PubMed Health⌕ Search

Biomedical subjects

G E Tempel

Publications and source records attributed to G E Tempel.

31 records · Page 2Linked to original sources
PubMed1982

Brain norepinephrine and serotonin in the golden hamster during heat and cold acclimation and hypothermia.

1. Norepinephrine (NE) and serotonin (5-HT) were simultaneously assessed in 4 discrete regions of the brain of the golden hamster. 2. Hypothalamic concentrations of both these amines are reported for the following groups: (1) normothermic controls; (2) heat acclimated; (3) cold acclimated; (4) helium-cold hypothermic; (5) rewarming; and (6) rewarmed. 3. Heat acclimated animals demonstrated approximately 35 and 25% decreases from control values for NE and 5-HT, respectively. Cold acclimated hamsters were not significantly different from controls. Helium-cold hypothermia resulted in approximately a 30 and 20% decrease in NE and 5-HT, respectively, with the latter returning to control values during rewarming. 4. The data provide indirect evidence for the involvement of NE in central pathways involving heat gain and 5-HT in pathways involving heat loss, and are discussed in terms of FELBERG & MYER'S (1964 J. Physiol., Lond. 173. 226-236) bioamine theory of thermoregulation.

Acclimatization↗
PubMed1977

Mechanisms responsible for decreased glomerular filtration in hibernation and hypothermia.

Mechanisms underlying the elimination or marked depression of renal function in hibernation and hypothermia were investigated through measurements of blood pressure, heart rate, red blood cell and plasma volumes, and relative distribution of cardiac output. Hamsters (Mesocricetus auratus) were made hypothermic (rectal temperature (Tre), 7 degrees C) by exposure to helox and cold, or permitted to hibernate with several weeks of cold exposure (Ta approximately 5 degrees C). Mean arterial pressure, 120 Torr in normothermic control animals, demonstrated a 55% and 60% decrease during hibernation and hypothermia, respectively. As the animals rewarmed from hypothermia or aroused from hibernation, blood pressure increased rapidly at 8-12 degrees C, more gradually at 12-17 degrees C, and plateaued thereafter. Blood pressure rapidly returned to near control levels whereas heart rate remained at less than one-half control value at the highest temperature examined. Red blood cell volume, 26.2 +/- 0.6 ml/kg body wt in the control animals appeared unaffected by hypothermia. Plasma volume, by contrast, decreased from control values of 33.0 +/- 0.8 to 21.3 +/- 0.6 ml/kg body wt in hypothermia, a decrease of approximately 35%. Distribution of cardiac output to various organs in hibernation and hypothermia followed a similar pattern. Relative flow to the heart, lung, diaphragm, and brown fat increased while the fraction distributed to the visceral organs appeared to decrease. The normothermic control kidney received approximately 16% of the cardiac output while the hibernating and hypothermic kidneys received approximately 10% and 6%, respectively. The data are discussed in terms of the determinants of glomarular filtration rate and explain, in part, the elimination or marked reduction in renal function observed in depressed metabolic states.

Animals↗
PubMed1976

Evidence for an intrarenal beta receptor in control of renin release.

Infusion of isoproterenol intravenously in normal dogs at rates of 0.10 or 0.018 mug/min per kg body wt increased renin secretion; at the lower infusion rate arterial pressure (AP) and renal blood flow (RBF) were unchanged. Isoproterenol was also infused into the renal artery in normal dogs at 0.10 mug/min per kg; renin secretion increased in association with an increase in RBF but AP was unchanged. Plasma K concentration was consistently decreased in all three of the above experiments and because hypokalemia is known to increase renin release isoproterenol was not infused intrarenally at the lower rate; the decrease in plasma K level precluded relating the entire response in renin release to isoproterenol. Intrarenal infusion of propranolol at 0.05 mg/kg per h in Na-depleted dogs decreased renin secretion whereas intravenous infusion at the same dose failed to alter renin release. Intrarenal infusion of propranolol at this rate in Na-depleted dogs with a denervated, nonfiltering kidney also decreased renin release. In contrast, intrarenal infusion of phentolamine or phenoxybenzamine in normal dogs failed to alter renin secretion in doses that blocked alpha-adrenergic receptors. These experiments provide strong evidence for an intrarenal beta-adrenergic receptor that mediates renin release, and it seems likely from the experiment in the denervated, nonfiltering kidney that the receptor is located in the juxtaglomerular cells.

Animals↗
PubMed1976

Mechanisms of temperature regulation in heat-acclimated hamsters.

