[The attenuation effectiveness of earplugs sold in local market].
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Biomedical subjects
Publications and source records attributed to R Y Chen.
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The effects of hypotension on systemic and renal hemodynamics, plasma renin activity (PRA), and renin secretion rate (RSR) were determined in dogs anesthetized with sodium pentobarbital plus chloralose. Renal blood flow (RBF) was determined with microspheres (15 micron) and with an electromagnetic flowmeter connected to an extra-corporeal circuit from the femoral artery to the renal artery. Hypotension was induced by nitroprusside infusion, which decreased peripheral resistance, and by hemorrhage, which reduced cardiac output. RSR increased in both forms of hypotension, but the increase following hemorrhage was greater than that after nitroprusside. Thus, when the mean arterial pressure (MAP) was reduced to 75 mmHg, RSR increased from 470 +/- 26 units/min to 990 +/- 12 units/min with nitroprusside and from 415 +/- 13 units/min to 1,509 +/- 21 units/min following hemorrhage. At MAP of 50 mmHg, RSR increased to 1,541 +/- 64 units/min with nitroprusside and to 2,254 +/- 98 units/min following hemorrhage. Nitroprusside increased renin secretion not only by an increase in sympathetic beta adrenergic activity through the baroreceptor reflex, but also by its direct vasolidatory effect in the renal circulation. In hemorrhagic hypotension, the increase in renin secretion was accompanied by renal vasoconstriction. The greater increase in RSR following hemorrhage than after nitroprusside at given levels of hypotension may be explained by a stronger beta adrenergic activation, the activation of prostaglandin and kallikrein systems, a lower microvascular pressure level, and/or smaller pulse pressure and lower sodium load in the macula densa. The comparison of renin secretion at the same degree of hypotension induced by different hemodynamic alterations serves to elucidate the mechanisms of renin secretion.
Ostwald solubility coefficients for 133Xe in plasma (Sp), red blood cells (Sc), and selected oral tissue homogenates (St) obtained from the dog were determined at 4, 20, 27 and 37 degrees C by counting the 133Xe activity of the air phase and the sample (liquid, red cells or tissue) in the same tube following equilibration. The partition coefficient for xenon (lambda, in ml/g) between red cells and plasma (lambda cp) and that between tissues and plasma (lambda tp) were calculated from the measured Sp, Sc and St. The tissue-blood partition coefficients (lambda tb) of oral tissues for 133Xe were then calculated using lambda cp, lambda tp and the haematocrit value. The calculated values of lambda tb at 37 degrees C and 50 per cent haematocrit were 0.650 for the pulp, 0.674 for the tongue, 0.828 for the submandibular gland and 0.881 for the gingiva of the dog. lambda cp increased and lambda tp decreased as the temperature was reduced from 37 to 4 degrees C.
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The baroreflex control of heart rate was investigated on 10 informed human subjects during light halothane anesthesia (0.3-0.5%, inspired concentration). The relationship of systolic pressure (SP) to the succeeding pulse interval (PI) was evaluated on a beat-to-beat basis during the entire course of sodium nitroprusside (SNP) depressor test. The initial slope of SP-PI plot (dPI/dSP) was used as an index of the sensitivity of baroreflex control of heart rate. Following an injection of SNP (4-6 micrograms/kg), dPI/dt was related directly to dPI/dSP, whereas the latter was inversely correlated with dSP/dt. The recovery of PI lagged behind that of SP, and there was a hysteresislike loop on the SP-PI plot. The time lag of PI recovery and the loop of SP-PI plot were markedly decreased by propranolol treatment and significantly increased by atropine. The slopes of SP-PI plot were significantly decreased by atropine but relatively unaffected by propranolol. These results indicate that SNP-induced hypotension in man during halothane anesthesia is associated with a withdrawal of parasympathetic inhibition and an enhancement of sympathetic activity. The autonomic control of heart rate in response to rapid changes in arterial pressure induced by SNP is dominated by parasympathetic influence; the more persistent sympathetic activity only becomes evident when the parasympathetic influence subsides quickly as the arterial pressure stays relatively constant at a new level. The slope of SP-PI plot (dPI/dSP) and the ratio of dPI/dt to dSP/dt during the decreasing pressure phase of SNP test can be used as indices for the sensitivity of baroreflex control of heart rate.
