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Biomedical subjects

E M Stricker

Publications and source records attributed to E M Stricker.

At least 145 records · Page 8Linked to original sources
PubMed1979

Thermal homeostasis in pregnant rats during heat stress.

Rats exposed to inescapable heat stress maintained a controlled hyperthermia while increasing heat loss by cutaneous vasodilatation and by grooming behavior. In nonpregnant rats, the evaporation of saliva groomed onto the body surfaces increased exponentially as a function of ambient temperature above 36 degrees C. This was associated with a decrease in the body temperature threshold for salivary secretion from the submaxillary gland, which then began at approximately the same body temperature as cutaneous vasodilatation. In addition, the pregnant rats maintained a lower level of controlled hyperthermia during heat stress than did nonpregnant rats. This appeared to result from a decreased production of metabolic heat, reduced insulation on the ventral surface, and an increased motivation to keep cool during heat stress. These changes met the increased need for thermolysis during pregnancy and provided for thermal homeostasis both in the pregnant rat and in the unborn fetuses.

Animals↗
PubMed1979

Acute homeostatic imbalances reinstate sensorimotor dysfunctions in rats with lateral hypothalamic lesions.

It has previously been demonstrated that rats recovered from aphagia and adipsia after large bilateral electrolytic lesions of the lateral hypothalamic area do not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glyol. The present work reveals that such homeostatic imbalances reinstate the profound sensorimotor impairments that are seen in the immediate postoperative period but abate in parallel with the gradual recovery of ingestive behaviors. Administration of alpha-methyltyrosine or spiroperidol produced sensory and motor dysfunctions in rats with lateral hypothalamic lesions that were similar to those observed after 2-deoxyglucose. These results suggest that the residual feeding and drinking deficits of rats with lateral hypothalamic lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. Instead, they may indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons.

Animals↗
PubMed1979

Renin and aldosterone secretions during hypovolemia in rats: relation to NaCl intake.

Plasma renin activities (PRA) and aldosterone concentrations increased in parallel over a wide range of plasma volume deficits produced in unanesthetized rats by extravascular administration of polyethylene glycol (PEG) solution. When PEG-treated rats were given water to drink, their intakes were proportional to PRA; when given water and 0.5 M NaCl, PRA and the steroid concentrations diminished concurrently in association with sodium consumption. Aldosterone concentrations and NaCl intakes were markedly enhanced after PEG treatment in rats maintained on a sodium-deficient diet for 4 days. On the other hand, a clear relation between PRA and water intake, and between circulating aldosterone levels and sodium intake, was not suggested by other experiments in this series. For example, bilateral nephrectomy abolished the rise in PRA during hypovolemia yet rats drank water normally. Moreover, aldosterone concentrations were substantially elevated by PEG treatment in the nephrectomized rats yet sodium appetite was abolished. These and other findings suggest that neither angiotensin nor aldosterone plays a prominent role in stimulating water and saline intakes during hypovolemia.

Aldosterone↗
PubMed1978

Hyperphagia.

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Animals↗
PubMed1978

Hepatic versus cerebral origin of stimulus for feeding induced by 2-deoxy-d-glucose in rats.

Intravenous administration of 2-deoxy-D-glucose (2-DG), a competitive inhibitor of glucose utilization, increased the food intake of rats. Infusions of glucose or mannose abolished this effect, whereas equimolar fructose solutions did not affect 2-DG-induced feeding. Similar results were obtained when 2-DG and the hexoses were administered into the hepatic portal vein. These findings suggest that 2-DG elicits feeding due to glucoprivation at a site that is inaccessible to fructose. This site is likely to be in the brain, not the liver, because all three sugars can nourish peripheral tissue but only fructose cannot penetrate the blood-brain barrier. Moreover, 2-DG-induced feeding was abolished by intravenous infusion of beta-hydroxybutyrate, a substrate that can be oxidized by brain and other tissues but not by the liver.

