Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model
1 Department of Medical Physiology, Institute of Medical Biology, and 2 Department of Anesthesiology, Institute of Clinical Medicine, University of Tromsø, Tromsø; 3 Department of Anesthesiology, University Hospital of North Norway, Tromsø; and 4 Section of Cardiology, Deptartment of Medicine, Sørla...
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Published in | Journal of applied physiology (1985) Vol. 100; no. 2; pp. 457 - 464 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Am Physiological Soc
01.02.2006
American Physiological Society |
Subjects | |
Online Access | Get full text |
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Summary: | 1 Department of Medical Physiology, Institute of Medical Biology, and 2 Department of Anesthesiology, Institute of Clinical Medicine, University of Tromsø, Tromsø; 3 Department of Anesthesiology, University Hospital of North Norway, Tromsø; and 4 Section of Cardiology, Deptartment of Medicine, Sørlandet Hospital, Kristiansand, Norway
Submitted 28 March 2005
; accepted in final form 28 September 2005
Rewarming from accidental hypothermia is often complicated by "rewarming shock," characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study, we tested whether epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1 , 2 , and 3 for dose-finding studies, and hypothermic groups 4 , 5 , and 6 . At 20 and 24°C during rewarming, group 4 (low-dose Epi) and group 5 (high-dose Epi) received bolus injections of 0.1 and 1.0 µg Epi, respectively. At 28°C, Epi infusion was started in groups 4 and 5 with 0.125 and 1.25 µg/min, respectively. Group 6 served as saline control. After rewarming, both CO and stroke volume were restored in group 4 , in contrast to groups 5 and 6 , in which both CO and stroke volume remained significantly reduced (30%). Total peripheral resistance was significantly higher in group 5 during rewarming from 24 to 34°C, compared with groups 4 and 6 . This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature-dependent adrenoreceptor affinity.
resuscitation; epinephrine; cardiovascular function; rat; cold; temperature
Address for reprint requests and other correspondence: T. V. Kondratiev, Dept. of Anesthesiology, Institute of Clinical Medicine, Univ. of Tromsø, 9037 Tromsø, Norway (e-mail: timoteik{at}fagmed.uit.no ) |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/japplphysiol.00356.2005 |