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Biomedical subjects

C F Rothe

Publications and source records attributed to C F Rothe.

At least 37 records · Page 2Linked to original sources
PubMed1985

Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs.

The magnitude of vascular capacitance change induced by hypercapnia, hypoxia, or hypoxic hypercapnia was estimated during the administration of experimental gas mixtures to anesthetized dogs for 25 min. Mean circulatory filling pressure (Pcf) was determined by fibrillating the heart and equilibrating arterial and venous pressures with a pump. We assumed that the total blood volume remained constant and that the magnitude of change in peripheral venous volume equaled the sum of the changes in blood volume in the cardiopulmonary and arterial beds. We further assumed that active (reflex) peripheral venoconstriction occurred if the cardiopulmonary and arterial bed blood volumes, as well as the Pcf, increased. Within 3 min, severe hypercapnia and hypoxic hypercapnia induced a 5.2 and 7.3 ml/kg reduction in systemic vascular capacity, and, by 19 min of experimental gas presentation, increased Pcf by 5.5 and 7.0 mmHg, respectively. Severe hypoxia had less effect (0.7 ml/ kg and 2.5 mmHg, respectively) at 19 min. Severe hypercapnia also increased the central venous, systemic arterial, and pulmonary arterial pressures and decreased heart rate. Hypoxic hypercapnia additionally increased cardiac output. We conclude that severe systemic hypercapnia, whether alone or in combination with hypoxia, causes a significant active reduction in vascular capacitance, but severe hypoxia is less effective.

Animals↗
PubMed1983

Total body vascular capacitance changes during high intracranial pressure in dogs.

The active capacitance response to increased intracranial pressure (Pic) was studied in nine chloralose-anesthetized dogs. The vena cavae were cannulated and drained into a reservoir as blood was pumped at a constant flow (Q) into the right atrium. Central blood volume was determined as Q times the mean transit time of dye from the right atrium to the aortic root. Arterial compliance (Ca) was determined from the monoexponential decay of systemic arterial pressure (SAP) during vagal cardiac arrest to compute changes in arterial volume (delta SAP X Ca). Atropine was administered to prevent bradycardia and dangerous, constant cardiac output-induced increases in pulmonary arterial (PAP) and right and left atrial pressures. Blood volume shifts indicative of active venoconstriction, included changes in reservoir, central, and arterial volumes during Pic of 100-200 mmHg. Raised Pic, after atropine, induced a tachycardia, increased systemic and pulmonary resistances, and increased SAP and PAP. Venoconstriction caused marked blood shifts between 125 and 200 mmHg Pic. The extrapolated response threshold was about 112 mmHg. In the most sensitive range, venoconstriction amounted to 3.9 ml X kg-1 per 25-mmHg change in Pic. These results indicate that intense active capacitance vessel constriction is an important part of cardiovascular hemostasis during rapidly increased intracranial pressure.

Animals↗
PubMed1982

Active hepatic capacitance responses to neural and humoral stimuli in dogs.

Active changes in hepatic capacitance were studied in pump-perfused dog livers during hepatic nerve stimulation or during intrahepatic arterial infusion of histamine (0.01-1 mg/l) or epinephrine (0.05 mg/l). Hepatic nerve stimulation at 5 pulses/s (pps) reduced hepatic blood volume by 76 +/- 39 (SD) ml/kg tissue and decreased the apparent hepatic compliance 36% from a control value of 25.6 +/- 9.3 ml.kg-1.mmHg-1, with constant flow perfusion. With a constant hepatic arterial pressure, 5 pps stimulation decreased hepatic arterial flow to 16% of control; the volume expelled was 91 +/- 33 ml/kg. Epinephrine caused hepatic artery constriction, the active expulsion of 71 ml/kg of blood, and a decrease of about 30% in hepatic compliance. Histamine dramatically reduced the hepatic vascular compliance, decreased the portal venous conductance, increased hepatic arterial conductance, and caused the apparent hepatic blood volume to double. Increased hepatic venous pressure, hepatic nerve stimulation, epinephrine, and, especially, histamine caused a significant filtration of fluid from the hepatic vasculature. We conclude that significant active capacitance changes and transsinusoidal fluid filtration can be induced in the canine liver by neural and hormonal stimuli.

