Glucose kinetics and body temperature after lethal and nonlethal doses of endotoxin

1985 ◽  
Vol 248 (4) ◽  
pp. R471-R478 ◽  
Author(s):  
C. H. Lang ◽  
G. J. Bagby ◽  
J. J. Spitzer
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Body Temperature ◽  
Lethal Dose ◽  
Temporal Response ◽  
Febrile Response ◽  
Glucose Kinetics ◽  
Arterial Blood ◽  
High Doses ◽  
Higher Doses

Rats were injected with doses of endotoxin ranging from 1,000 [lethal dose approximately 50% (LD50)] to 0.01 microgram/100 g, and alterations in hemodynamics, glucose kinetics, and body temperature were studied over the subsequent 4 h. Doses of 10 micrograms/100 g or less were consistently nonlethal over 72 h. Decreases in arterial blood pressure and cardiac output were evident in rats receiving 1,000-10 micrograms/100 g endotoxin. Doses of endotoxin between 1,000 and 10 micrograms produced an early hyperlactacidemia evident by 1 h, whereas the lower doses (1 and 0.1 microgram) induced elevations that exhibited a delayed temporal response. The rates of glucose appearance (Ra) and disappearance (Rd) were increased early and transiently by the higher doses of endotoxin. Lower doses increased glucose Ra and Rd between 2 and 4 h after endotoxin. A febrile response was elicited by 10, 1, and 0.1 microgram/100 g endotoxin, while hypothermia was seen in animals receiving higher doses. Thus high doses of endotoxin induced metabolic and hemodynamic alterations that were temporally associated. Very low nonlethal doses of endotoxin (up to 4 orders of magnitude less than LD50) induced metabolic changes that appeared to be independent of hemodynamic disturbances but were temporally associated with the observed hyperthermia.

Norepinephrine elevation in the fetal lamb: oxygen consumption and cardiac output

1980 ◽  
Vol 239 (1) ◽  
pp. R115-R122 ◽  
Author(s):  
R. H. Lorijn ◽  
L. D. Longo
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Diffusing Capacity ◽  
Blood Flows ◽  
Umbilical Blood ◽  
Arterial Blood ◽  
Fetal Lamb ◽  
O2 Diffusion ◽  
Umbilical Blood Flow ◽  
Higher Doses

In an effort to determine if placental diffusion reserves exceed fetal O2 requirements, we increased fetal O2 consumption (VO2) by infusing 1.7-11.5 microgram of norepinephrine (NE) . min-1. After 50 min of infusion VO2 rose 25% to 10.2 from 8.2 ml . min-1 . kg fetal wt-1. Placental CO diffusing capacity remained essentially unchanged from control, 0.49 +/- 0.05 (SE) ml . min-1. Torr-1 . kg-1, During the first 5 min of NE infusion fetal arterial blood pressure increased 29%, while heart rate decreased 15%. In addition, coronary, pulmonary, and umbilical blood flow, expressed per kilogram of fetal weight as determined by use of labeled microspheres, increased 50, 162, and 25%, respectively (P less than 0.05), although fetal cardiac output remained constant at 538 +/- 23 (SE) ml . min-1 . kg-1. Finally, we determined the NE-blood pressure dose-response relations for the fetus; Blood pressure increased with doses up to 1 microgram . min-1 . kg-1, but failed to rise further with higher doses. We conclude that 1) fetal VO2 increases with NE infusion 2) the placental reserve for O2 diffusion exceeds normal requirements, and 3) NE infusion is associated with increased blood pressure, bradycardia, and a redistribution of blood flows to the heart, lungs, and placenta despite a constant cardiac output.

Alterations in glucose kinetics induced by pentobarbital anesthesia

1987 ◽  
Vol 253 (6) ◽  
pp. E657-E663 ◽  
Author(s):  
C. H. Lang ◽  
G. J. Bagby ◽  
D. M. Hargrove ◽  
P. M. Hyde ◽  
J. J. Spitzer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Temperature ◽  
Glucose Metabolism ◽  
Carbohydrate Metabolism ◽  
Whole Body ◽  
Metabolic Clearance ◽  
Glucose Kinetics ◽  
Arterial Blood ◽  
Anesthetized Rats

Because pentobarbital is often used in investigations related to carbohydrate metabolism, the in vivo effect of this drug on glucose homeostasis was studied. Glucose kinetics, assessed by the constant intravenous infusion of [6-3H]- and [U-14C]glucose, were determined in three groups of catheterized fasted rats: conscious, anesthetized and body temperature maintained, and anesthetized but body temperature not maintained. After induction of anesthesia, marked hypothermia (5 degrees C decrease in core temperature) developed in rats not provided with external heat. Anesthetized rats that developed hypothermia showed a decrease in mean arterial blood pressure (25%) and heart rate (40%), whereas no differences were seen in blood pressure and heart rate of conscious and euthermic anesthetized rats. Likewise, the plasma lactate concentration and the rates of glucose appearance, recycling, and metabolic clearance were reduced by 30-50% in the hypothermic anesthetized rats. Changes in whole-body carbohydrate metabolism were prevented when body temperature was maintained. Because plasma pentobarbital levels were similar between the euthermic and hypothermic rats during the first 2 h of the experiment, the rapid reduction in glucose metabolism in this latter group appears related to the decrease in body temperature. The continuous infusion of epinephrine produced alterations in glucose kinetics that were not different between conscious animals and anesthetized rats with body temperature maintained. However, marked differences were seen in hypothermic rats. Thus pentobarbital-anesthetized rats became hypothermic when kept at room temperature and exhibited marked decreases in glucose metabolism. Such changes were absent when body temperature was maintained during anesthesia.

