ABSTRACT
Spatial distribution of pulmonary blood flow (SDPBF) during 2- to 3-min exposures to 6-8 Gy acceleration was studied, using radioactive microspheres in dogs, and compared to previously reported 1 Gy control distributions. Isotope distributions were measured by scintiscanning individual 1-cm-thick cross sections of excised, fixed lungs. Results indicate: 1) the fraction of cardiac output traversing left and right lungs did not change systematically with the duration and magnitude of acceleration; but 2) the fraction is strongly affected by the occurrence or absence of fast deep breaths, which cause an increase or decrease, respectively, in blood flow through the dependent lung; and 3) Gy acceleration caused a significant increase in relative pulmonary vascular resistance (PVR) in nondependent and dependent regions of the lung concurrent with a decrease in PVR in the midsagittal region of the thorax. Result 3 may be mediated primarily by changes in regional alveolar volume and geometry in the nondependent hemithorax conbined with hydrostatic effects of extravascular fluid and active hypoxic response in the dependent region and is superimposed on, and may override, hydrostatic effects of perfusion pressures on SDPBF during acceleration.
Subject(s)
Gravitation , Pulmonary Circulation , Vascular Resistance , Adaptation, Physiological , Animals , Cardiac Output , Dogs , Dye Dilution Technique , Lung/physiology , Lung Volume Measurements , Regional Blood FlowABSTRACT
Regional displacements of lung parenchyma due to respiratory movements at 1 G and 7 Gy were studied in anesthetized dogs in the left decubitus position in a water-filled respirator that provided control of respiratory volumes and rate and minimized inertial shifts in position and shape of the thorax and abdominal contents and related effects on the lungs. Inspiratory movements at 1 G were relatively uniform, although regional volume increased more in the nondependent (right) lung than in the dependent (left) lung. Regional functional residual capacity (FRC) increased in the nondependent lung and decreased in the dependent lung during exposures to 7 Gy. The greatest inspiratory increase in volume occurred near the midlung, where regional FRC changed the least during acceleration. The decrease in dependent and increase in nondependent lung volumes during acceleration are attributed to the increased weight and consequent downward displacement of the higher specific gravity mediastinal contents concomitantly with upward displacement of pulmonary gas, producing an exaggeration of the dependent-to-nondependent gradient in alveolar size.
Subject(s)
Adaptation, Physiological , Gravitation , Lung/physiology , Animals , Dogs , Lung Volume Measurements , Male , Posture , RespirationSubject(s)
Biomedical Engineering/instrumentation , Computers , Oscillometry , Tape Recording , Laboratories , Paper , Physiology/instrumentation , Time FactorsABSTRACT
Lethal gas embolism always occurs after FC 80 liquid fluorocarbon is injected intravenously (0.1 ml/kg body mass) in dogs breathing room air but not in dogs breathing oxygenated FC 80 liquid fluorocarbon. Gas embolism is not prevented in dogs that have been injected intravenously with FC 80 when they are exposed to 2 ATA (atmospheres absolute) 20% 02-80% N2, 9 ATA 5% O2-95% He, or 1 ATA 100%, O2. In dogs that die of FC 80-induced gas embolism, free gas in the right atrium contains approximately 0.5 g FC 80/liter, and Po2 and Pco2 in the gas are in equilibrium with their corresponding tensions in right atrial blood. These observations are consistent with the hypothesis that PFC 80 in alveolar gas does not equilibrate with PFC 80 (55 mmHg) in blood. The total gas tension in pulmonary capillary blood containing FC 80 and its vapor thus exceeds the total tension of alveolar gases (atmospheric pressure). Bubbles of O2, CO2, N2, FC 80, and water vapor form in the regions of the pulmonary capillary bed where the total tension of gases dissolved in blood exceeds the absolute blood pressure.