The relationship of bypass shunt blood flow to arterial pressure and stump pressure was studied in 12 informed patients undergoing carotid endarterectomy. These patients were anesthetized with halothane plus nitrous oxide. Systemic arterial blood pressure was measured with a radial artery catheter, and stump pressure as well as distal shunt pressure (carotid pressure distal to the shunt) were measured with a 25-gauge needle inserted cephalad to the bypass shunt. From the pressure drop across the bypass shunt, blood viscosity, geometry of the bypass tubing and the use of Poiseullie's law, the shunt blood flow can be calculated. The calculated shunt flow shows a close correlation with the difference between arterial pressure and stump pressure (r = 0.91) as well as with the slope of arterial pressure increase following carotid occlusion (r = 0.82); but it is poorly correlated with the stump pressure. Administration of 100 ml low molecular weight dextran solution does not improve the shunt blood flow, whereas 500 ml low molecular weight dextran significantly decreases blood viscosity. The patency of the carotid artery as assessed by angiogram does not give a proper indication of the need for a bypass shunt. The shunt flow as well as the need of such a shunt might be predicted by the use of the difference of arterial pressure and stump pressure. If the slope of arterial pressure increases rapidly following carotid occlusion, it can also be used to determine the necessity of such a shunt.
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The responses of alterations in regional hemodynamics and oxygen transport rate to hematocrit (Hct) were studied in 20 pentobarbitalized dogs. Hemodilution was carried out by isovolemic exchange with plasma in 12 dogs and the hemoconcentration with packed cells in 8 dogs. The cardiac output and regional blood flows were determined with the microsphere technique. In hemodilution, the increases of blood flow to the myocardium and the brain were out of proportion to the increase of cardiac output; the oxygen supply to the myocardium remained unchanged while that to the brain decreased only slightly. In hemoconcentration, vasodilation occurred in the myocardium and the brain to maintain constant oxygen supply. Splenic vessels had marked vasoconstriction with Hct alteration in either direction. Blood vessels in the liver, intestine, and kidney responded with a milder vasoconstriction and maintained a constant oxygen supply between Hct of 30-55%. Therefore, during Hct alteration, redistribution of blood flow to myocardium and brain occurred. The optimal Hct range for constant oxygen supply was different among various organs.
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The effects of surface hypothermia (25 degrees C) on arterial hematocrit value (by microcentrifuge) and plasma protein concentration (by refractometry) were studied in infants undergoing surface cooling for cardiac operations. To analyze in detail the mechanisms leading to the observed changes in patients, we performed parallel studies on normal dogs and permanently splenectomized dogs. In these dogs, measurements were also made of plasma volume (by 125I-albumin) and red cell volume (by 51Cr-erythrocytes). Arterial hematocrit value increased progressively during surface cooling in infants. Assuming that red cell volume remained constant and that the ratio of whole body red cell percentage to arterial hematocrit value during surface cooling in infants as in splenectomized dogs, we estimated percent changes in plasma volume in infants from arterial hematocrit data. The computed plasma volume decreased progressively as the body temperature was decreased. Since plasma protein concentration remained constant, the loss of plasma volume suggested a sequestration of whole plasma in portions of the circulatory bed and/or an extravasation of whole plasma into the interstitial space.
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In 17 pentobarbitalized dogs, the shunting of 15-micrometer and 9-micrometer microspheres was studied in the brain, myocardium, kidney, intestine, and lung. The veins of these organs were catheterized for constant blood withdrawal for 2 min by direct venipuncture. The ratio of microsphere radioactivity in the venous blood to that in the arterial blood gave the shunting of microspheres by the venous sampling technique. The 15-micrometer microspheres showed 2% or less shunting for all organs studied, whereas the 9-micrometer microspheres had shunting ranging from 3% in the coronary sinus to 24% in the portal vein. The shunting of 9-micrometer microspheres was also calculated from direct tissue counting, where the 15-micrometer spheres were considered to be completely entrapped. The results of direct tissue counting indicate that the 2-min venous sampling underestimates microsphere shunting. CO2 administration increased significantly the shunting of 9-micrometer spheres, whereas the shunting of 15-micrometer spheres determined by venous sampling remained less than 2%. Consideration of shunting indicates that the 15-micrometer microspheres might be more appropriate for regional organ blood flow measurements, including the myocardium.
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Hemodynamic functions and blood viscosity changes in hypothermia (core approximately 25 degrees C) were studied in 14 pentobarbital-anesthetized dogs subjected to surface cooling. The viscosity of blood (eta B) increased progressively to 173% of that at 37 degrees C when body temperature was lowered to 25 degrees C. The increase in blood viscosity was caused by: a) the direct effect of low temperature on plasma viscosity, b) hemoconcentration as a result of plasma loss, and c) the low-flow (low-shear) state induced by hypothermia. A larger portion of the increased viscosity was caused by the low-flow state in hypothermia. The systemic flow resistance (SFR) increased to 271% of control, and this was attributable about equally to the increases in blood viscosity and systemic vascular hindrance (SFR/eta B). Similarly, the viscosity of blood contributed significantly to raising the pulmonary flow resistance. The relative constancy of mixed venous O2 saturation suggests that the cardiac output at low body temperature is generally adequate to meet the metabolic needs.