasispecies are important in emergence because they are a major source of viral evolution. We identify the “wild type” gene amongst quasispecies as a distribution of genes that characterize that viral species (consensus gene); even though amongst different quasispecies they may be found in different places in the genome. This is where the existence of quasispecies propels viral evolution forward. When you mix up the genome so much, you can create mutations that change nothing in the functional portions of the genome, but create subpopulations that are fine tuned to conditions that may not yet be occurring. As an example, it’s been assumed that SARS was introduced to humans through Civet cats, when it was originally a virus transmitted by bats. Contact with civets is common in areas surrounding SARS outbreaks (where they are raised for food), where contact with bats is much less common. It is possible that there was a quasispecies subpopulation of SARS carrying a mutation allowing it to jump species to humans long before it was even introduced to civets. When the disease was contained to bats, this mutation has no fitness advantage, but it can sit idle until a change in the environment (higher infection rates in civets, civets brought from more rural areas, there are unlimited possibilities) gives it an advantage. This essentially allows virus to be proactive in its evolution. Instead of waiting for selective pressure, new genes are created spontaneously in the event that they may become useful.
The article continued to discuss different factors in emergence, primarily focusing on new host emergence, and brought it all together as an example of biological complexity. My personal favorite example for biological complexity is the realization that we’ll probably never fully understand the complete pharmacology associated with feelings of hunger and satiety. Alternatively you can illustrate this principal by asking someone to model the weather. The idea is that there are so many variables, all interdependent on each other, that it is pretty much impossible to trace all of the factors that led to an event such as the host change SARS made from civets to humans. They illustrate this by showing that even if viral variation is sufficient to promote a host change, there are numerous other roadblocks that have to be surmounted to allow it to take place (interaction with the new host, sufficient amounts of virus introduced to the system of the new host, fitness of the mutated virus, exposure to multiple quasispecies or serovars, future shedding of virus adapted to that host species, etc.). It’s a paradoxal idea, because we have been able to successfully model systems like these through the CDC and WHO, and we have been able to successfully model complex systems like the weather, even when there are countless interactions that we can’t even begin to measure.
Read this article if you have any interest in virology at all. I learned a lot, and it’s interesting and fluid reading if you have a basic understanding of cell biology.
I recently had a professor tell me that if I didn’t let them know if I made it into vet school, they would forever curse me with fat, in heat, Labrador spays for the rest of my career. I can think of few fates worse for a future veterinarian (though I did mention that the owners also had to have no way to pay, and will forget to mention this until after the procedure). Today’s article is really cool and discusses the prevalence of ovariohysterectomy and orchiectomy (spaying and neutering, fixing, castration, gonad removal,de-nutting, whatever you prefer to call it) in the USA. It breaks the percentages down into region, animal species, animal breed, animal age, and enrollment in wellness plan from Banfield (animal health insurance).
Banfield Pet Hospital is an amazing organization for animal research because all of their records are computerized and kept in a central database (I should mention that the man who made Banfield what it is today is an OSU alum, go beavs). Because of this treasure trove of data, this study was able to get a sample size of over 300,000 cats and over one million dogs. While this represents less than 1% of the US pet population, its still a valuable amount of data, and we can reasonably assume that Banfield has a decent representation of the rest of the pet population that regularly visits private clinics. The article mentions that one of the only large differences is the mean age at clinics (Banfield’s is slightly lower). The numbers found in this study also line up well with previous examinations using distributed surveys to collect data.
I’m very proud to say that the Northwest region (making up Washington, Oregon, Idaho, and Montana) has the highest percentage of castrated cats and dogs compared to any other region (tied with the North Central region for percentage of dogs) according to the study. The region with the lowest percentage was the Southeast region (making up Alabama, Florida, Georgia, Mississippi, North Carolina, South Carolina, and Tennessee). That’s an area of the country I haven’t ever visited, so I can’t comment on cultural factors that may influence the decision to castrate pets, but clearly more outreach could be focused on that area.
