Thermal reactions of blood vessels in vascular stroke and heatstroke.
Research on the pathophysiology and treatment of brain damage with special focus on thermal vascular responses is the subject of this minireview. Interruption of cerebral blood supply by vascular obstruction, temporary cardiac arrest or hyperthermia causes a sudden attack of vascular stroke or heatstroke with serious consequences. It may not induce immediate cell death, but can precipitate a complex biochemical cascade leading to a delayed neuronal loss. When testing thermal vasomotor responses by stepwise cooling of isolated carotid arteries, a temperature-proportional dilatation was observed while heating induced the opposite response: a marked vasoconstriction. General hyperthermia with an increased oxygen demand combined with a reduction of blood supply therefore is a serious consequence. At the cellular level an important mechanism involving hyperthermia is the temperature-dependent regulation of K(+) channel tone of vascular smooth muscle. Further, their inhibition through temperature elevation causes vasoconstriction. In heatstroke, which can induce platelet aggregation and the release of the vasoconstrictor serotonin, arterial cooling attenuates this response. General hypothermia is induced to prevent or attenuate neurological damage in stroke. The procedure is not without serious side effects. Therefore, rapid institution of selective brain cooling has been considered in adults and in infants with postpartum encephalopathy.
Thulesius
Olav
O
Department of Clinical Physiology, Faculty of Medicine, University Hospital Linkoping, Sweden. olva.thulesius@telia.com
D000818:Animals; D001808:Blood Vessels / Q000503:physiopathology*; D001921:Brain / Q000098:blood supply; D002339:Carotid Arteries / Q000503:physiopathology; D005334:Fever / Q000503:physiopathology; D018883:Heat Stroke / Q000503:physiopathology*; D006801:Humans; D006979:Hyperthermia, Induced; D007035:Hypothermia / Q000503:physiopathology; D007036:Hypothermia, Induced; D020521:Stroke / Q000503:physiopathology*