| pubmed-article:2645461 | pubmed:abstractText | Altered vascular reactivity to numerous vasoactive substances in hypertension formed the basis for studying the in vivo microcirculation of skeletal muscle tissue during high cardiac output bacteremia and low cardiac output sepsis. Large and small arteriole and venule diameters of the cremaster muscle were measured via videomicroscopy in normotensive and 1K-1C-renovascular hypertensive rats before and after the infusion of live Escherichia coli bacteria. During hyperdynamic bacteremia and during hypodynamic sepsis, large arterioles constricted and small arterioles dilated in normotensive animals. During hyperdynamic bacteremia, this differential arteriolar response was blunted in hypertension. In hypodynamic sepsis, large arterioles did constrict in the hypertensive animals, but small arteriolar dilation was still blunted. Sodium-nitroprusside, a postreceptor acting agent applied locally, maximally dilated small arterioles to the same level in all groups to indicate that the ability of vascular smooth muscle to relax is intact in hypertension. We conclude that the failure of the small arterioles to dilate during sepsis in hypertension is not due to a loss of vascular smooth muscle function, but that hypertension may functionally alter arteriolar reactivity at the receptor and/or endothelial level to interfere with E. coli-mediated responses in the skeletal muscle microvasculature. | lld:pubmed |
