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(Hypertension. 1999;34:212-216.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Microvascular Responses to Ischemia/Reperfusion in Normotensive and Hypertensive Rats

Iwao Kurose; Robert Wolf; Wolfgang Cerwinka; D. Neil Granger

From the Departments of Molecular and Cellular Physiology (I.K., W.C., D.N.G.), and Medicine (R.W.), Center of Excellence in Arthritis and Rheumatism, Louisiana State University Medical Center, Shreveport, La.

Correspondence to D. Neil Granger, PhD, Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, 1501 Kings Hwy, PO Box 33932, Shreveport, LA 71130-3932. E-mail dgrang{at}lsumc.edu

Abstract—The objective of the present study was to determine whether long-term arterial hypertension renders the microvasculature more vulnerable to the deleterious inflammatory responses elicited by ischemia and reperfusion (I/R). Intravital fluorescence microscopy was used to monitor leukocyte adherence and emigration, platelet-leukocyte aggregation, and albumin extravasation in mesenteric postcapillary venules of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) after 10 minutes of ischemia and subsequent reperfusion. Significant and comparable increases in leukocyte adherence/emigration and the formation of platelet aggregates were elicited by I/R in both WKY and SHR. Albumin extravasation was enhanced after I/R in SHR, but not in WKY. Monoclonal antibodies directed against the adhesion glycoproteins CD18, P-selectin, or ICAM-1 showed similar patterns of protection against the I/R-induced inflammatory responses in WKY and SHR. The enhanced albumin extravasation noted in postischemic venules of SHR was prevented by immunoneutralization of either CD18 on leukocytes or ICAM-1 on endothelial cells. These results suggest that, whereas long-term arterial hypertension does not significantly modify the leukocyte and platelet recruitment normally elicited in venules by I/R, it does result in an exaggerated albumin leakage response, which is mediated by an interaction between ß₂ (CD18) integrins on leukocytes and ICAM-1 on endothelial cells.

Key Words: leukocytes • integrins • oxidative stress • mast cells

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