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Biomedical subjects

C V Gisolfi

Publications and source records attributed to C V Gisolfi.

At least 91 records · Page 5Linked to original sources

New apparatus for exercising a monkey seated in a primate chair.

A new apparatus and method for exercising a monkey seated in a primate chair are described. The apparatus consists of a set of hand and foot bars mounted at either end of a rocker arm that pivots in a vertical plane. This arm is connected by a steel cable to a wooden box that houses lead weights. By simultaneously pushing the foot bar and pulling the hand bar, the monkey lifts a weight and triggers a microswitch which releases a banana-flavored food pellet into a well close to the animal's mouth. The amount of work performed is varied by changing the a) amount of weight to be lifted, b) distance the weight must be lifted, or c) number of times that the animal lifts the weight for a single reward. During 30 min of exercise, the heart rate of a given monkey rose 120 beats/min, respiratory rate 24/min, and colonic temperature 1.2 degrees C above base-line values. Total work performed in 30 min varied from 250 to 360 kpm. Major advantages of this apparatus over a treadmill or bicycle ergometer are that the animal 1) is restrained sufficiently to permit the delicate experimental manipulations and physiological measurements, 2) can be exercised strenuously in a quantitative fashion, and 3) is readily trained to perform the task in a short time.

Animals↗

Work-heat tolerance of distance runners.

Physical training in a cool environment by subjects not previously trained improves their work-heat tolerance, but can not replace heat acclimatization to the standard heat stress conditions employed by a variety of investigators. This is attributed to the inability of these subjects to sustain prolonged work at high metabolic rates. Thus, they are not maintaining high core body temperatures long enough to bring about an adaptive change to heat. On the other hand, the intense and prolonged (years) training of long distance runners in a temperature environment at high metabolic rates has acclimatized them for at least 4 hours of mild work (MR 160 kcal/m2-hr) in both hot dry (50/27 C db/wb) and hot wet (36.7/33.1 C db/wb) environments, but not for work at high energy expenditures (MR 540 kcal/m2-hr) in a less severe thermal stress (35/21 C db/wb). These highly trained athletes can improve their work-heat tolerance at high metabolic rates in a warm climate by training at competitive speeds in a cool environment dressed in sweat clothing or by training at near competitive speeds in the heat. In either of these situations the athlete is cautioned to consume water at frequent intervals to offset the dehydration associated with excessive sweating under these conditions.

Acclimatization↗

Diencephalic efflux of calcium ions in the monkey during exercise, thermal stress and feeding.

1. The diencephalon of the unanaesthetized macaque monkey was radio-labelled with calcium by a microinjection of 6-8 muC (45)Ca(2+) into the third cerebral ventricle through a permanently implanted cannula. Successive 5 min push-pull perfusions of the mid-line hypothalamic region with an artificial C.S.F. were carried out at a rate of 28 mul./min every 20 min. A washout curve of declining (45)Ca(2+) radioactivity was thus generated.2. When the monkey exercised strenuously on a special ;rowing machine' to obtain highly palatable banana pellets, its body temperature rose sharply. As the monkey exercised, during a sequence of push-pull perfusions, the concurrent efflux of (45)Ca(2+) ions increased markedly in the corresponding samples of diencephalic perfusate. This enhanced activity of calcium ions continued throughout a 30 min work period and persisted as long as the monkey's temperature was elevated in the interval immediately following exercise.3. Exposure of the monkey's trunk, between neck and thigh to cold air of 5 degrees C likewise augmented the amount of (45)Ca(2+) ions in the diencephalic push-pull perfusates; however, a similar exposure to air warmed to 35 degrees C failed to alter the pattern of (45)Ca(2+) efflux from the animal's diencephalon. If a fasted monkey consumed only the banana pellets but was not exercised, the level of (45)Ca(2+) in the perfusate also increased transiently, just at the onset of feeding.4. We conclude that a local change in calcium transport, binding or other cellular activity of the cation within the diencephalon could play an important role in the central mechanism underlying the set-point rise in a primate's temperature which accompanies vigorous exercise. Further, the results support the idea that this cation functions in the diencephalic control of metabolic heat production as well as in the overall processes of energy metabolism, particularly in relation to feeding.

Animals↗

Thermal responses to intermittent work in selected enironments.

Acclaimed subjects exercised intermittently for 8 hrs in 25 to 50 degrees environments. Thermal and metalobic determinations were made. Results showed the time-weighted WBGT heat strain index for intermittent work needs re-evaluation. For acclimated subjects working steadily at 350 kcal/hr, 30% max, the ULPZ is more than 33% WBGT.

Acclimatization↗

Autonomic effects of central injections of D-Ala2-Met-enkephalinamide (DAME) in the conscious monkey.

