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.

The responsiveness of the microvasculature and arteries during cerebral cortical autoregulation in rats was determined from measurements of microvascular pressures and blood flow as the systemic arterial pressure was altered. At systemic arterial pressures from 65 to 155 mmHg, cortical blood flow was essentially constant. Arterioles with a resting internal diameter of 20-70 microns responded by nearly equal proportional changes in diameter over this pressure range, but microvascular pressures were a linear function of arterial pressure. The percent of control changes in arterial and microvascular resistances at systemic pressures from 80 to 180 mmHg were nearly identical. Therefore, the microvasculature and arterial vasculature were approximately equally responsive to changes in arterial pressure over most of the autoregulatory pressure range. In addition, the arterial vasculature controlled 45-50% of the total vascular resistance at systemic arterial pressures from 40 to 180 mmHg. These data indicate that the cerebral vascular autoregulation in the rat depended substantially on the approximately equal responsiveness of the arterial vasculature and microvasculature. Similar results have been reported in cats and may indicate a common form of cerebral vascular control, which involves both the microvasculature and brain arteries among different species.

The role of neural, metabolic, physical, and humoral factors in the intestinal hyperemia associated with chronic portal hypertension was examined by use of the rat portal vein stenosis model. Intestinal blood flow and splenic pulp pressure were increased, while systemic arterial pressure and total vascular resistance were reduced in portal vein-stenosed rats as compared with controls. The reduction in total vascular resistance was entirely due to a fall in precapillary resistance and was accompanied by an increase in intestinal capillary pressure, which exceeded that produced by acute portal pressure elevation to the same level. Arteriovenous shunting of 15-micron microspheres was four times higher in portal-hypertensive rats. Cross-perfusion of control intestinal preparations with arterial blood from portal-hypertensive rats produced a 30% increase in blood flow. Plasma glucagon levels in portal-hypertensive rats were three times higher than in controls. Intra-arterial infusion of glucagon (at a rate that achieved the concentration measured in portal-hypertensive animals) produced a 20% reduction in intestinal vascular resistance. The results of these studies indicate that humoral factors, including glucagon, are primarily responsible for the hyperemia associated with portal hypertension.

A deep-tissue pressure injury (DTPI) is a serious type of pressure injury that begins in tissue over bony prominences and can lead to the development of hospital-acquired pressure injuries (HAPIs). Using a commercially available thermal imaging system, study authors documented a total of 12 thermal anomalies in 9 of 114 patients at the time of admission to one of the study institution’s ICUs over a 2-month period. An intensive, proven wound prevention protocol was immediately implemented for each of these patients. Of these 12 anomalies, 2 ultimately manifested as visually identifiable DTPIs. This represented a 60% reduction in the authors' institution’s historical DTPIs/HAPI rate. Because these DTPIs were documented as present on admission using the thermal imaging tool, researchers avoided a revenue loss associated with nonreimbursed costs of care and also estimated financial benefits associated with litigation expenses known to be generated with HAPIs. Using thermal imaging to document DTPIs when patients present has the potential to significantly reduce expenses associated with pressure injury litigation. The clinical and financial benefits of early documentation of skin surface thermal anomalies in anatomical areas of interest are significant.