Central arginine vasopressin and endogenous antipyresis

1992 ◽  
Vol 70 (5) ◽  
pp. 786-790 ◽  
Author(s):  
Quentin J. Pittman ◽  
Marshall F. Wilkinson
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Arginine Vasopressin ◽  
Septal Area ◽  
Host Defence ◽  
Neonatal Rat ◽  
Prostaglandin E ◽  
Febrile Response ◽  
Arterial Blood ◽  
The Brain

Arginine vasopressin (AVP) is a centrally synthesized nonapeptide that exerts classical endocrine effects as well as a host of centrally mediated actions. A strong case can be argued in support of a neurotransmitter–neuromodulator role for AVP. Acting within the central nervous system (CNS), AVP has been demonstrated to be involved in the modulation of febrile body temperature. Because AVP acts to reduce pyrogen-induced fevers, but not normal body temperature, its actions are deemed to be antipyretic. However, to demonstrate an endogenous antipyretic function, AVP must be shown to be active during conditions where fever is naturally suppressed. This review will focus on five such conditions where the absence of pyrogen-induced fever can be linked to the endogenous activity of AVP within the brain. In the neonatal rat pup, the use of specific antagonists to the AVP receptor has revealed a role for CNS AVP in the absence of fever following peripheral injections of bacterial endotoxin. These results may help to explain a similar lack of fever in other newborn species. In parturient animals a reduced or absent febrile response has been linked to the increased presence of AVP within the septal area of the brain. The combined use of AVP receptor antagonism as well as immunohistochemistry has shown enhanced AVP activity within the ventral septal area of the rat and guinea pig brain during tolerance to intravenous pyrogens. These results suggest that the mechanism of fever suppression following repeated systemic injections of bacterial pyrogen includes centrally acting AVP. Recent observations from our laboratory have revealed a suppression of fever during the rising phase of arterial blood pressure in the one-kidney, one-clip model of hypertension. The normal febrile response to prostaglandin E1 can be restored in this instance by blockade of ventral septal AVP receptors. A similar situation of lack of response to pyrogens occurs in hypotensive animals in which pressor mechanisms are activated to restore blood pressure to normal. In this, and the previous four examples, centrally acting AVP has been linked to the natural suppression of pyrogen-induced fevers. Using these models of endogenous antipyresis we will continue to investigate this phenomenon to assess the benefits to the organism as well as to examine other nonthermal host defence responses.Key words: fever, antipyretic, pyrogen, host defence, vasopressin.

Effect of hemorrhage on fever: the putative role of vasopressin

1981 ◽  
Vol 59 (4) ◽  
pp. 324-328 ◽  
Author(s):  
N. W. Kasting ◽  
W. L. Veale ◽  
K. E. Cooper ◽  
K. Lederis
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arginine Vasopressin ◽  
Febrile Response ◽  
Arterial Blood ◽  
Conscious Sheep

The effects of hemorrhage on the febrile response of the sheep was examined because hemorrhage is a potent stimulant for arginine vasopressin (AVP) release into cerebrospinal fluid and blood. Removal of 20% of the estimated blood volume of the conscious sheep led to small physiologic changes and significantly decreased fevers in response to bacterial endotoxin. Mean arterial blood pressure decreased in hemorrhaged febrile sheep to a siginificantly greater extent than in nonhemorrhaged febrile sheep. AVP levels were considerably greater in the blood of hemorrhaged febrile sheep than in nonhemorrhaged febrile sheep and the concentrations correlated with the magnitude of the decrease in fever. Sheep hemorrhaged in the cold had changes in body temperature similar to control sheep. These experiments support the hypothesis that AVP may be an antipyretic neuromodulator.

EFFECT OF ENDRIN ON VENOUS RETURN AND CATECHOLAMINE RELEASE IN THE DOG

1966 ◽  
Vol 44 (1) ◽  
pp. 59-67 ◽  
Author(s):  
D. A. Reins ◽  
J. A. Rieger Jr. ◽  
W. B. Stavinoha ◽  
L. B. Hinshaw
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Adrenal Glands ◽  
Venous Return ◽  
Lethal Dose ◽  
Peripheral Resistance ◽  
Primary Source ◽  
Arterial Blood ◽  
Total Body ◽  
The Relationship

Previous reports have shown that dogs treated with the insecticide endrin develop marked changes in blood pressure and heart rate accompanied by convulsions terminating in death. The present study was designed to determine the relationship between venous return (cardiac output), total peripheral vascular resistance, and hypertension seen in succinylcholine-treated dogs after a lethal dose of endrin. Experiments were performed on "intact" (viscera intact) and eviscerated dogs under conditions of total body perfusion. Results indicate that the rise in systemic arterial blood pressure depends primarily on increased cardiac output due to an elevated venous return. Total peripheral resistance does not change significantly in either group of animals. The abdominal viscera were the primary source of the increase in venous return after endrin. Adrenal glands were partially depleted of adrenaline, and increased levels of adrenaline and noradrenaline found in blood plasma may explain the marked alterations in systemic hemodynamics.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

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