Search PubMed⌕ Search

Biomedical subjects

R L Prewitt

Publications and source records attributed to R L Prewitt.

At least 55 records · Page 3Linked to original sources

Arteriolar dimensions from unanesthetized rabbits.

Arteriolar dimensions were determined during vasodilated states of natural vasomotion in unanesthetized rabbits using the ear chamber technique. Analysis of 383 arteriolar segments were made in 16 New Zealand white rabbits, 8-9 weeks after implantation of the ear chamber under the conditions of 25.5 +/- 0.5 degrees C (room temperature), 33.6 +/- 1.4 degrees C (ear surface temperature), 38.3 +/- 0.5 degrees C (rectal temperature), 66.5 +/- 3.2 mmHg (aortic mean blood pressure) and 238.6 +/- 33.0 beats/min (heart rate). Inside diameter (ID) and outside diameter were measured by closed circuit television microscopy using a Vista model 308 video image splitter. Wall thickness (WT) vs. ID, wall-to-lumen ratio (W/L) vs. ID and cross-sectional wall area (CSWA) vs. ID were fitted to the formulae: WT = 0.14 X ID + 3.8 (r = 0.76, p less than 0.001), W/L = 4.23 divided by ID + 0.12 (r = 0.84, p less than 0.001) and CSWA = 0.57 X ID2 + 11.0 X ID + 93.7 (r = 0.93, p less than 0.001), respectively. W/L increased rapidly in precapillary arterioles, especially below 30 micron ID, since WT has a finite size while ID does not. This structural property of resistance vessels is important in regulating peripheral resistance, blood flow, and downstream capillary density.

Animals↗

Microvascular alterations in the one-kidney, one-clip renal hypertensive rat.

The microcirculation was studied in one-kidney, one-clip renal hypertensive rats ( 1KG ) and uninephrectomized controls at 4-6 and 8-10 wk postoperation. Under chloralose-urethan anesthesia the gracilis muscle was transilluminated in situ with a light pipe. Measurements of arteriolar and capillary density and arteriolar diameter were made in three consecutive states: innervated, denervated, and vasodilated with nitroprusside. Arteriolar wall-to-lumen ratio was measured after vasodilation. At 4-6 wk vasoconstriction was significantly greater in 1KG and vasodilated arteriolar diameter was significantly smaller, partially because of an elevated wall-to-lumen ratio. Capillary density in 1KG was reduced in the innervated and denervated states compared with controls. At 8-10 wk in the 1KG , arteriolar vasoconstriction was no longer significantly elevated. However, the vasodilated arteriolar diameter was smaller, wall-to-lumen ratio had increased further, and rarefaction of arterioles and capillaries was present. Thus, with time, structural mechanisms for increasing vascular resistance were seen to displace the active mechanism of vasoconstriction.

Animals↗

A mathematical representation of the microvascular network in the bat's wing.

We previously have published a description of a mathematical representation for general vascular networks. In this paper we will illustrate the application of this operator representation to the microvascular network found in the wing web of the bat. We will show that this method follows the rules of vector algebra, it can be used for determination of Orthogonality of two vectors, and can be used in calculating resistance through the microvascular network. The method can also be used for representation of vessel networks in three dimensions.

Animals↗

Capillary pressure gradients in cremaster muscle of normotensive and spontaneously hypertensive rats.

The purpose of this investigation is to test the hypothesis that capillary pressure gradients are elevated in spontaneously hypertensive rats (SHR) and to determine the mechanism for the elevation. The cremaster muscle was prepared for microscopic examination under chloralose-urethane anesthesia in seven SHR and eight Wistar-Kyoto (WKY) rats 4-6 weeks of age. Capillary hematocrit, diameter, and red cell velocity were measured. Capillary flow induced by a time-varying pressure gradient was treated mathematically. A finite Hankel transformation was applied to the Navier-Stokes equation for capillary vessels. The solution was expressed as a Fourier-Bessel series, and the fluctuation of capillary flow induced by a time-varying pressure gradient was studied. It was shown that if the velocity fluctuation depended only on the pressure gradient, then the velocity fluctuation would be diminished almost instantly after the capillary started to flow. Capillary pressure gradient and shear stress were evaluated according to two different flow models, Newtonian and Casson. The capillary viscosity was obtained from the capillary hematocrit based on the empirical correlation of viscosity vs hematocrit. Calculations based on both flow models indicate that the capillary pressure gradient and shear stress of SHR is higher than in WKY, especially in vessels near 6 microns in diameter. The elevated pressure gradient is due to a combination of reduced capillary density, causing a higher red cell velocity and a tendency toward smaller capillary diameters in the SHR. Capillary hematocrit and viscosity were not elevated in the SHR.

Animals↗

Development of microvascular rarefaction in the spontaneously hypertensive rat.

