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Biomedical subjects

D Mitchell

Publications and source records attributed to D Mitchell.

At least 325 records · Page 18Linked to original sources
PubMed1977

Motion sickness-induced pica in the rat.

Two experiments investigating the effects of motion sickness on pica (the consumption of non-nutritive substances) are reported. In the first experiment rats subject to rotational stimulation subsequently engaged in geophagia (clay consumption). In the second experiment use of a conditioned aversion paradigm confirmed that the method of rotational stimulation used in the first experiment causes motion sickness in rats. The results of these experiments indicate that simple gastrointestinal malaise in the absence of a deficiency state or acute toxemia will elicit pica. It is suggested that gastrointestinal distress may be a significant factor in the etiology of pica and its relationship to other causes of pica is discussed.

Animals↗
PubMed1977

Effects of prostaglandin antagonism on sodium arachidonate fever in rabbits.

1. Sodium arachidonate, the prostaglandin precursor substance, when injected intraventricularly into rabbits, results in dose-dependent hyperthermia, which is rapid in onset and of several hours duration. 2. Arachidonate fever was inhibited by intraventricular injection of indomethacin, but not by the simultaneous intraventricular injection of either of the two prostaglandin antagonists SC 19220 or HR 546. 3. Both antagonists effectively inhibited the fever induced by the intraventricular injection of an equipotent dose of PGE1. 4. Our results show that a derivative of arachidonic acid other than prostaglandin is pyrogenic.

Animals↗
PubMed1976

Experiments on neophobia in wild and laboratory rats: a reevaluation.

Two experiments using food-container avoidance as an index of neophobia are reported for two strains of laboratory and one strain of wild rats. In Experiment 1 rats were fed from a single familiar container until their consumption had stabilized. Upon replacing the familiar container with a novel container, the latency of all three strains to begin feeding increased. In Experiment 2 rats were offered a choice between a familiar and a novel container containing identical food. Though there was considerable individual variation among the three strains, the wild strain was more reluctant to eat from the novel container than a hooded laboratory strain, which, in turn, was nore reluctant than an albino laboratory strain. Nonetheless, all three strains showed an initial avoidance of the novel container. It was concluded that both wild and laboratory strains are neophobic and that strain differences are ones of degree, not of kind.

Animals↗
PubMed1976

Thermoregulation in rabbits during fever.

1. We have studied the effect of fever on the efficacy of the thermoregulatory control system in conscious rabbits. 2. The control system was challenged by a series of systemic thermal loads produced by the intravenous infusion of hot or cold isotonic solutions. The time integral of the consequent upward or downward displacement of brain temperature was used as an index of the response of the control system. Steady-state fever was induced by intravenous infusion of plasma containing leucocyte pyrogen. 3. With cold loads there was a linear relation between load and response. The regression coefficients were not significantly changed by fever in any of the six rabbits. Wth hot loads given to afebrile rabbits the regression of response on load was generally not statistically significant, but the responses were not demonstrably greater in the febrile state. 4. We were not able to demonstrate impairment in the capacity of the febrile animal to compensate for systemic thermal loads.

Animals↗
PubMed1976

Evidence that brain prostaglandin synthesis is not essential in fever.

1. We have tested the hypothesis that a fever caused by pyrogen depends upon the synthesis of prostaglandin E in the brain and that the prostaglandin in turn acts on the hypothalamus to produce fever. 2. In rabbits, fever was produced by the injection of leucocyte pyrogen in a lateral cerebral ventricle. The latency, rate of rise and magnitude of the fever was unaffected by the simultaneous intraventricular injection of two prostaglandin antagonists, SC 19220 and HR 546. 3. Both antagonists effectively attenuated the fever caused by the intraventricular injection of prostaglandin E2. 4. This evidence is not consistent with the hypothesis that prostaglandin E is the principal mediator of fever.

Animals↗
PubMed1976

Acclimatization in a hot, humid environment: energy exchange, body temperature, and sweating.

Four trained young men, worked for 4 h/day at 43-50% of their maximum aerobic capacity for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Their thermal status was assessed using direct calorimetry. As a group, the men showed classical acclimization responses, but there were marked individual differences. The calorimetric analysis revealed that reductions in strain were associated with minor changes in heat balance confined to the first and last hours of exposure. Events occurring within the first 4 days appeared to have little effect on body temperatures. Significant decreases in body temperature took place only when sweat and evaporation rate increased. A 10% increase in evaporation rate was accompanied by a 30% increase in sweat rate and a 200% increase in unevaporated sweat; thus, there is a wasteful overproduction of sweat. By the 10th day skin temperature was confined to the level necessary to evaporate sufficient sweat to achieve thermal balance with a fully wet body surface. The efficiency of heat transport within the body did not change with acclimatization.

