The American journal of physiology
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Lipopolysaccharide (LPS) or partially purified endogenous pyrogen (EP) was injected intravenously into rats of both sexes to induce fever. In LPS fever, which was easily produced in 24-h dehydrated rats with an intravenous injection of LPS, the female rats showed an attenuated febrile reaction as measured by both the maximum increase of rectal temperature (Tre) and the thermal response index (TI). Although castrated female rats showed the same magnitude of febrile reaction to that in normal female rats, castrated male rats had less of a febrile response than normal male rats. ⋯ However, castration of rats of both sexes did not affect the febrile reaction to intravenous injection of EP. Ten-week-old female rats, treated by a subcutaneous injection of testosterone propionate on the 1st day after birth, produced a similar magnitude of febrile reaction to that in the normal male rats that were comparable in age. It is concluded that there are sex-related differences in fever development, due both to EP production and structural sexual differences in the central nervous system pathways regulating fever.
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A volume-resuscitated porcine endotoxin shock model was used to evaluate the effect on organ blood flow of increasing systemic arterial blood pressure with vasopressors. Administration of 0.05-0.2 mg/kg of Escherichia coli endotoxin (E) reduced mean arterial blood pressure (MAP) to 50 mmHg, decreased systemic vascular resistance to 50% of control, and did not change cardiac output or heart rate. Blood flow to brain, kidney, spleen, and skeletal muscle was reduced during endotoxin shock, but blood flow to left ventricle, small and large intestine, and stomach remained at pre-endotoxin levels throughout the study period. ⋯ Kidney, splanchnic, and skeletal muscle blood flow did not change with vasopressor administration. The dose of norepinephrine required to increase MAP by 20-25 mmHg during E shock was 30 times the dose required for a similar increase in MAP in animals not receiving E. We conclude that hypotension in the fluid resuscitated porcine E shock model is primarily the result of peripheral vasodilatation, that the vascular response to vasoconstrictors in this model is markedly attenuated following E administration, that blood pressure elevation with norepinephrine, dopamine, and phenylephrine neither decreases blood flow to any organ nor increases blood flow to organs with reduced flow, and that norepinephrine, dopamine, and phenylephrine affect regional blood flow similarly in this model.