Effects of peritoneal dialysis solutions on human clearance and rat arterioles.
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Biomedical subjects
Publications and source records attributed to D L Wiegman.
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Closed-circuit television microscopy was used to quantitate the in vivo response of small arteries (approximately 100 micron) and small veins (approximately 150 micron) to topically applied norepinephrine in the rat cremaster muscle. Rats were anesthetized with pentobarbital (50 mg/kg), or urethane (1200 mg/kg) or a combination of urethane (800 mg/kg) and chloralose (60 mg/kg). Complete concentration-response curves were obtained for an artery and vein pair in each rat and pD2 values (-log ED50) were used to evaluate the vascular sensitivity to norepinephrine. Both the artery and the vein in urethane-anesthetized animals had decreased sensitivity to norepinephrine in comparison to the vessels of animals anesthetized with pentobarbital or urethane-chloralose. Pretreatment with cocaine (10(-5) M) significantly increased the sensitivity of both the artery and vein in pentobarbital-anesthetized animals but did not affect the vessels in urethane-chloralose-anesthetized animals. These results are consistent with two opposing effects of the urethane-chloralose combination. The first is an increased sensitivity to norepinephrine via blockade of neuronal uptake and the second is a decreased sensitivity of norepinephrine via a vascular inhibitory effect of urethane.
Television microscopy was used to quantitate the responses of small arteries and veins, in the wings of unanesthetized bats, to alterations in the inspired concentrations of O2 and CO2. Mean arterial pressure, heart rate, and the diameters of small arteries (28-54 mum) and veins (50-128 mum) were measured during a 90-min protocol--30 min with an inspiratory gas mixture of 20% O2 and 80% N2 (control period); 30 min with a gas mixture containing 5% O2 (hypoxic period) or 12, 20, or 28% CO2 (hypercapnic period); and 30 min with the original control gas. The hypoxic responses were dilatation of arteries and no change in the veins in both innervated and surgically denervated wings. Hypercapnia resulted in artery dilatation in innervated wings. Hypercapnia resulted in artery dilatation in innervated wings and constriction in denervated wings. The veins constricted in both innervated and denervated wings during the hypercapnia period. In another series, topical application of Krebs solutions (pH ranging from 7.7 to 6.7) to exposed segments of small arteries and veins produced dilatation of both vessels with decreasing pH. Artery dilatation during hypoxia and vein constriction during hypercapnia involve non-neural mechanisms, while both a neural stimulus for dilatation and a non-neural stimulus for constriction are components in the response of innervated arteries to hypercapnia. The non-neural stimulus for artery and vein constriction during hypercapnia is not a local decrease in pH.
In the past 10 years, microcirculation studies have emphasized quantitative measurements of microvascular diameters to characterize in vivo small vessel responses to experimental forcings such as hemorrhage, anesthesia, and hypoxia. We have developed an instrument to obtain continuous diameter measurements of a small artery and vein (40-200 mu) via closed-circuit television microscopy. The outputs are analog voltages proportional to the vessel diameters. Video processing is limited to two image areas termed "windows," which are defined by markers on the monitor and positioned over separate vertically aligned vessels. Each vessel, which appears darker than the surrounding tissue, is located by comparing the video signal to a reference voltage that adapts to changes in the relative contrast within the window. In the presence of a vessel, a ramp voltage is generated, the peak value of which is proportional to the vessel diameter. These peaks are averaged over the 15-video lines of the window and over several video frames to reduce noise sensitivity. In order to accommodate preparation movement such as skeletal muscle contraction, window position and width automatically adapt to changes in vessel position and width. Visual verification of system performance is provided by clamping the video signal to white on that portion of the image which the instrument identifies as vessel.
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Aerobic and anaerobic energy transformations were measured in two trained runners during 90-sec treadmill runs at 23.6 km/hr (2% grade). The runs were preceded by rest or either of two warm-ups: 1) 15-min run at 10 km/hr, or 2) 15-min run at 10 km/hr followed by 3-min standing. Compared with runs without warm-up, during the third half minute of runs following both types of warm-up 11% greater heart rates (HR), 8% greater oxygen consumption (Vo2), and unchanged ventilation were recorded. The rate constant of the approach of Vo2 to O2 in the first minute of work was unaffected by warm-up. Runs following either warm-up resulted in 25% lower lactate production; during these runs 3 to 4 degrees C higher gastrocnemius muscle temperatures (Tm) were maintained. The differences in HR, Vo2, and Tm continued throughout exhausting 5-min runs at 20.9 km/hr (2% grade). An elevated muscle temperature may therefore be requisite for the maximal aerobic response to a short exhausting run.
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Norepinephrine-induced changes in diameters of first- (1A), second- (2A), and third-order (3A) arterioles in the exposed cremaster muscles of normotensive and renovascular hypertensive rats were quantitated via television microscopy. By 2 weeks following the surgery to induce hypertension, we found that 3A sensitivity to norepinephrine had increased and the 1As had chronically constricted. By 4 weeks, the constriction had progressed to include both 1A and 2A. Sensitivity was no longer increased in 3As and, in fact, sensitivity had decreased in 1As and 2As. The 1As and 2As could not be dilated with isoproterenol or nitroprusside; thus, the vessels appeared to have undergone a structural alteration. We suggest from these results that the early increased 3A sensitivity contributes to the initial development of hypertension. The larger arterioles then constrict to protect the downstream vessels from increased luminal pressure. As the hypertension develops, the constriction progresses to smaller arterioles in an attempt to maintain normal pressure in the capillaries (site of water exchange). The constricted arterioles contribute to increased total peripheral resistance, and with the constriction, there occurs a general decrease in vessel responsiveness.