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Am J Physiol Heart Circ Physiol 273: H2072-H2077, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 4, H2072-H2077, October 1997

SPECIAL COMMUNICATION
Involvement of interleukin-1 receptor mechanisms in development of arterial hypotension in rat heatstroke

M. T. Lin1, H. H. Liu2, and Y. L. Yang2

1 Department of Physiology, National Yang-Ming University, School of Medicine and Life Science, Taipei; and 2 Department of Physiology, National Cheng-Kung University, Medical College, Tainan, Taiwan, Republic of China

Rats, under urethan anesthesia, were exposed to a high ambient temperature (42°C) to induce heatstroke and to assess the hemodynamic changes associated with heatstroke. Compared with normothermic controls, rats with heatstroke showed higher values of colonic temperature, heart rate, and plasma levels of interleukin (IL)-1 but lower values of R wave amplitude, P-R and Q-T intervals, systolic wave amplitude, diastolic and dicrotic wave duration, mean arterial pressure, stroke volume, and cardiac output. Animals injected intravenously with an IL-1-receptor antagonist at the time of heatstroke induction were protected from some of the cardiovascular effects of heatstroke, such as depressed ventricular depolarization, decreased stroke volume, decreased cardiac output, and arterial hypotension. The hemodynamic changes associated with heatstroke could be mimicked by IL-1beta administration. Other cardiovascular parameters such as total peripheral vascular resistance were unaffected by heatstroke induction or IL-1beta treatment. The results indicate that a selective decline in stroke volume or ventricular depolarization resulting from increased plasma levels of IL-1 may be an important mechanism signaling arterial hypotension or circulatory failure in rat heatstroke.

stroke volume; arterial hypotension; interleukin-1; cardiac output


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