World Laboratory Animal Liberation Week 2007

Tuesday, April 24th, P.O.E.T. demonstrated against the use of animals in experimentation on the OSU campus.

Where: Biomedical Research Tower (map with building shown) located at 460 W. 12th Ave.

The Research Tower, which opened on Nov. 3rd with a dedication and protest by members of P.O.E.T., has remained empty of animals due to problems with setting up the vivarium including water damage.

Animals have yet to be moved into the vivarium.

Last year OSU used 9,100 rats and 98,506 mice in experimentation. A large number of the mice are not even used in the final experiment, because they are transgenic animals and their genes do not match the experimental criteria. The animals are killed. The Tower will be the location for much of the transgenic work that will occur on campus.

We received coverage from News Center which is the ABC and Fox affliate. There was live coverage at 12:30 and other stories ran on the evening and late news. We were able to highlight the cats are being killed for an EMT course. OSU attempted to change the subject by saying they didn't know for sure if the cats were killed (which THEY ARE) and claimed that simulators are used before the cats. If you read the justification for using animals in this lab, simulators do not enhance job performance so why would they be used at OSU. Even though plenty of other locations use simulators. More information can be found at http://www.poetwill.org/cat_intu.htm

Another experiment covered was Billman and his running dogs on a treadmill, giving them a heart attack, and soon after they are killed. Click here to read more information about the current renewal of one of his experiments.

Dr. Billman published a paper in 2006, A comprehensive review and analysis of 25 years of data from an in vivo canine model of sudden cardiac death: Implications for future anti-arrhythmic drug development.

The paper is a summary of all his work over the last twenty-five years of killing dogs. Some highlights:

In 1980, I joined the laboratory of Dr. H. Lowell Stone, and together with Dr. Peter Schwartz, we developed a canine model of sudden cardiac death

A detailed description of this canine model has been recently published (Billman, 2005). Therefore, the following paragraph contains only a brief description of the model. After 3–4 weeks of recovery period following the surgery and myocardial infarction, the animals learn to run on a motor-treadmill (usually over 3 or 4 days). The susceptibility to VF is then assessed using an exercise plus ischemia test. The animals run on a motor-driven treadmill for 15–18 min until a criterion heart rate of 210 beats/min has been achieved ( 70% of maximum heart rate). The workload is increased every 3 min during this test (initial level, 0% grade 4.8 kph, 0% grade 6.4 kph, 4% grade 6.4 kph, 8% grade 6.4 kph, 12% grade 6.4 kph, and finally, 16% grade 6.4 kph). During the last minute of the exercise the left circumflex occluder is inflated, the treadmill is then stopped and the occlusion maintained for an additional minute. The occlusion therefore lasts 2 min: 1 min during exercise and 1 min post exercise. This allows for the differentiation of arrhythmias induced during exercise, post exercise, and post occlusion release. The occlusion is immediately released in those animals that exhibit ventricular tachyarrhythmias (most frequently ventricular flutter that rapidly deteriorates into VF). Large flexible metal pads (approximately 11-cm diameter) are placed across the animal's chest and are connected to an external defibrillator. A major advantage of this model is the identification of 2 highly reproducible and stable populations of animals: those resistant and those susceptible to VF (Billman et al., 1982, Schwartz et al., 1984 and Billman, 2005).

To date, I have produced an anterior wall myocardial infarction in a total of 768 animals (male, n = 287; female, n = 481) (Fig. 1). Two hundred and thirteen (27.7%) dogs died acutely either during surgery or usually within the next 4 days following surgery. The distribution of the timing of the early mortality is displayed in Fig. 2. The majority of the dogs died either during surgery (n = 90) or within the first 24 hr (n = 52) after the myocardial infarction. Over the years the survival rate has improved, as highlighted by comparing the results from the first 100 animals with studies completed on the most recent set of 100 dogs. Thirty of the first 100 dogs died before studies began (13 died during surgery) while only 19 dogs in the most recent set of 100 dogs died acutely (only 2 died during surgery). Thus, like mastering a complex piano sonata or learning a new language, practice makes perfect.

Although, during the last 25 years, the canine model of sudden cardiac death described in this article has provided invaluable information concerning factors involved in VF, there remain many unanswered questions. The mechanisms responsible for VF at the cellular and subcellular level remain largely to be determined. It, therefore, is very likely that this canine model for sudden death will continue to stimulate new research and produce interesting results for the next 25 years.

Well not if we have any say in the matter. Expect more demonstrations to take place in the near future.

Thursday, April 26th, we demonstrated outside of the Math building . We highlighted the use of non-human primates in experiments being conducted at OSU and The University of Utah. (http://www.poetwill.org/primates_usage.htm)

WOSU conducted a radio interview which ran in the afternoon. On note the Math building is directly across from the Journalism building and were the Lantern is published. No one from the paper came out to take a photo or conduct an interview. One protester went to the Lantern offices and noted that we were demonstrating. They were aware but declined to do any story.

Dr. John Buford arrived at OSU in 1999 and since his arrival has been conducting experiments on
primates to study carpal tunnel syndrome and study movement (reaching).

Goggle carpal tunnel syndrome and you'll find many articles discussing what can be done to prevent the
disorder. But at OSU they create primates with carpal tunnel syndrome.
Attending the ILACUC meeting (2/24/06) we learned that Dr. Buford requested a change of primate from
cynomolgous monkeys to rhesus monkeys because their muscles and brain are larger and provide precise
locations of tracer injections. Does that mean his previous work was NOT precise? A statement in a recent
Columbus Dispatch indicated that maybe that is true.
The monkeys, a species related to rhesus monkeys known as fascicularis, are killed and their
brains dissected after the research so Buford knows he has recorded activity in the correct part
of the brain. (3/13/05 - Primate research slow but not stopped - Dispatch)

This week, a primate experimenter from The University of Utah, is delivering a series of lectures at OSU.
While her field of research is vision, both researchers use primates to simulate human conditions.

A review of published papers by Alessandra Angelucci, indicates that holes are drilled into the primates
skulls (as in Buford's primates to attach electrodes) and then strapping the animal to a chair in front of a
screen displaying light patterns to test the brain's responses. Pretty much the same technique Buford uses
on his primates except:

"... the monkey began the trial by waiting in the start position, and then an instruction (target
cue) was presented to direct movement to one of the 4 targets. The monkey was then given the
movement cue and he subsequently moved to contact the correct target and held his hand on the
target until the reward was given. After the reward, a new trial began."

Both animal researchers kill their primates at the end of the experiments to verify correct placement of electrodes, etc.