The breed distribution is interesting, but doesn’t offer too much information for most breeds. In my own head I see the Labs’ and Retrievers’ high numbers understandable, as you can in some ways consider them “white-collar” or suburban dogs. This would be associated with a higher income and thus one less roadblock to castration. Pit Bulls can maybe be considered a “blue-collar” dog, but that can’t be the only reason their numbers are so low. I’m actually at a loss as to why the castration rate of Pit Bulls is so much drastically lower than all the others. It’s an obvious outlier. I myself love Pits and believe that in the right hands they make great dogs. But considering their stigma, low rate of adoption (and consequently high euthanasia rate), insurance liability, and higher risk, I do believe we should make castrating Pits a priority. I’ll definitely be looking for more literature that attempts to explain the demographics and other factors that create this problem. The second lowest group, Chihuahuas, is also interesting. Again, I’m not sure why the numbers for this breed are so low, but one factor may be that many Chihuahua’s are kept as indoor-only dogs, and that may reduce the motivation to perform the procedure, as the largest benefit is wasted on them (as seen by those owners).
I’m not surprised to see that mixed animals were more likely to be castrated, and I really have no problem with that. There aren’t too many unwanted animals that come from intentional breeding, and purebred animals generally don’t have trouble finding homes (pending behavioral issues). Responsible breeding doesn’t contribute to the pet overpopulation problem significantly, and leaving that option open to purebred owners is acceptable. With cats on the other hand, I’m happy to see the extremely high rate of castration. Cats are allowed to roam unsupervised much more than dogs, and we have enough trouble controlling the feral population without accidental pregnancies also occurring in animals that could have been easily castrated.
One rather frightening statistic was the percentage of dogs and cats from shelters that do not return for castration. This concerns me as in many cases the cost is free or subsidized to less than $50. In a private clinic you can pay upwards of $200, but this seems to be little incentive as 40-60% of animals are returned for the procedure when it is already paid for. To me, this is indicative that some of those owners will provide a low level of veterinary care for the lifetime of that animal, when they already haven’t taken advantage of a free procedure. This is pure conjecture however, and there could be a host of reasons that owners do not return. However, because the rate is so low, I would bet that there is some significant factor that is relatively consistent among owners who adopt from shelters, whether that be income (shelter’s are a very inexpensive option to get a purebred-looking dog) or attitude.
All in all, a good look at where castration is common, and where education and improvement needs to be made. I do think that many PSA’s, advertizements, and advocacy campaigns are too often directed at groups that are already in agreement. Even looking the statistics from a PSA I made back in high school show that the primary people concerned with animal welfare are women over 35, and it’s clear that similar announcements are marketed at that group. New campaigns should focus on a new approach to educate people why castration is important, and maybe spend less time showing us pictures of sad puppies. Tell me why I personally should do it, because until it’s too late to change anything, there’s no reason I should think I’m part of the problem.
Trevejo R, Yang M, & Lund EM (2011). Epidemiology of surgical castration of dogs and cats in the United States. Journal of the American Veterinary Medical Association, 238 (7), 898-904 PMID: 21453178
Veterinary ethics are especially touchy and complex because the general public often has strong opinions on every animal issue, including: euthanasia, animal welfare, animal rights, cosmetic surgery, private breeding, puppy mills, spaying and neutering, pit bulls, leash laws, animals as food, veal, genetic engineering, hormone use, vaccination, preventative care, training techniques, feral cats, dogs and livestock, licensing, service animals, classroom animals, TV animals, animal research, animal testing, animal waste, grazing on public lands, raw-food diets, alternative medicine, hunting, population control, use of animals in sports, no-kill shelters, captive wild animals, and a million others that people will vehemently defend their side on.
There are many on that list that I myself have strong opinions on, but its my responsibility as a scientist and my benefit as a debater to approach conflict on this issues as discussions, not arguments. I’m not always the best at it, but I pride myself on my willingness to be proven wrong. I like to think that when shown data, presented in a clear and unbiased way, I can base my decisions on all the information presented, rather than simply reject new opinions. Terry Etherton had a few great posts about communicating with non-scientists, and how there’s a need to reach out even when you receive a poor response. This isn’t just a scientist vs. the lay public thing, this is for anyone who wants to be part of a productive discussion of these issues. Everyone is entitled to an opinion, but unless we listen to each other and work toward middle ground, nothing ever gets done.
With my little editorial finished, lets jump into this article on branding and microchip use in foals.
“For animal welfare reasons, many veterinarians are currently promoting the method of implanting a microchip over the traditional practice of branding, while officials of major sport horse breed registries deny that branding really causes pain or stress to foals.” (ScienceDaily, 2011)
I’m a big promoter of microchipping, it’s hardly an invasive procedure, and causes little more pain than a vaccine. At my animal shelter, almost all microchipped animals we received were reunited with owners, as long as the chip data was current. They’re especially great for cats, who have a knack of removing collars with identification information when lost, and are more likely not to carry identification in the first place. The data shows that microchipped animals are much more likely to be returned home from shelters than non-microchipped animals. I haven’t heard much about microchipping in large animals until now, but I can understand why there’s a debate there.
