We conclude that the investment of resources in our rural campus may add an increment to rural practice choice beyond the established associations with rural upbringing and family medicine residency. The decision of practice site choice is complex, and collaborative studies that include data from several schools with differently structured rural exposures, including those with rural clinical campuses, are needed.
Factors that alter peritoneal blood flow may influence the clearance of solutes during peritoneal dialysis. Arteriolar vasodilation, for instance, could increase the delivery of solutes to the capillaries and venules leading to an increase in solute transport into the peritoneal cavity. This study was designed to identify the vasoactive effects of several major components of McGaw and Dianeal peritoneal dialysis solutions to understand how the composition of these solutions may alter in vivo blood flow in the peritoneum. Because the major differences between these solutions and Krebs solution are a high osmolality, a high dextrose concentrations, and an acetate or lactate buffer system, we investigated the effects of these components. Rats were anesthetized with the combination of urethane and chloralose. The cremaster muscles, with the nerve and blood supplies from the rat still intact, was placed in a specially designed tissue chamber that was filled with Krebs solutions. A port permitted microscopic observations of the blood vessels. In vivo television microscopy observations was used to quantitate changes in small arteriole diameters induced by changes in the composition of the solution bathing the cremaster or by the addition of nitroprusside. Hyperosmolality produced by the addition of dextrose, sucrose, or sodium chloride to the Krebs solution induced a submaximal dilation of the small arterioles of the cremaster. The rate of dilation differed depending on the substance used to increase osmolality. A normal osmolality acetate (74 mM) or lactate (45 mM) solution produced a slow, submaximal dilation of the cremaster arterioles. Hyperosmolar acetate (37 or 74 mM) or lactate (45 mM) solutions produced a rapid, maximal dilation of these vessels. Because the rate of dilation and maximal effect produced by the commercial dialysis solutions were similar to these same parameters produced by the high-osmolality acetate or lactate solutions, the dilatory effects of McGaw and Dianeal solutions appear to be due to the combinations of high osmolality and the buffer anion acetate or lactate.
The autoregulatory ability of the renal vascular system in the split hydronephrotic kidney was quantitated with intravital microscopy. The luminal diameters of the arcuate and interlobular arteries as well as the afferent and efferent arterioles were measured. Glomerular blood flow was determined by the dual slit technique. In the first series of experiments, the renal perfusion pressure was reduced by graded clamping of the abdominal aorta. Pressure reduction from 118 mm Hg to 95 mm Hg induced dilation of all preglomerular vessels except for the distal afferent arteriole; there was no change in the efferent arteriole and the blood flow was maintained. Further pressure reductions to 71 and 43 mm Hg caused additional dilations of the preglomerular vessels, a marginal reduction in diameter of proximal efferent arterioles and flow reductions by 15% and 41%, respectively. In the second series, systemic blood pressure was increased by continuous i.v. infusions of norepinephrine (NE). NE constricted pre- and postglomerular vessels except for the distal afferent arteriole; glomerular flow was decreased. Reduction of renal perfusion pressure during NE infusion to the preinfusion value did not diminish glomerular blood flow, but reduced the constrictor response to NE in preglomerular vessels. In a third series of experiments we examined the effect of atrial natriuretic factor (ANF) on renal autoregulation. Addition of ANF (10(-9) to 10(-7) M) to the renal bath induced a dose-dependent dilation of all preglomerular vessels and a constriction of the efferent arteriole. Pressure reduction from 120 to 95 mm Hg resulted in a further preglomerular vasodilation. These experiments demonstrate that autoregulation is mediated primarily by diameter changes in all preglomerular vessels excluding the distal segment of the afferent arteriole. Further, these data suggest that ANF induced dilation of preglomerular vessels does not impair the myogenic response of these vessels.
The objectives of this study were the development of a skeletal muscle microcirculatory preparation, in which the complications of drug anesthesia were minimized, and the quantitation of the effects of urethan and chloralose anesthesia on the microcirculation. Rats were initially anesthetized with urethan and chloralose and decerebrated by a midcollicular transection. The cremaster skeletal muscle, with intact circulation and innervation, was prepared for intravital microscopy by placement in a tissue bath. Arterioles (9-70 micrometers diam) at several anatomic levels were observed during the initial period of urethan-chloralose anesthesia (period 1), after recovery from the anesthesia (period 2), and again following reanesthetization (period 3). During period 2, respiratory rate, heart rate, and mean arterial pressure were significantly greater than during periods 1 and 3. Smaller arterioles (8-50 micrometers diam) exhibited vasomotion (mean amplitude 35% of mean diameter; mean frequency 31 cycles/min) during period 2. Urethan-chloralose anesthesia during periods 1 and 3 inhibited vasomotion and increased arteriolar diameters by 16-36%. This study quantitates the depressant effects of urethan-chloralose anesthesia on the cardiovascular system and demonstrates the feasibility of using decerebration to circumvent the necessity of continuous drug anesthesia for in vivo microvascular studies.
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