The use of naloxone (NAL), an opioid receptor antagonist, has provided indirect evidence that endogenous opioids contribute to cardiovascular depression during shock. To determine if endogenous opioids act centrally to influence cardiovascular function, injections of D-Ala2-Met-enkephalinamide (DAME), a potent Met-enkephalin analog, were made into the 3rd cerebral ventricle (ICV) of 5 conscious cynomulgus monkeys restrained in primate chairs. Systolic blood pressure (SBP) and heart rate (HR) were determined every 10 min during a 30-60 min control period and for up to 5 hr post-injection. Colonic temperature (Tc) was monitored continuously. SBP declined from baseline values with 50 and 100 micrograms (85.2 and 170.4 nM) doses but was significant (p less than 0.001) for only the 100 micrograms dose between 15-125 min post-injection. HR also decreased but did not exhibit any significant variation with time. However, when averaged across time, HR fell significantly (p less than 0.001) from baseline: -9.1 +/- 2.3 and -15.0 +/- 2.1 b/min for 50 and 100 micrograms DAME, respectively. Tc displayed a nonsignificant, delayed (greater than 2 hr) rise in Tc with the 50 micrograms dose, whereas the 100 micrograms dose caused a significant (p less than 0.001) decline in Tc (from 65-125 min post-injection). NAL injected ICV attenuated the effects of DAME but had no effect on SBP, HR or Tc when injected alone. Systemic injection of DAME (300 micrograms) in one monkey produced a transient decline in SBP (26 mmHg within 2 min) which returned to baseline values 4 min post-injection. HR and Tc were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of opiate receptor drugs injected intracerebrally into the normovolemic and hypovolemic monkey.

Systemic injection of naloxone (NAL), an opioid-receptor antagonist, significantly elevates systolic blood pressure (SBP) in anesthetized hypovolemic monkeys, providing indirect evidence that endogenous opioids contribute to cardiovascular depression during shock. The purpose of this study was to identify specific centrally located opioid receptor sites that participate in SBP regulation under normovolemic and hypovolemic conditions. In 6 monkeys, bilateral guide cannulae were stereotaxically implanted above areas ranging from the diencephalon to the lower medulla. Microinjections (1 microliter) of D- Ala2-Met-enkephalinamide (DAME) (3.4-27.2 nM) into normovolemic unanesthetized monkeys reduced SBP by 10-65 mm Hg in a dose-related fashion. Subsequent injection of NAL (12.2 nM) attenuated this hypotensive response. Heart rate fell 20-40 bpm with DAME, but not in response to dose. In the anesthetized animal rendered hypotensive (SBP = 45 mm Hg) by hemorrhage. NAL injected into predetermined DAME-sensitive sites failed to increase SBP more than 5 mm Hg. Even consecutive injections into multiple sites elevated SBP only 20 mm Hg. We conclude that the centrally located opioid-sensitive sites tested exert only a mild influence in mediating hemorrhagic hypotension.

Animals↗

Feeding and body temperature in the rat: diencephalic localization of changes produced by excess calcium ions.

In the unanesthetized rat, Ca++ ions in solutions ranging from 2.6 to 112.0 mM in excess of the normal level in CSF were applied at different sites in the brain and by three separate procedures, Colonic temperature was monitored and in certain experiments, the amount of food pellets and water consumed was measured simultaneously following the administration of excess Ca++ ions. An infusion into the lateral cerebral ventricle of excess calcium in a volume of 5.0 mul produced a concentration-dependent hypothermia, This fall in temperature was not attenuated by a prior intraventricular infusion of mecamylamine and often enhanced by atropine. Depending on the site, a microinjection of excess Ca++ ions in a volume of 0.5 to 1.0 mul directly into the hypothalamus produced hypothermia or feeding. The sites of maximum sensitivity at which excess calcium caused a decline in temperature were clustered in the caudal hypothalamus, whereas those at which calcium elicited feeding were distributed widely in caudo-lateral, medial and rostral hypothalamic areas. Push-pull perfusions at a rate of 20 to 25 mul per min for 10 to 20 min at homologous sites caused similar responses but the cation concentration required to evoke feeding or hypothermia was significantly less than that of either microinjection or intraventricular infusion. These findings demonstrate species continuity in the rat concerning anatomical localization of the postulated set-point mechanism for body temperature. Several different pathways in the feeding system are affected by an alteration in the hypothalamic level of calcium.

Animals↗

Influence of EGTA on an exercise-induced elevation in the colonic temperature of the rat.

The purpose of this study was to determine if an exercise-induced rise in body temperature could be affected by the chelation of Ca++ in the extracellular fluid surrounding the hypothalamus of the rat. Following the implantation of a guide tube above the hypothalamus, each animal was familiarized with exercising on a motor-driven treadmill. In random order, on separate days, a solution containing 3.6 mM EGTA, 26 mM Ca++ or an artificial cerebrospinal fluid (ACSF) solution was perfused through the guide tube while the animal was running. Colonic (Tc) and tail-skin (Tt) temperatures were monitored continuously. The perfusion of EGTA produced a significant increase in Tc when compared with the perfusion of the ACSF solution. The perfusion of excess Ca++ produced a significant decrease in Tc. These results suggest that Ca++ may play an important role in the mediation of heat dissipation during exercise.

Animals↗