Animals↗
PubMed1978

Osmoregulatory thirst in rats after lateral preoptic lesions.

In confirmation of previous observations, lesions of the lateral preoptic area in rats abolished water ingestion during a 4-hr test following an intraperitoneal injection of hypertonic NaCl solution. However, it was observed that these animals increased their water intakes when tests were prolonged to 24 hr and drank almost exactly what they needed for osmoregulation. Furthermore, they increased their water intakes normally when NaCl was given in their diet, when NaCl was administered intravenously, or when they were water deprived and given preloads of isotonic saline to remove hypovolemia. These findings indicate that rats with lateral preoptic lesions do experience osmoregulatory thirst, and consequently, they raise new doubts about whether osmoreceptors located in the lateral preoptic area mediate thirst following the administration of osmotic loads.

Animals↗
PubMed1978

Water and NaCl intake after furosemide treatment in sheep (Ovis aires).

Intravenous infusion of the natriuretic drug furosemide in sheep led to the excretion of large quantitites of hypotonic urine. The sheep consumed more water than was needed simply to restore osmotic equilibrium. The stimulus for the additional intake was presumably hypovolemia resulting from the loss of sodium in urine. Despite the natriuresis, in only 2 of 15 experiments did sheep drink significant amounts of .5 M NaCl solution during the first 10 hr after the onset of furosemide treatment, and hemoconcentration and arterial hypotension were evident during this time. By 24 hr, however, the saline consumption in all but three experiments had increased and compensated adequately (together with the water intakes) for the furosemide-induced loss of sodium-rich fluid in urine. These results provide evidence that following acute hypovolemia in sheep, as in rats, the onset of sodium appetite is delayed relative to the appearance of thirst.

Animals↗
PubMed1978

The renin-angiotensin system and thirst: some unanswered questions.

Recent experiments dispute the significance of four findings that usually are cited to support the hypothesis that angiotensin is a natural dipsogen. First, although administration of exogenous renin consistently increases water intake, the plasma renin activities that are produced seem to be outside of the normal physiological range when the elicited drinking is substantial. Second, although plasma renin activities are elevated following caval ligation, colloid, or isoproterenol treatment, this activity of the renin-angiotensin system appears to account for only a small portion of the observed water intake. Third, although bilateral nephrectomy abolishes the water intake that otherwise occurs after caval ligation or isoproterenol treatment, the observed blood pressure appears to be so low as to preclude drinking behavior. Finally, although drinking can be stimulated in these hypotensive rats by various treatments, in each case a pressor response also is observed that might have restored the ability to drink. These new observations have provoked a reevaluation of the circumstances in which endogenous angiotensin stimulates thirst and the magnitude of its contribution then. At present, there is no persuasive evidence that the renin-angiotensin system normally plays a direct and substantial role in mediating the ingestion of water or saline.

Angiotensin II↗
PubMed1977

Caffeine restores feeding response to 2-deoxy-D-glucose in 6-hydroxydopamine-treated rats.

A large portion of the central catecholaminergic nerve terminals of the rat are destroyed by administering 6-hydroxydopamine (6-HDA) via the cerebrospinal fluid. Animals lesioned in this way often appear normal, yet show many subtle behavioural abnormalities. We have been examining one example of this phenomenon, the failure of 6-HDA-lesioned rats to increase food intake when given a systemic injection of 2-deoxy-D-glucose (2-DG) (refs 5, 6). This glucose analogue seems to elicit feeding in intact rats due to its inhibition of glycolysis in cerebral chemoreceptor cells. We have proposed that lesioned animals do not eat because of an insufficient central catecholaminergic response to the severe decrease in glucose utilisation induced by 2-DG (ref. 10). If so, then pretreatments which serve to augment this neurochemical response might be expected to reinstate behavioural function. Consistent with this hypothesis, very large increases in telencephalic tyrosine hydroxylase activity in 6-HDA-lesioned animals, which occur following chronic insulin treatment, are associated with the restoration of 2-DG-induced feeding. Many of the physiological effects of catecholamines in the sympathetic nervous system seem to be mediated by an increase in the cyclic AMP concentration of the target cells. Methylxanthenes, such as caffeine and theophylline, inhibit phosphodiesterase, prevent cyclic AMP degradation, and thereby potentiate the catecholamine-stimulated rise in cyclic nucleotide. They also enhance many of the behavioural and physiological effects of catecholamines, presumably by the same mechanism. We therefore sought to determine whether the acute administration of those sympathomimetic agents, in intact and 6-HDA-lesioned rats, also would potentiate 2-DG-induced feeding, a behaviour that seems to be mediated, in part, by central catecholaminergic neurons. We report that caffeine restores the 2-DG-induced feeding response.