Mechanisms of temperature regulation were assessed by measurements of oxygen consumption (VO2), body temperature (Rre = rectal, Tsk = skin), evaporative water loss (EWL), regional distribution of blood flow, and blood volume. Hamsters (Mesocricetus auratus) were acclimated to ambient temperatures of 34 or 22 degrees C. VO2 of 34 degrees C-exposed animals was reduced to 50% of that of controls at 22 degrees C, whereas EWL with heat exposure was almost double that of controls. Heat-acclimated animals had a slightly elevated Tre in comparison to 22 degrees C-acclimated animals, whereas there was a marked elevation in Tsk with heat exposure, in contrast to control animals at 22 degrees C. Blood flow distribution measurements indicated that with 34 degrees C exposure there was a decreased flow in liver, kidney, and intestine, whereas there was an increase to the carcass. Red cell and plasma volumes in heat-acclimated hamsters were decreased belwo the values of the 22 degrees C controls. Heat acclimation of the fhamster appears to involve reduced VO2 and increased WEL. Convective and radiative heat loss appear to be maintained by increased Tsk with heat exposure. Nonevaporative heat dissipation mechanisms are of primary importance in thermoregulation of the heat-acclimated hamster, and it is suggested that this is mediated by increased peripheral blood flow with reduced flow to the viscera.

Acclimatization↗
PubMed1975

Renal function in the hibernating, and hypothermic hamster Mesocricetus auratus.

Plasma and urine concentrations of Na+, K+, and urea were examined in hibernating, hypothermic, and normothermic hamsters. Plasma Na+ and K+ appear unaffected by 48 h of hypothermia (T-re 7 degrees C); however, plasma Na+ increased (P smaller than 0.05) from control values of 125.8 plus or minus 10.2 to 173 plus or minus 9.2 meg/liter in hibernators. Plasma K+ of the hibernator increased to 9.6 plus or minus 3.2 meq/liter from control values of 5.5 plus or minus 0.8 meq/liter (P smaller than 0.05). Plasma urea concentrations were increased (P smaller than 0.05) in both metabolically depressed groups from a control value of 0.5 plus or minus .05 to 0.8 plus or minus .16 and 7.2 plus or minus 2.8 mM in hypothermic and hibernating groups, respectively. Urine concentrations of solute for the hypothermic animals showed no detactable change from control values for Na+ and a decrease for both K+ and urea. Concentrations from hibernators showed a decrease from control values for both Na+ and K+ with no detectable change in urea. Renal tissue slice analysis demonstrated a marked corticomedullary solute gradient for Na+ and urea in normothermic control animals which is eliminated in hamsters hypothermic for 48 h and reduced in animals hypothermic for 15 min. Rewarming animals did not show a return of the solute gradient at T-re 18 degrees C. However, animals that had rewarmed to T-re 37 degrees C demonstrated a complete return with no difference (P greater than 0.05) from control values. Hibernators showed a slight (P smaller than 0.05) gradient for Na+ and no gradient for urea. Animals in all instances demonstrated a decrease in K+ concentration from cortex to papilla. A greater concentration of K+ was found in the renal cortex of animals hypothermic for 15 min and in hibernators (P smaller than 0.05).

Animals↗
PubMed1975

Influence of peritoneal dialysis on factors affecting oxygen transport.

To determine the effect of changing concentrations of uremic metabolites on factors affecting oxygen transport, without the effects of extracorporeal blood pumping, we studied five patients before, during and after peritoneal dialysis. Significant decreases in serum urea, creatinine and phosphate and increase in serum bicarbonate were not associated with changes in P50, a reflection of hemoglobin-oxygen affinity. High erythrocyte 2,3-DPG concentrations decreased only slightly. Arterial pO2 increased slightly as negative fluid balance was achieved. The slight changes in oxygen transport parameters with dialysis suggest an interplay of compensatory factors and do not warrant modifying dialysis to limit the correction on acidosis or hyperphosphatemia. Effects on hemoglobin and pO2 resulting from fluid loss can be the dominant influence of peritoneal dialysis on tissue oxygenation.

Creatinine↗
PubMed1975

Erythrocyte 2,3-diphosphoglycerate concentrations in hibernating, hypothermic, and rewarming hamsters (38589).

Hematocrit, hemoglobin and erythrocyte 2,3-DPG concentrations were examined in normothermic control, hibernating, and helium-cold hypothermic hamsters. Hematocrit was not signigicantly different (P greater than 0.05) between groups, but did reflect alterations reported for hemoglobin. Hemoglobin concentration did not change from control values during 12 hr at Tre 7 degrees; however, approximately a 20% decrease occurred in hibernators (48 hrs) and animals hypothermic (24 hr). 2,3-DPG concentrations declined 39.1 and 33.9% from control values in the hibernating and 24 hr hypothermic groups, respectively. No change was observed in animals hypothermic for 12 hr. Both parameters were studied in the aroused animal. Hemoglobin returns to control values immediately after the animals reached a stable Tre approximately equal to 37 degrees. Although 2,3-DPG levels increased during arousal, they were still 10% lower than control values in both metabolically depressed groups. 2,3-DPG remained approximately 10% less than controls in rewarmed hypothermic animals studied 2 hr after reaching stable Tre approximately equal to 37 degrees. The data are discussed in terms of cold depression of erythrocyte glycolysis.

Animals↗
PubMed1975

Effect of hemodialysis on factors influencing oxygen transport.