Microchipping would be a difficult identifier in any large group of horses, as you need to get within inches of the animals, and there’s no way to simply view the identification. Ear tagging is unwanted aesthetically in horses, which leaves branding as a useful permanent mark. Freeze branding is an option the article doesn’t discuss, but it’s expensive, not always recognized by the state, and will be less visible depending on the animal’s color. The University of Veterinary Medicine in Vienna has done a study concluding that hot branding causes more long term stress from the injury, assuming that the short term stress is mostly due to restraining procedures the foals must go through to be microchipped or branded. The fact remains however, that branding in many ways is superior to microchipping depending on the management of the animals.
The counter argument to using microchips is further strengthened by the comparing the procedure to other common practices with foals. Castration, tail docking, and (in cattle) polling can be considered far more traumatic, and have similar debatable merits depending on the management strategy. The article also mentions a tradition component that it doesn’t elaborate on. Many county fairs have branding competitions and branding is often made into an event in rural areas, implying that the tradition of branding animals has a cultural component independent of animal welfare.
While branding may be more stressful for the animals, I do not think that microchipping is an adequate replacement as the only means of identification in large animals. The specific purpose microchips serve well in companion animals doesn’t translate into the same needs we have for livestock. Hopefully another solution will eventually be available, but for now it seems that the use of brands, ear tags, and microchips will be determined by management, not its effect on the animal.
The first of a bunch of articles I recently picked out of JAVMA was interesting because while I never got any readings without some form of anesthesia, I imagine that hypertension was extremely common in many of the dogs I saw at Lapaw Animal Hospital. Whether it’s a result of obesity, illness, or hospital stress, systemic hypertension is usually an indicator of some other problem, and therefore important in the analysis of the patient.
The article is a bit confusing, because it goes into great detail the different potential causes of both hypertension and ocular lesions, and the significance of the data based on which was diagnosed first with each case. I began to lose track when on one hand they would mention that the data may be too biased to determine a cause and effect relationship between the two symptoms due to a preexisting condition, but then also said that those preexisting conditions had such a relationship. It does seem clear that ocular lesions are promoted by the presence of hypertension in both dogs and cats, while the disagreements in the literature are mainly in how much one is indicative of the other. The relationship of hypertension correlating with ocular lesions in cats has varied from 50-100%, which tallied with the frequency of 62% in this case review. While these frequencies don’t prove any sort of direct relationship, they do support the evidence we do have that hypertension can lead to ocular lesions, and that if one is discovered in a patient, it’s worth looking for the other.
This is the first case study I’ve looked at in detail, and I’ll certainly be reading more as I move into veterinary medicine. It was really interesting to me how they selected cases, and how thoroughly they reviewed the significance of possible bias in each case. I absolutely understand why it’s so important, and the way each patient is presented changes how each symptom is portrayed in relation to the others, which makes the range of values for this specific correlation so understandable. Owners are much more likely to bring their dog into the clinic when seeing a clouded or irritated eye
than hypertension would be found during a routine exam. Then you have to examine old clinic notes to see if other conditions led to either event, or to see if the veterinarian made the assumption that they were related, and though the situation was resolved, no lab work supports their theory. Some of the limitations mentioned in the study were the fact that they lad a low sample of normotensive dogs with ocular lesions, and that diagnosis of hypertension is difficult due to situational stress interpretation in the face of blood pressure values and varied measurements within the “grey area” of test results. They also did significant analysis within the cases that took into account patients that were taking anti-hypertensive drugs for other conditions, but mention that those patients might have skewed the data, because there is no way to ensure that there was owner compliance in administration.
An interesting note is that all 5 dogs in the study that were currently taking Phenylpropanolamine either acutely or chronically were all hypertensive, supporting anecdotal evidence that it can promote hypertension. This makes sense to me, as PPA is controlled due to its potential use in creating amphetamine, and its inclusion in many prescription stimulants (Adderall, etc.).
All in all, a good article, and a good look at the relationship between ocular findings and hypertension. Though a large part of me does feel for those research assistants at the University of Wisconsin School of Veterinary Medicine who combed through thousands of patient files to find these 65 cases.