Acclimatization↗
PubMed1976

Acclimization in a hot, humid environment: cardiovascular adjustments.

Four trained young men worked for 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb, and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. This portion of the study was mainly concerned with central circulatory changes during acclimatization. The central circulatory adaptation to work in heat could be divided into four distinct phases: phase I (day 1) was characterized by a progressive fall in stroke volume (SV) during heat exposure but cardiac output (CO) was maintained above control values by high heart rates. Phase II (days 2 and 3) was marked by increases in SV ande decreases in heart rate but with little change in CO from phase I. During phase III (days 4-8 of acclimatization), CO increased due to increases in SV. Phase IV (days 6-8) was associated with decreases in rectal and skin temperature towards control levels. SV and HR both decline in this phase so that CO was not elevated greatly above control levels. The results indicated that central circulatory and temperature regulating events are not casually associated in acclimatization.

Acclimatization↗
PubMed1976

Acclimatization in a hot, humid environment: body fluid adjustments.

Four trained men worked 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Between days 1 and 2 of heat exposure mean total circulating protein (TCP) and plasma volume (PV) increased 11.6% and 9%, respectively. Preexposure TCP and PV increased until day 6 of heat exposure. Of the protein fractions beta-globulins underwent the largest relative increase. During work movement of protein into and out of the vascular compartment was similar in control and acclimatizing subjects but the latter generally maintained a greater amount of protein and fluid within the vascular volume. There was no evidence of salt and water retention. The increase in vascualr volume was ascribed to transfer of interstitial protein and water to the vascular volume. Regression coefficients indicated significant correlations for changes in plasma volume versus heart rate, stroke volume, and cardiac output during acclimatization. It was concluded that the most critical event in heat acclimatization is the expansion of the plasma volume.

Acclimatization↗
PubMed1976

Meningoencephalomyelitis in horses associated with equine herpesvirus 1 infection.

During an outbreak of abortion caused by equine herpesvirus 1, a neurologic disease characterized clinically by dullness and ataxia occurred in several mares. Equine herpesvirus 1 was isolated from brain and lung of two severely affected mares. Histologically, both mares had disseminated meningoencephalomyelitis characterized by necrotizing arteritis, focal malacia in grey and white matter of brain and spinal cord, and accumulation of lymphocytes and neutrophils in paravertebral ganglia. Eosinophilic intranuclear inclusion bodies occurred in foci of necrosis in thyroid adenomas of both mares.

Abortion, Veterinary↗
PubMed1976

Abnormal regulation of plasma pyridoxal 5'-phosphate in patients with liver disease.

UNLABELLED: Pyridoxal 5'-phosphate (PLP), the coenzyme form of vitamin B6, is essential for many biochemical reactions in the body. Studies in experimental animals have suggested that the liver is a primary site for the formation of PLP circulating in the plasma, and that it may also participate in its degradation. This study evaluates, for the first time, the effects of liver disease in man on the regulation of plasma PLP. The plasma PLP level was measured before and sequentially after the rapid intravenous administration of 50 mg of pyridoxine to patients with alcoholic cirrhosis, acute hepatitis, and extrahepatic obstruction, and to normal control subjects. The base line plasma PLP concentration was significantly lower in cirrhotic patients than in normal persons (P less than 0.025), and there was a tendency for it to be reduced in patients with extrahepatic obstruction. After administration of pyridoxine there was a significant increase in the plasma PLP level over a 2- to 12-hr period, after which the concentration returned gradually toward the initial value. The area under the concentration/time curve was from 2 to 8 times smaller (P less than 0.002) in the patients with liver disease. To assess possible mechanisms of this change, 5 mg of PLP were intravenously administered to the various patient groups and the pharmacokinetics of the disposition were assessed. The initial and steady state volumes of distribution of PLP were comparable in cirrhotics and controls (P greater than 0.05), but the clearance of plasma PLP in cirrhotics was much faster (63.0 +/- 7.4 versus 31.7 +/- 2.7 ml per min, P less than 0.004). Similar findings were obtained in the other liver disease subjects. The in vitro plasma binding of PLP at supracirculatory concentrations was comparable in cirrhotics and controls (99.4 versus 99.5%, P greater than 0.05). IN CONCLUSION: (1) plasma PLP regulation in patients with liver disease is abnormal, (2) a significant factor in the decrease in plasma PLP after intravenous pyridoxine administration in these patients appears to be an increase in the total plasma clearance of the coenzyme, and (3) it is postulated that this may be due to increased degradation of PLP by the diseased liver.

Acute Disease↗