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Biomedical subjects

C F Rothe

Publications and source records attributed to C F Rothe.

49 records · Page 3Linked to original sources

Reflex vascular capacity reduction in the dog.

The maximum degree and time course of active reflex venoconstriction in chloralose-anesthetized dogs was studied. The mean circulatory filling pressure (Pmc) was measured by fibrillating the heart and rapidly pumping blood from the aorta to the vena cava until the systemic arterial pressure equaled the central venous pressure. Ventricular fibrillation was continued for 1 minute and was assumed to induce maximal sympathetic discharge to the capacity vessels. Blood was removed to maintain the Pmc constant at the level determined at 8 seconds after the start of fibrillation. It was necessary to remove 13.8 ml/kg by the end of 1 minute. After autonomic nervous system blockade by hexamethonium only 4.8 ml/kg were removed to hold the Pmc constant. Thus, in conclusion, the maximal degree of active venoconstriction induced by circulatory arrest was 9.0 ml/kg during the 1st minute of cardiac fibrillation. A basal capacity vessel tone was present, equivalent to 10 ml/kg under the experimental conditions used.

Animals↗

Assessing microvascular volume change and filtration from venous hematocrit variation of canine liver and lung.

The volume increase of canine liver after 1 min of a 10 mmHg elevation in hepatic venous pressure has been reported as 251 ml/kg tissue. An analysis of the transient hematocrit variation in hepatic venous blood indicated that 16% of the volume change results from transcapillary filtration, 72% from microvascular expansion, and 12% from macrovascular expansion. In the analysis, we first used the temporal change of the liver volume to determine the time course of the filtration and microvascular and macrovascular volume change. We next deduced, for a permeable microcirculation with a microvascular hematocrit lower than the feed hematocrit (the Fahraeus effect), how the filtration and microvascular volume change (MVC) produce a hematocrit variation in the blood leaving microcirculation. By accounting for the dispersion of the blood flow, the analysis predicted a hematocrit variation in the hepatic venous blood that matched well with the measured variation over the 1-min course of experiment. A reasonable fit with the hematocrit variation of pulmonary blood also was obtained for experiment with an 8 mm/Hg increase in the arterial and venous pressure perfusing the canine left lower lung lobe. The tissue and vascular volume increase at 1 min was 149 ml/kg tissue with 4% as a result of filtration, 41% as a result of microvascular expansion, and 55% as a result of macrovascular expansion. The large MVCs from the hepatic and pulmonary circulation indicate their microcirculations function as a reservoir in controlling blood volume redistribution.

Animals↗