Leblanc NL, Stepien RL, & Bentley E (2011). Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005-2007). Journal of the American Veterinary Medical Association, 238 (7), 915-21 PMID: 21453181
I enjoy looking at animal science from a public health perspective, but I usually just think about it in terms of zoonoses and food safety, I hadn’t dwelled too much about animal health being directly related to whether or not someone eats tonight.
It was apparently a big deal when the United Nations announced that Rinderpest was eradicated just a few months ago. Rinderpest is credited with speeding the fall of the Roman Empire, and for the bankruptcy and starvation of many farmers/communities in 3rd world or war-torn regions. Now that the attempted eradication of Rinderpest was successful, veterinary experts are recommending that the next target be “goat plague.”
Pest de Petits Ruminants or “goat plague” is a viral infection related to rinderpest that affects sheep, goats, and deer (important as vectors for the virus). It’s pretty nasty and comes with a host of upper respiratory symptoms, gastrointestinal upset, and causes characteristic lesions on the mouth, lips, and gums. Mortality and rates of transmission are high, so I understand why it would be such an issue in prevalent countries. Additionally, goats are the “poor mans cow”, meaning that disease afflicting goat stock generally will affect people who can’t afford to lose a portion of their herd to an outbreak of disease.
Some of the economic returns associated with the eradication of Rinderpest are pretty amazing, so it seems like PPR would be a reasonable next step. No one can argue that helping impoverished parts of the world feed themselves is a bad cause, and the economic benefits of helping other countries be more successful are far reaching. Many times I have to explain to friends and acquaintances of the roles that animal scientists and veterinarians play in public health through the USDA, and that’s just a product of how little people stop to think how their food gets to Safeway. I found that I also don’t stop to think that while I look at disease prevention from a profits and and animal welfare standpoint, in other areas of the world it can be a matter of life or death for the farmers themselves.
When I first started working in an actual clinic, I was blown away with the education I received in vaccine administration. Before at the shelter my instruction included solely how to administer them and not to be bitten while doing so. Spending a minute to educate clients on vaccine reactions, the steps we took to prevent them from happening, and the importance of the proper scheduling of a series were all new to me, and considering how seriously we took all these things, it vastly contrasted with my training at the shelter. How vaccines work has always been interesting to me, and the immunology involved isn’t terribly complicated on the surface. Even if the mechanisms escape me, I can still visualize the flowchart (something I wish I could consistently do with G-proteins, a crucial topic but one I constantly have to review).
Anyway, the point is I was really interested in this article. Bleeding calf syndrome is technically called bovine neonatal pancytopenia (BNP), but is probably still a frightening thing to see. It actually only emerged in 2007. The characteristic bleeding is caused by thrombocytopenia after the calf’s bone marrow becomes compromised. The lack of platelets causes the appearance of bleeding through the skin the name refers to. A group of doctors in Germany were able to determine the etiology of the condition (which has a calf mortality rate of 90%). Based on another study, they knew that the colostrum given to affected calves could also induce the symptoms in other unrelated calves, and after not finding evidence from pathogenic or genetic causes looked at an “immune mediated process” (Deutskens, 2011).
What they found was that there was a correlation between cows vaccinated for Bovine Viral Diarrhea Virus (BVDV) and calves suffering from BNP. After a lot of spectroscopy and protein identification, they found that the vaccine actually was the cause. What the issue was, is that the BVDV vaccine is made using kidney cells from cows, instead of another species (for example many human vaccines are cultured in pig cells). Here’s how that works: there is a specific protein “map” coating all nucleated cells that the immune system uses to identify which team they play for. Anything with a different protein coat is assumed to be foreign, and is attacked. This is the major reason why donated organs are rejected, because the donor has a slightly different “map” than you and your immune system assumes it’s trying to hurt you. With the vaccine grown in bovine cells, remnants or copies of this Major Histocompatability Complex (MHC, the “map”) are introduced to the mother, who has an immune response to them.
This is where it gets interesting, the antibodies the mother makes to attack this are called alloantibodies, and they don’t hurt the mother. They just become another antibody she reserves along with the ones that attacked the rest of the BVDV vaccine. None of her cells have that foreign “map”, so none of her cells need to worry about that extra antibody she created. However, the alloantibody gets stowed away in the colostrum along with all the others just before partuition, still ready to attack the MHC the vaccine was made with. If by coincidence the MHC of the calf is the same as the one in the vaccine cultures, then those alloantibodies given to the calf through the dam’s colostrum will attack cells within the calf, starting with blood cells and moving to the bone marrow. Making it technically not an auto-immune response, because it comes from a foreign immune system, but still a case of friendly fire. Those alloantibodies in the colostrum treat every calf cell featuring that MHC as if it’s an infection.
