Hemodynamic characteristics of the intestinal microcirculation in renal hypertension.

Abstract

SUMMARY This study investigated the microvascular changes that affect vascular resistance in the rat small intestine during two-kidney, one clip renal hypertension 4 weeks after renal artery stenosis. To study the intestinal microcirculation, a loop of the small intestine was exteriorized with intact circulation and innervation and a section of the bowel wall was prepared for observation with an intravital video microscopy system. Microvascular diameter, pressure, and flow velocity were measured for first, second, and third branch order arterioles and venules, using an image shearing monitor, servo-null micropipette system, and an optical Doppler velocimeter, respectively. The diameters of the first order arterioles and venules were significantly (p < 0.05) reduced in hypertensive rats; however, diameters were unaltered in smaller second and third order arterioles and venules as compared with normotensive vessels. In hypertensive rats, mean arterial pressure was significantly (p < 0.05) elevated (47%) and pressures also were elevated significantly (p < 0.05) throughout the microcirculation, although by a proportionally smaller amount. Total network flow (i.e., first order arteriole flow) was significantly (p < 0.05) reduced (40%) in hypertensive rats, but volume flows in individual second and third order arterioles were similar to flows measured in normotensive rats. Calculated total network resistance was increased (124%) in hypertensive rats. Thus, the intestinal microcirculation in rats with two-kidney, one clip renal hypertension is disturbed by elevated pressure and decreased total flow. The presence of normal flows in individual second and third order arterioles without any demonstrable difference in their diameters suggests that the predominant cause of elevated resistance across this segment of the intestinal microcirculation is a reduction in the number of perfused small arterioles. (Hypertension 8: 66-75, 1986) KEY WORDS • microvascular pressures • microvascular flows • microvascular diameters • vascular resistance • splanchnic circulation • two-kidney, one clip Goldblatt hypertension T HE microvascular characteristics that determine vascular resistance in hypertension have received increased attention over the last decade. This is principally because the microcirculation is a primary site of peripheral resistance and is controlled by neural and hormonal mechanisms of blood pressure regulation, which are well known to be altered in various forms of experimental hypertension.

Alterations in flow-dependent vasomotor tone in spontaneously hypertensive rats.

“…22 -25 Furthermore, it has been suggested that the macroarteries contribute to the increased peripheral resistance observed in anesthetized hypertensive rats. 22 - 24 Christensen and Murvany 26 recently reported that in normotensive and unanesthetized SHR, approximately one third of the resistance of the mesenteric bed lies in macroarteries. In addition, the perfusion pressure recorded in the larger mesenteric arteries reflects the resistance of the overall mesenteric bed (macroarteries and microarteries) calculated as the pressure-flow ratio.…”

Location of Resistance Arteries

“…In the cerebral circulation of adult SHR, Harper and Bohlen [33]found that although fractional blood pressures were 10% elevated throughout the microvasculature compared to WKY, there was reduced fractional blood pressure in feed arteries. This suggests that hypertension may be sustained primarily by the microvasculature [34]. In the cerebral circulation, the same has been shown, namely that in stroke-prone SHR proportionally more of the pressure drop occurs over the feed arteries than in WKY [35].…”

A New in Vitro Pulsatile Perfusion System that Mimics Physiological Transmural Pressure and Shear Stress in Any Size of in Vivo Vessel

“…However, in the same species and same anatomical location, hypertension elevates blood pressure. In hypertensive rats, mean arterial pressure is significantly elevated (32) (33) . As just described, the magnitude of pressure and shear stress in in vivo vessels vary greatly due to cross-species differences, differences in anatomical locations, and disease.…”