The mucosal microcirculation in innervated and denervated small intestine was studied using anesthetized rats. Denervation did not cause significant (P greater than 0.05) diameter changes in the precapillary vasculature; however, venules did constrict significantly. These results indicate minimum neural control in the precapillary vasculature during the resting state. The innervated precapillary vasculature constricted during both the carotid occlusion reflex and hemorrhagic hypotension. The diameter of the denervated precapillary vasculature was unchanged during the carotid occlusion reflex and dilated during hemorrhage. The responses of innervated and denervated precapillary vasculatures were attributed to increased neural activity and autoregulatory mechanisms, respectively. Neither innervated nor denervated venules responded during the carotid occlusion reflex. During hemorrhage, however, innervated venules constricted and denervated vessels dilated. The vasoconstriction of the innervated vasculature during hemorrhage contributed to a stoppage of blood and epithelial detachment; these responses did not occur in the dilated, denervated vasculature. Therefore, neural vasoconstriction, qualitatively similar to that in normal animals during the baroreceptor reflex, is a contributing cause to the vascular and tissue impairment in the intestinal mucosa during hemorrhage.

Animals↗

PubMed1975

Pressure regulation in the microcirculation.

The results of direct pressure measurements are described which demonstrate that pressures in a certain fraction of mesenteric capillaries remain remarkably constant during large changes in systemic pressure. The results of isogravimetric studies, reported in the literature, are also described which indicate that this phenomenon may also occur in the intestine. The question is raised whether capillary pressures may therefore be regulated. Pressures recorded from mesenteric arterioles and capillaries are shown which indicate that maintenance of a constant capillary pressure is primarily the consequence of the vascular architecture peculiar to this tissue, and is merely a secondary reflection of mechanisms associated with flow regulation. The results of direct pressure measurements recorded in the microcirculation of intestinal muscle are also shown. These data indicate that capillary pressures in innervated, denervated, and xylocaine-treated intestinal muscle change in direct proportion to variations in arterial pressure. It is concluded that capillary pressures in the intestinal muscle layers are therefore not regulated, so that the observation that capillary pressures may be maintained is probably a phenomenon unique to the mesentery. Pressures recorded from capillaries in the mucosal villi are also shown and compared to capillary pressures measured in the microvasculature of mesentery and intestinal muscle. When systemic pressure was normal (107 +/- 10 mm Hg), capillary pressure in the mesentery averaged 30 to 33 mm Hg; capillary pressures in the intestinal muscle averaged 22 to 24 mm Hg; and capillary pressures in the mucosal villi averaged 13 to 15 mm Hg. These data suggest that mesenteric capillaries are primarily a filtering network; intestinal muscle capillaries are normally in fluid balance; whereas at rest mucosal capillaries are primarily absorptive. These pressures, recorded from the three major regions of the rat intestine, were used to calculate a weighted average for the whole organ. The calculated value, based on assumed values for relative capillary densities, was 17 mm Hg. This result compares favorably with data from whole organ, isogravimetric studies, and may clarify some of the apparent discrepancies between previous isogravimetric and servopressure studies.

Animals↗

PubMedDate not supplied

Intestinal microvascular adaptation during maturation of spontaneously hypertensive rats.

Adaptive microvascular changes in increased arterial pressure were investigated in the intestine of spontaneously hypertensive rats (SHR). In 4- to 5-week-old normal Wistar-Kyoto (WKY) and SHR ras, as well as in 18- to 21-week-old WKY rats, the number of arterioles of a given type per milligram of tissue were very similar. However, 18- to 21-week-old SHR had 30% to 35% fewer arterioles in the diameter range of 25--35 mu, as if intestinal vessels were lost or failed to grow during maturation. The largest and smallest arterioles in the intestine of adult SHR were constricted by 20% to 25%, but other vessels in the SHR had an equal or increased diameter relative to those in WKY rats. As a result of rarefaction and selective vasoconstriction in SHR, microvascular pressures in the intestinal muscle of SHR were near those in WKY rats, and those in villi of SHR were equal to those in WKY rats despite a 60% to 70% increase in mean arterial pressure in SHR. The percentage of small arterioles (less than 15 mu) that were intermittently closed to flow at rest was minimal, and the total number of small vessels per milligram of tissue was equal in WKY and SH rats. These data indicate that the adaptive changes in the intestinal vasculature of SHR do not include the loss of small arterioles as occurs in skeletal muscle but that the vascular branching pattern is disturbed, and the largest and smallest arterioles are constricted in the intestine of SHR.

Adaptation, Physiological↗

PubMedDate not supplied

Microvascular adaptation in the cerebral cortex of adult spontaneously hypertensive rats.

The purpose of this study was to determine the microvascular characteristics that cause cerebral cortical blood flow autoregulation to shift to a higher range of arterial pressures during established hypertension in spontaneously hypertensive rats (SHR). An open-skull technique with constant suffusion of artificial cerebrospinal fluid (PO2 = 40-45 mm Hg, PCO2 = 40-45 mm Hg, pH = 7.35-7.45) was used to view the parietal cortex of 18- to 21-week-old SHR and Wistar Kyoto (WKY) normotensive control rats. The resting inner diameters of first (1A)-, second (2A)-, and fourth (4a)-order arterioles were significantly (p less than 0.05) smaller, and the wall thickness/lumen diameter ratios were significantly (p less than 0.05) larger in SHR compared to WKY. Only 1A and 4A has significantly (p less than 0.05) increased vessel wall cross-sectional area in SHR. At the resting mean arterial pressures of WKY and SHR, the passive (10(-4) M adenosine, topical) diameters of comparable types of arterioles were not significantly different (p greater than 0.05). At reduced arterial pressures, however, the arterioles in SHR had smaller maximum diameters than in WKY. Cortical blood flow in WKY and SHR was constant at arterial pressures from 70-150 mm Hg and 100-200 mm Hg, respectively. Resting arteriolar pressures in 1A, 2A, and 3A of SHR were substantially and significantly (p less than 0.05) elevated, although pressures in the smallest arterioles and venules of WKY and SHR were similar. Therefore, it is possible that cerebral capillary pressure is only slightly elevated, if at all, in SHR as a result of the vasoconstriction. The number of arterioles per unit area of brain surface at rest was equal in WKY and SHR. In addition, the number of vessels was equal in WKY and SHR during maximal dilation, and neither type of rat demonstrated an opening of previously closed vessels upon maximum dilation. Therefore, the cerebral arteriolar constriction in SHR, which was probably potentiated by vessel wall hypertrophy of the largest and smallest arterioles, was the major contributor to an upward shift in the autoregulatory range, the protection of exchange vasculature pressures, and the increase in vascular resistance.

Adaptation, Physiological↗