It should be noted that other vaccines for BVDV that are grown using non-bovine cultures do not cause these problems. This is because if the mother creates antibodies for the MHC of another species, there is no way that the calf can be affected by them. The authors of both the news article and the journal article mention that this serves as an example why same-species vaccine cultures and formation of alloantibodies should be avoided.
Check out the journal article for yourself, the introduction and discussion are well written and interesting. There’s also a similar alloantibody caused disease in humans called Neonatal Alloimmune Thrombocytopenia that’s interesting, the major difference being that the alloantibodies are introduced through the placenta instead of ingested through colostrum.
Deutskens F, Lamp B, Riedel CM, Wentz E, Lochnit G, Doll K, Thiel HJ, & Rumenapf T (2011). Vaccine-induced antibodies linked to Bovine Neonatal Pancytopenia (BNP) recognize cattle Major Histocompatibility Complex class I (MHC I). Veterinary research, 42 (1) PMID: 21878124
Madeline McCurry-Schmidt is a great writer, and like me, didn’t grow up in an animal science background. She writes for ASAS Graduate BULLetin and does a great job of detailing her experience and providing great information for graduate students, including job postings! I also discovered the American Society of Animal Science through her site, and am now an undergraduate member. I probably won’t be able to take advantage of many of the benefits, but for undergraduates, membership is free, so you have nothing to lose by joining.
Anyway, after reading some of her stuff, I asked Madeline if I could write a guest post for the Graduate BULLetin and she was kind enough to publish it. So feel free to go read it there, and check out some of the other great content on her site.
Well, it’s about time I mentioned an article I didn’t particularly enjoy on here. It’s not like I think it’s a waste of paper, it’s an important topic, but it does nothing creative and does little to contribute to the understanding of the subject. The article looks at the effects of different rates of Lactated Ringers Solution administered while under isoflurane anesthesia. It uses healthy animals, discusses well documented effects in humans, and just reinforces common practice.
Lactated Ringers is the most frequently prescribed fluid for maintenance of homeostasis in surgery and pretty much any other health stress event. I know when any patient wasn’t feeling well from any situation at my clinic, we always administered LRS either through a catheter or subcutaneously for outpatients, the dosage based on weight and severity of condition. We know how to use it, and it’s gotten a proven history of effectiveness in both humans and animals. The article justifies itself by saying that fluid therapy in dogs is largely based on human evidence, and that the formulas we use to determine rates have not been thoroughly investigated. Yet throughout the article they repeatedly compare their results to similar studies, and make no conclusions that aren’t already accepted in human and animal medicine. Additionally, the gaps in the literature they identify can’t even be answered using the methods and results of this study, so you can’t use them to justify its existence.
So the big conclusions they determined were that providing LRS increased plasma volume and cardiac output, didn’t increase urine production, and appears to leave the blood volume and remain in extracellular space. These are important points, but they were accepted unanimously without the presence of this study. Further, if their goal was to confirm these assumptions, their results are pretty much irrelevant with a sample size of only 8 animals, all in perfect health, similar size (26-41 lbs isn’t a lot of variance in the world of dogs), and undergoing no medical stress other than common anesthesia and mechanical ventilation.
My impression after finishing the paper was that the people at QTest labs (associated with Ohio State University College of Veterinary Medicine) needed a study to do, needed to get a grant proposal ready, and did enough research on the subject to sell this trial. It’s well written and the authors do a great job of placing their results in context of the literature, mostly because it all agrees. But it can’t hide the fact that it does nothing revolutionary other than providing history on the subject, and giving an excellent account of the methods used in the study. With such great, specific, and controlled procedures, this facility could be solidifying other theories that have conflicting data, if they’d use a sample size large enough. I’m sure that they don’t always do milk run trials such as this one, and I look forward to seeing their name again in future articles.
William W. Muir III, Anusak Kijtawornrat, Yukie Ueyama, Steven V. Radecki, & Robert L. Hamlin (2011). Effects of intravenous administration of lactated Ringer’s solution on hematologic, serum biochemical, rheological, hemodynamic, and renal measurements in healthy isoflurane-anesthetized dogs JAVMA, 239 (5), 630-637