Animals↗
PubMed1981

Hepatic capacitance responses to changes in flow and hepatic venous pressure in dogs.

The effect of changes in inflow and hepatic venous pressure (Phv) on the hepatic vascular bed was studied in denervated, pump-perfused canine livers. Hepatic arterial, portal venous, and hepatic venous pressures and flows were continuously monitored as was the hepatic venous hematocrit (Hct). The hepatic venous outflow, which averaged 1179 +/- 356 (SD) ml x min-1 x kg tissue-1 at control conditions, was controlled by a servosystem set to keep Phv at the desired level. Hepatic volume changes (delta V) were determined by integration of the difference between hepatic inflow (Fin) and outflow (Fhv). Over the range of Phv of 0-15 mmHg, the delta V-to-delta Phv ratio (apparent compliance C) was linear; C = 19.8 ml x mmHg-1 x kg tissue-1. These increases in Phv caused transient and plateau increases in Hct of 1.26 and 0.42%/mmHg, respectively. Varying inflow over the range of 0-156% of control by changing hepatic arterial and/or portal venous flow(s) resulted in delta V of 0.066 ml/kg per ml x min-1 x kg tissue-1 change in flow. We conclude that changes in Fin as well as changes in Phv cause changes in liver volume; and that a significant fraction of the volume shift accompanying changes in Phv is due to transsinusoidal plasma movement.

Animals↗
PubMed1980

Measuring systolic arterial blood pressure. Possible errors from extension tubes or disposable transducer domes.

The purpose of this study was to evaluate the magnitude of possible error in the measurement of systolic blood pressure if disposable, built-in diaphragm, transducer domes or long extension tubes between the patient and pressure transducer are used. Sinusoidal or arterial pressure patterns were generated with specially designed equipment. With a long extension tube or trapped air bubbles, the resonant frequency of the catheter system was reduced so that the arterial pulse was amplified as it acted on the transducer and, thus, gave an erroneously high systolic pressure measurement. The authors found this error to be as much as 20 mm Hg. Trapped air bubbles, not stopcocks or connections, per se, lead to poor fidelity. The utility of a continuous catheter flush system (Sorenson, Intraflow) to estimate the resonant frequency and degree of damping of a catheter-transducer system is described, as are possibly erroneous conclusions. Given a rough estimate of the resonant frequency of a catheter-transducer system and the magnitude of overshoot in response to a pulse, the authors present a table to predict the magnitude of probable error. These studies confirm the variability and unreliability of static calibration that may occur using some safety diaphragm domes and show that the system frequency response is decreased if air bubbles are trapped between the diaphragms. The authors conclude that regular procedures should be established to evaluate the accuracy of the pressure measuring systems in use, the transducer should be placed as close to the patient as possible, the air bubbles should be assiduously eliminated from the system.

Air↗
PubMed1980

Linearity of the vascular pressure-volume relationship of the canine intestine.

To test whether the pressure-volume relationship of the canine small intestinal vasculature is linear over the normal range of portal venous pressures (5 to 35 mm Hg), we used two methods to measure volume: (1) the integral of inflow minus outflow (IFD), and (2) tissue activity of 51Cr-labeled erythrocytes (Cr-51). Venous pressures were changed in steps of 5 mm Hg with a servo-controlled system. The tissue was perfused at a constant rate. With venous pressures of 3.6 to 38.6 mm Hg, the vascular compliance was 2.19 +/- 0.42 (SD) ml/kg x mm Hg using IFD, and 1.87 +/- 0.50 ml/kg x mm Hg using Cr-51. Although a quadratic term significantly improved the fit, the effect was small (less than 3 ml/kg with a 30 mm Hg venous pressure change). The control blood volume of the intestinal loop at a venous pressure of 8.6 +/- 1.5 (SD) mm Hg was 86.2 +/- 19.1 ml/kg tissue weight using the mean transit time of a step input of indocyanine green at a perfusion pressure of 106 +/- 29 mm Hg and a flow of 556 +/- 147 ml/min x kg. We conclude that there is no significant change in compliance over the normal venous pressure range of 5-35 mm Hg.