Animals↗
PubMed1977

Homeostasis during hypoglycemia: central control of adrenal secretion and peripheral control of feeding.

Intravenous infusions of manose or B-hydroxybutyrate, metabolic fuels which can be oxidized by brain, abolished adrenal discharge of epinephrine in rats during insulin-induced hypoglycemia, whereas infusion of fructose, a sugar which does not cross the blood-brain barrier, did not. In contrast, increased feeding behavior during hypoglycemia was prevented both by the sugars and by B-hydroxybutyrate. Thus, while the sympathetic response during marked hypoglycemia may have been initiated by alterations in cerebal metabolism, the feeding response evidently was not, and a decrease in the utilization of glucose per se does not appear to be the critical stimulus in either case.

Animals↗
PubMed1977

The renin-angiotensin system and thirst: a reevaluation. II. Drinking elicited in rats by caval ligation or isoproterenol.

Ligation of the inferior vena cava and administration of isoproterenol have been shown to stimulate renin secretion and to augment water intake in rats. However, the present experiments suggested that the plasma renin activities produced by these treatments do not account for more than 20% of the observed drinking behavior. Direct measurements of arterial blood pressure further indicated that nephrectomized rats go into hypotensive shock after caval ligation or isoproterenol treatment. Drinking was elicited in these hypotensive animals by systemic injection of hypertonic NaCl solution, renin, or Pitressin, or by intracranial injection of angiotensin, but in each case a rapid increase in blood pressure also was observed. Thus, it appears that nephrectomy reduces water intake in these animals by undermining their general capacity to behave rather than by removing a specific dipsogenic stimulus. These and other results suggested that drinking elicited in rats by caval ligation or isoproterenol is not mediated by the renin-angiotensin system.

Angiotensin II↗
PubMed1977

Effects of dopaminergic agonists and antagonists of feeding in intact and 6-hydroxydopamine-treated rats.

The effects on food intake of treatments which alter central dopaminergic function were examined in rats. Doses of d-amphetamine that increased the conversion of 3H-tyrosine to 3H-dopamine in the brain were found to decrease food intake, an effect that was reduced by the systemic administration of the dopaminergic antagonists alpha-methyltyrosine, haloperidol or spiroperidol. The dopaminergic agonists, apomorphine, dopa, cocaine and methylphenidated, also reduced feeding and these effects were attenuated by low doses of spiroperidol. In larger doses, spiroperidol itself decreased feeding, and this effect was potentiated by alpha-methyltyrosine. The ability of dopaminergic agonists and antagonists to inhibit food intake was also observed in rats treated with 6-hhyroxydopamine so as to produce a selective 83% depletion of dopamine. In these animals, d-amphetamine was found to be less effective as an anorexic agent, whereas dopa, apomorphine, alpha-methyltyrosine and spiroperidol each was more effective in reducing food intake. These alterations in sensitivity may reflect neurochemical changes which occur at residual dopaminergic synapses after subtotal lesions of dopaminergic neurons. We conclude that both increases and decreases in central dopaminergic activity can reduce feeding and propose that some intermediate rate of dopamine release provides an optimal level of neuronal activity for feeding by the hungry animal.

Animals↗