Coronary vasomotor dysfunction following hemorrhagic shock

Abstract

Myocardial dysfunction and subendocardial ischemia have been described during hemorrhagic shock, but technical limitations have precluded the in vitro examination of coronary reactivity following hemorrhage. We tested the hypothesis that in vitro coronary artery contraction and relaxation are impaired by hemorrhagic shock (HS). HS was produced in awake rats ( n = 6) 24 hr after surgery for arterial cannulation, by bleeding to a mean arterial pressure of 50 mm Hg for 2 hr followed by reinfusion of shed blood. Using a small vessel myograph, reactivity of coronary arterial ring segments from three groups of rats not undergoing HS were compared to coronaries harvested from rats after HS (Group 4). The three nonshock treatments included normal rats without pretreatment (Group 1), rats undergoing prior surgical cannulation alone (Group 2), and rats undergoing prior surgical cannulation followed by nonhypotensive hemorrhage (Group 3). Responses to 125 m M potassium (KCl) and to 10 −6 M serotonin (STN) determined smooth muscle contraction. Acetylcholine administration determined endothelium-mediated smooth muscle relaxation, whereas acetylcholine plus nitroprusside combined determined maximum smooth muscle relaxation. Rats following HS demonstrated impaired coronary arterial smooth muscle contraction to KCl when compared to normal rats, but the response to STN did not differ among groups. Maximum smooth muscle relaxation was significantly lower in rats following HS as compared to rats in Groups 1 and 2. Endothelium-dependent relaxation was significantly impaired when compared to each of the three nonshock groups. Thus, in coronary arteries isolated from neurohumoral influences, HS was associated with diminished smooth muscle contraction and relaxation as well as impaired endothelium-mediated relaxation. These vasomotor abnormalities may contribute to subendocardial ischemic injury described in hemorrhagic shock.