[Role of calcium desensitization in vascular hyporeactivity in hemorrhagic shock]

To evaluate the role of calcium desensitization of vascular smooth muscle in vascular hyporeactivity following hemorrhagic shock (HS) in rats.

The superior mesenteric artery (SMA) from HS model of rat was adopted to assay the vascular reactivity and calcium sensitivity by observing its contractibility initiated by norepinephrine (NE) and Ca2+ under depolarizing conditions (120 mmol/L K+) with the aid of an isolated organ perfusion system. The experiment was conducted in two parts. In the first part, calcium desensitization was present whether or not in the response-decreased blood vessels was observed, and in the second part, whether angiotensin II (Ang II) and insulin which were calcium sensitivity regulating agents, and a relatively selective inhibitor of Rho-kinase, Fasudil, could regulate the vascular reactivity through regulating the calcium sensitivity was tested.

As compared with the normal group, the cumulative dose-response curve of SMA to NE and Ca2+ in shock group was shifted to the right, the maximal contraction (Emax) and -lg(EC50)(pD2) of NE and Ca2+ were decreased significantly(P<0.05 or P<0.01). Ang II shift the cumulative dose-response curve of NE and Ca2+ to the left, and increased the contractile response of NE and Ca2+ (P<0.05 or P<0.01). On the contrary, insulin rendered the cumulative dose-response curve of NE and Ca2+ shift to the right and decreased the contractile response of NE and Ca2+ (P<0.05 or P<0.01). Pretreatment with Fasudil abolished the enhancing effect of Ang II on vascular contraction produced by NE, and reduced the calcium sensitivity.

Calcium desensitization is a physiological condition which exists in the vascular smooth muscle of HS rat, and it plays an important role in vascular hyporeactivity, which is one of the important mechanism of the abnormal condition of vascular hyporeactivity.