Failure of microscopic metarterioles to elicit vasodilator responses to acetylcholine, bradykinin, histamine and substance P after ischemic shock, endotoxemia and trauma: possible role of endothelial cells.

We have noted, recently, that early after experimental intestinal ischemia, endotoxemia or whole-body trauma in rats, that the endothelial cells (EC) lining splanchnic precapillary microvessels (i.e., arterioles and metarterioles) appear to be contorted, often exhibit swelling and appear to have lost a great deal of their normal wetable surfaces as evidenced by sticking of white blood cells and platelets. Using identical circulatory shock and trauma models, we now report that irrespective of the ischemic or traumatic etiology, neither of four vasodilators, e.g., acetylcholine, bradykinin, substance P or histamine, were able to elicit much in the way of vasodilatation of metarterioles (10-12 microns in size) early after induction of intestinal ischemia, endotoxemia or whole-body trauma. Irrespective of the mechanism(s), if our results are seen in other organ regions as well, the end result would be a severe reduction in lumen sizes of the microscopic resistance and capacitance vessels in the lung ("shock lung"), kidneys, liver, etc., resulting in multiple organ failure.