Hypothermia and Rewarming after Hypothermic Exposure Alter Venous Relaxation
| Autor: | Mark G. Davies, Mark A. Hopkin, Kelvin G.M. Brockbank, Per Otto Hagen |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
Hot Temperature Contraction (grammar) Endothelium chemistry.chemical_element Isometric exercise 030204 cardiovascular system & hematology Calcium Muscle Smooth Vascular 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Hypothermia Induced medicine Animals 030212 general & internal medicine Analysis of Variance Forskolin business.industry Hypothermia Vasodilation Logistic Models medicine.anatomical_structure chemistry Anesthesia Endothelium Vascular Rabbits Sodium nitroprusside Jugular Veins medicine.symptom Cardiology and Cardiovascular Medicine business Acetylcholine medicine.drug |
| Zdroj: | Vascular Medicine. 1:103-107 |
| ISSN: | 1477-0377 1358-863X |
| DOI: | 10.1177/1358863x9600100203 |
| Popis: | Hypothermia has pathophysiological consequences on endothelial and smooth muscle cell function. This study investigates the impact on venous relaxation of hypothermia and rewarming following hypothermic exposure. In vitro isometric relaxation responses of norepinephrine precontracted rabbit external jugular veins to a panel of endothelium-dependent and -independent agonists were assessed in controls at 37 degrees C, and in an experimental group after cooling to 20 degrees C and after rewarming to 37 degrees C. On cooling, the endothelium-dependent responses to acetylcholine became multiphasic with initial contraction at low concentrations followed by relaxation at higher concentrations, the maximum of which was significantly diminished compared to controls. Incubation with indomethacin did not affect this response. Rewarming re-established a monophasic dose-dependent acetylcholine induced relaxation response but the maximal response was significantly augmented. This augmentation in relaxation on rewarming could be prevented by preincubation with indomethacin. The maximal response to calcium ionophore was reduced at 20 degrees C and augmented upon rewarming to 37 degrees C. All veins relaxed in a dose-dependent manner to the non-endothelium-dependent agonists forskolin and sodium nitroprusside; the maximal responses were significantly reduced at 20 degrees C and returned to normal upon rewarming. This study suggests that short-term exposure of venous tissue to hypothermia impairs the vessel's ability to produce endothelium-dependent relaxation. Rewarming does not re-establish normal endothelium-dependent relaxation but results in an enhanced, partially indomethacin-sensitive, response which appears to be independent of changes in non-endothelium-dependent mediated relaxation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|