Ten patients underwent 4 study hemodialyses, one with standard dialysis conditions, one with an isophosphate dialysate, one with simultaneous ammonium chloride loading, and other, after pretreatment, with sodium bicarbonate. Measurement of hemoglobin oxygen affinity (P-50), erythrocyte 2,3-DPG, blood-gasses, and serum chemistries revealed biochemically effective hemodialyses and slight changes in oxygen transport parameters. The P-50 (in vivo) values decreased slightly but significantly (p greater than 0.05) with dialysis. When corrected to pH 7.4, eliminating the Bohr effect, P-50 increased (p greater than 0.05). With unmodified dialysis elevated values of 2,3-DPG (in comparison to normal) decreased, a change that did not correlate with delta-p-50, delta-serum phosphate, or delta-serum creatinine. With standard and isophosphate dialyses Po-2 decreased significantly. The decrease correlated with delta-hydrogen ion concentration and did not occur with dialyses designed to maintain pH constant. Thus, hemodialysis influences many factors that affect oxygen transport in different and counterbalancing directions. These changes are not totally explained by alterations in 2,3-DPG, pH or serum phosphate. Maintenance of acidosis or hyperphosphatemia during dialysis is not recommended.

Adolescent↗
PubMedDate not supplied

Alterations in the myocardial capillary vasculature accompany tachycardia-induced cardiomyopathy.

Changes in capillary structure and distribution within the left ventricle (LV) occur with pressure and volume overload hypertrophy. These changes may cause an impairment in myocardial blood flow (MBF) and oxygen delivery resulting in myocyte injury and LV dysfunction. However, it is unknown whether changes in the capillary vasculature accompany the development of LV dysfunction in dilated cardiomyopathies. Accordingly, this study examined the relation between LV function, MBF and capillary architecture after the development of dilated cardiomyopathy in pigs produced by chronic supraventricular tachycardia (SVT). LV function was examined by echo-catheterization, and capillary morphometrics were computed using lectin histochemistry in two groups of pigs: sham controls (n = 8); and after 3 weeks of pacing-induced SVT (n = 8). Chronic SVT resulted in significantly increased LV end-diastolic dimension and pressure with a 50% reduction in LV fractional shortening compared to CON (p less than 0.05). Although no significant change in capillary density (2180 +/- 164 vs 2402 +/- 147/mm2, p = 0.25) occurred in the SVT group compared to CON, a significant reduction in the volume fraction of capillaries (12.2 +/- 0.5 vs 9.9 +/- 0.7%, p less than 0.05) and increased capillary diffusion distance (8.4 +/- 0.5 vs 7.5 +/- 0.3 microns, p less than 0.05) was observed. Frequency distribution analysis revealed a higher percentage of smaller diameter capillaries with chronic SVT vs CON (p less than 0.05). Ultrastructural examination revealed an increased capillary-myocyte distance with chronic SVT (0.95 +/- 0.08 vs 1.95 +/- 0.12 microns, p less than 0.05). These changes were accompanied by ultrastructural evidence of significant subendocardial injury (p less than 0.05). MBF was measured using microspheres in five additional conscious pigs in each group. MBF was significantly reduced and coronary vascular resistance increased in the SVT group compared to CON (p less than 0.05). Chronic SVT caused significant remodeling of the capillary vasculature; these changes were associated with reduced MBF, myocyte injury, and LV dysfunction.

Animals↗
PubMedDate not supplied

Improvement in organ blood flow by inhibition of thromboxane synthetase during experimental endotoxic shock in the rat.

Endotoxic shock is associated with increased metabolism of arachidonic acid to thromboxane (Tx) and prostaglandins. This investigation examined the effects of two structurally dissimilar inhibitors of (Tx) synthetase on Salmonella enteritidis endotoxin (LPS) (15 mg/kg)-induced alterations in cardiac output and organ blood flow in Long-Evans rats. An imidazole derivative, 7(1-imidazolyl) heptanoic acid (7-IHA), and sodium -(E)-3-[4-(3-pyridyl-methyl)phenyl]-2-methacrylate (OKY-1581) were injected intravenously at 30 and 5 mg/kg, respectively, 30 min before injection with endotoxin. Cardiovascular function was assessed 30 min post-LPS with Sr-85 labeled microspheres under light ether anesthesia. Injection of endotoxin caused a 60% decrease in cardiac output (34.0 +/- 2.7 ml/min/100 g body weight in control rats) and a 38.9% decrease in systolic arterial pressure. Both Tx synthetase inhibitors significantly (p less than 0.05) attenuated the decrease in cardiac output, although only 7-IHA improved blood pressure. Pretreatment with 7-IHA or OKY-1581 significantly (p less than 0.05) attenuated the LPS-induced decrease in renal perfusion. Lung nutrient blood flow (1.1 +/- 0.2 ml/min/g lung) decreased nearly 70% in shock. Both Tx synthetase inhibitors prevented this reduction. LPS shock resulted in approximately a 30% decrease in brain blood flow. 7-IHA significantly (p less than 0.05) improved flow, while OKY-1581 was without apparent effect. Splanchnic blood flow was likewise improved by 7-IHA and OKY-1581. Liver blood flow, 55% less than values of the control group in shock (p less than 0.05), was returned to values of the controls by both inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylates↗