Using stereological methods in vivo, we have investigated the rarefaction of arterioles and capillaries in male spontaneously hypertensive rats (SHR) and the Wistar-Kyoto controls (WKY) at 6-8, 12-14, and 16-18 wk of age. Under chloralose-urethan anesthesia, the gracilis muscle was isolated for microscopic observation. Vessel length and surface area per unit volume of tissue (density) were determined during three consecutive states: innervation, denervation, and vasodilation with nitroprusside. Arteriolar wall-to-lumen ratio was measured after vasodilation. At 6-8 wk capillary density was reduced in the SHR. At 12-14 wk there was a reduction of arteriole and capillary density under innervated and denervated conditions but not after vasodilation (a state of functional rarefaction). At 16-18 wk there was a reduction of arteriolar and capillary density under all three conditions (a state of anatomical rarefaction). At 12-14 and 16-18 wk there was an elevated level of arteriolar vasoconstriction in the SHR that was masked in any one state by the closure of the smaller arterioles. Arteriolar wall-to-lumen ratio was not elevated in the SHR at any time. Arteriolar closure was not reversed by acute denervation.

Aging↗

Microvascular rarefaction in spontaneously hypertensive rat cremaster muscle.

We have investigated the neural and local vascular effects on vessel length and surface area per unit volume in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) by quantitative stereology. Fourteen SHR and 14 KWY (70-130 g) were anesthetized with chloralose-urethan, and the cremaster muscle was exposed for microscopic observation. The large arterioles entering the muscle were termed the first order, and consecutive branches were termed second-, third-, and fourth-order arterioles. The data were collected in three consecutive states: innervated, denervated, and vasodilated with nitroprusside. The third- and fourth-order arteriole and capillary lengths per unit volume in the SHR were less than those of the WKY in all three states. The vessel surface area per unit volume was also reduced in the SHR. Denervation and sodium nitroprusside (Nipride) resulted in larger percent increases in vessel length and surface area in the SHR than in the WKY. We conclude that in the SHR cremaster muscle there are fewer terminal arterioles and capillaries anatomically present, and, under resting conditions, a greater percentage but similar absolute number of them are closed to flow.

Animals↗

The effects of allopurinol on skeletal muscle microcirculation in normal and dystrophic mice.

Allopurinol lowers peripheral vascular resistance in dogs, and it has beneficial effects upon muscular dystrophy patients. Since it has been suggested that muscular dystrophy may result from muscle ischemia, we decided to investigate the effects of allopurinol on skeletal muscle blood flow in normal and dystrophic mice. Arterioloar red cell velocity and diameters were measured in the cremaster muscle and used to calculate blood flow. Allopurinol (5 mg/kg, i.p.) resulted in an 81% increase in arteriolar blood flow in normal mice and a 102% increase in dystrophic mice. Such an increase in microcirculatory perfusion could be a mechanism contributing to the clinical effects of allopurinol.

Allopurinol↗

Oxygen uptake and tissue oxygen tension during adrenergic stimulation in canine subcutaneous adipose tissue.

The effect of sympathetic nerve stimulation (NS) and injected noradenaline (NA) or isoprenaline (Iso) on PVO2, VO2 and PtO2 was studied in isolated canine subcutaneous adipose tissue. These effects were compared to those produced by mechanical blood flow reduction (clamping). Resting VO2 measured 13.0+/- 2.3 mumol X min-1 X 100 g-1. When blood flow was reduced by 20% or less there was no significant change of VO2. Reducing blood flow to 50% of control or less by NS caused a parallel reduction in VO2, while clamping reduced VO2 significantly less. NA gave effects similar to those of NS. After NS or NA there was a period of hyperemia and increased oxygen extraction which more than compensated for the decrease in VO2 during vasoconstriction. Such a net increase in VO2 was not produced by clamping. Control PtO2 averaged 29+/-2 mmHg. NA reduced it by 70% and clamping to the same blood flow level only by 14% (p less than 0.01). Thus, a mere reduction in blood flow has little effect on PtO2, while blood flow reduction combined with redistribution of blood flow and an increased oxygen deman can lead to tissue hypoxia.

Adipose Tissue↗

Mechanisms of radio-protection by catecholamines in the hamster (Mesocricetus auratus).

Whole-body exposure to 1000 or 2000 rads in a 60Co source was used to study radio-protection by norepinephrine, isoproterenol, and phenylephrine in normal and splenectomized hamsters. After exposure, the animals were caged individually, and percent survivals were recorded daily. The aortic blood pressure of permanently cannulated, unanaesthetized hamsters was measured to test the vasoconstriction-hypoxia mechanism of radio-protection, and plasma calcium levels were measured to test the hypothesis that isoproterenol protects through a mechanism of hypercalcaemia-stimualted cell proliferation. The data support the vasoconstriction-hypoxia mechanism for agents stimulating the alpha receptors, while beta agonists seem to protect through a hypotensive-hypoxia mechanism similar to that of histamine. All the catecholamines protect against the haematopoietic syndrome, but show no evidence of protection against the gastrointestinal syndrome.

Animals↗