Animals↗
PubMed1979

Actively circulating blood volume in endotoxin shock measured by indicator dilution.

To estimate the size of the actively circulating blood volume of splenectomized dogs during control conditions and after endotoxin infusion, the pattern of concentration changes of 51Cr-labeled erythrocytes and 125I-labeled albumin was monitored. A dual exponential equation was fitted to the data. The total red blood cell and albumin volumes of distribution were determined from the slow exponential disappearance curves. The active red blood cell and albumin volumes were 89.8 +/- 5.3% and 92.0 +/- 2.0% of the total volumes, respectively. After endotoxin shock (mean arterial blood pressure 49.1 +/- 17.8 mmHg) the active volumes fell to only 60.0 +/- 10.3% and 56.2 +/- 20.0% of the total volumes, respectively. The fast-mixing time constants were similar (3.1 +/- 1.4 min and 2.5 +/- 2.7 min, respectively) and did not change significantly during the endotoxin shock, indicating that the albumin tag mixed into its larger volume of distribution as rapidly as the cells mixed into their indicated volume. We conclude that 1) an active blood volume can be distinguished, 2) it decreases for both red blood cells and albumin in endotoxin shock, and 3) a major part of the "extravascular plasma volume," as estimated by albumin dilution, is in the actively circulating circulation.

Animals↗
PubMed1978

Vascular capacitance of dog intestine using mean transit time of indicator.

Changes in vascular volume of dog jejunum caused by norepinephrine, isoproterenol, or acetylcholine at constant=flow perfusion, were compared to changes in volume caused by changes in blood flow or venous pressure. Vascular volume was measured by indicator dilution mean transit time, using a step input of indocyanine green (125 microgram/min). Venous pressure was held at 10 mmHg; control arterial pressure was about 110 mmHg. At a control flow of 521 ml/min.kg of tissue, the vascular volume was 104 +/- 14 (SD) ml/kg of tissue. Reducing flow by 75 percent caused the volume to decrease by 29 percent (--31 ml/kg); maximal norepinephrine infusion at constant flow and venous pressure decreased the vascular volume by 24 percent, and a 10-mmHg reduction in venous outflow pressure caused a 25 percent (--27 ml/kg) reduction. On the other hand, isoproterenol (100 microgram/liter) at constant flow caused a 245 percent increase in conductance and only a 12 percent increase in vascular volume. Thus, active venoconstriction, changes in venous pressure, or changes in flow independently may cause changes in vascular volume of the intestine. Active smooth muscle changes in the venous capacitance vessels are not necessarily correlated with changes in the arterial resistance vessels.

Acetylcholine↗
PubMed1976

Vascular capacitance and fluid shifts in dogs during prolonged hemorrhagic hypotension.

The mean circulatory pressure (Pmc) in dogs anesthetized with chloralose-urethane was estimated from 0.5 to 150 minutes after hemorrhages of 0, 17, or 34 ml/kg, or that volume giving an arterial pressure (Pa) of 40 mm Hg. The Pmc was determined by fibrillating the heart and then rapidly pumping blood from aorta to vena cava until Pa=venous pressure (Pv)=Pmc. Within about 10 seconds, the heart was defibrillated. Vascular compliance was estimated as the ratio of a test blood volume change (0, +/- 8.5, or 17 ml/kg) to the change in Pmc, determined 0.5 minute after the start of the test volume change. Erythrocyte and plasma volumes were measured by 51Cr-erythrocyte and 125I-albumin dilution. In response to prolonged hemorrhage: (1) the total vascular compliance apparently decreased; (2) most of the changes in capacity vessels occurred within 5 minutes, and indeed a large part of the response probably had occurred by the time of the first measurement at 30 seconds; (3) the progressive recovery in Pmc after 5 minutes was primarily from fluid shifting into the vasculature; (4) even after 2 hours of severe hemorrhagic hypotension, the venoconstriction was not lost; but (5) after an hour of severe hemorrhagic hypotension (arterial pressure of 40 mm Hg) there was water loss from the vasculature, because plasma protein and erythrocyte concentrations and plasma oncotic pressure increased.

Animals↗