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J L Robotham

Publications and source records attributed to J L Robotham.

100 records · Page 6Linked to original sources
PubMed1979

A model of the effects of respiration on left ventricular performance.

We have investigated the interaction of left ventricular afterload and right-heart volume on left ventricular performance. By utilizing a right-heart bypassed heart-lung preparation, we have been able to control independently each factor. We have previously suggested that the major influences of the inspiratory decrease in pleural pressure in decreasing left ventricular stroke volume (LVSV) may be via the inspiratory increases in left-heart afterload and right-heart volume (RHV). Thus, our preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Our results show that increases in transmural (relative to pleural pressure) aortic pressure (Pao) caused an increased left ventricular end-diastolic pressure (LVEDP), and that the effect of equivalent increases in Pao was greater when RHV was greater. Increase in RHV had minimal effects at low volume, but resulted in large increases in LVEDP at large RHV. These effects were markedly attenuated after pericardiectomy. Rapid increases in either RHV or Pao produced transient falls in LVSV. Our results are consistent with the hypothesis that increases in both right-heart volume and LV afterload contribute to the inspiratory decrease in LVSV and increase in LVEDP.

Animals↗
PubMed1979

Left ventricular hemodynamics during respiration.

We have investigated the mechanisms involved in the inspiratory fall in left ventricular stroke volume (LVSV), utilizing a spontaneously breathing dog on right-heart bypass (RHBP). We have been able to control lung volume, pulmonary artery inflow, and right-heart volume (RHV). During Mueller maneuvers in one series, RHV was allowed to increase as pleural pressure (Ppl) fell; in a second series, changes in RHV were excluded. In both series LVSV fell significantly, associated with a significant rise in the transmural (relative to Ppl) aortic diastolic pressure, reflecting an increase in the effective LV afterload. The transmural left ventricular filling pressure did not fall, a fact inconsistent with decreased pulmonary venous return, causing the fall in LVSV. The LVSV fell significantly more when RHV was allowed to increase as when it was held constant with all other variables showing no statistical change. Thus, increases in both RHV and effective LV afterload are created by the inspiratory fall in Ppl and summate to decrease LVSV.

Airway Obstruction↗
PubMed1979

Distribution of interstitial compliance and filtration coefficient in canine lung.

Utilizing a modification of the isogravimetric methodology, we have estimated the perivascular interstitial compliance and filtration coefficient in the canine lung. These values averaged 1.8 g/cm H2O and 34 (g/h)/cm H2O, respectively, per 100 g lung wet weight. By studying lungs at both low and high states of inflation (where the alveolar septae are collapsed) we were also able to determine the spatial distribution of both the interstitial compliance and filtration coefficient. We estimate that of the above total interstitial compliance a maximum of 55% is around alveolar septal vessels, 20% around extra-alveolar arteries and 25% around extra-alveolar veins. Of the above total filtration coefficient, 50% represents filtration from alveolar septal vessels, 23% from extra-alveolar arteries, and 27% from extra-alveolar veins. Our results imply that there are finite interstitial compliances communicating with all permeable vessels. Significant pressures can be built up in these spaces, thereby acutely limiting the further formation of interstitial edema.

Animals↗
PubMed1978

Effects of respiration on cardiac performance.

The conventional explanation for the fall in left ventricular stroke volume (LVSV) with inspiration is that blood pools in the lungs, thereby decreasing pulmonary venous return. In anesthetized dogs, we have found an increase in left ventricular filling pressure (LVFP) with both constant and increasing lung volume during an inspiratory effort. Transmural aortic diastolic pressure rises as LVSV falls and LVFP rises consistent with the hypothesis that a fall in pleural pressure afterloads the left ventricle. Additionally the increase found in right ventricular filling pressure with inspiration may adversely affect LV performance by decreasing LV compliance and/or contractility. Our findings are incompatible with pooling of blood in the lungs being the primary determinant of the fall in LVSV with inspiration.

Animals↗
PubMedDate not supplied

Hepatic and renal blood flow responses to a clinical dose of intravenous cyclosporine in the pig.

The immunosuppressant Cyclosporine A (CsA) is considered to induce nephrotoxicity in part by causing vasoconstriction of the glomerular afferent arterioles. Although CsA is widely used in hepatic transplantation, little is known concerning its effects on hepatic blood flow. We used ultrasonic flow probes in an anesthetized swine model to measure the effects of a single 60 min infusion of a clinically comparable dose of CsA (5 mg/kg per h) on hepatic, renal, and supraceliac descending aortic blood flows (n = 7 swine). To account for any change in systemic output or systemic vascular resistance during the 60 min CsA infusion that may non-specifically affect hepatic and renal blood flows, the total hepatic (portal vein plus hepatic artery) and renal blood flows were reported relative to the supraceliac descending aortic blood flow (termed 'fractional' total hepatic and renal blood flows). The fractional total hepatic blood flow decreased significantly (p < 0.05) by 40 min of CsA infusion vs baseline, and continued to decrease throughout the infusion (baseline = 0.38 +/- 0.03 units vs 0.28 +2- 0.05 units by 60 min of CsA infusion). During the recovery period, the fractional total hepatic blood flow increased to a value which was not different from baseline (recovery = 0.38 +2- 0.03 units). Fractional right renal artery blood flow did not change significantly from baseline at any time during the CsA infusion or during the recovery period. We conclude that a single, clinically comparable dose of CsA results in a significant decrease in total hepatic blood flow, and that this decrease is greater than that seen in renal blood flow.

Animals↗