Journal of applied physiology
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We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. ⋯ When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.
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We investigated the effects of high-frequency chest wall compression (HFCWC) on peripheral and tracheal mucus clearance in anesthetized spontaneously breathing dogs. HFCWC was achieved by oscillating the pressure in a thoracic cuff with a piston pump. Regional lung retention of a technetium-99m sulfur colloid aerosol was monitored with a gamma camera. ⋯ Phase III: HFCWC at 13 Hz with Pcuff = 50-60 cmH2O was found to significantly enhance PMCI in five dogs without the consequence of hemorrhage. Correlations were found between the enhancement of PMCI and TMCR by HFCWC. These results demonstrate that HFCWC is effective in enhancing both peripheral and central mucus clearance in dogs and safe when moderate pressures are applied.
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We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). ⋯ Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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By using adult rabbits in which the lung surfactant had been reduced by repeated whole-lung lavage, we examined the effects of surfactant supplement and positive end-expiratory pressure (PEEP). The rabbits were anesthetized with pentobarbital sodium and mechanically ventilated with pure O2. Surfactant that was extracted from pigs' lungs was supplemented to the rabbits through the trachea. ⋯ The 18 rabbits that were ventilated with either the supplement or the PEEP showed some elevations of arterial O2 tension, but 9 of them died within 4 h. After application of both the surfactant supplement and the PEEP, six out of the eight rabbits survived for more than 11 h with nearly normal values of blood gases and compliance. We concluded that the combination of the transtracheal surfactant supplement and ventilation with PEEP has favorable therapeutic effects on surfactant deficiency.
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Values of the classical Haldane coefficient, i.e, the change in the concentration of total CO2 in whole blood per unit of change in the concentration of total O2 at constant PCO2, have been calculated at different combinations of plasma pH (range 7.25-7.50), erythrocyte 2,3-diphosphoglycerate (DPG) concentration (range 3.5-6.5 mM), PCO2 (range 25.0-65.0 Torr), initial hemoglobin O2 saturation (range 0.50-0.80), and erythrocyte volume fraction (range 0.25-0.55). The principle of the calculations is to utilize the so-called reciprocity relations to determine the amount of protons and CO2 released from hemoglobin on oxygenation and to estimate the resulting change in the concentration of total CO2 from published data on the interaction coefficient for the binding of O2 and protons to hemoglobin, the interaction coefficient for the binding of O2 and CO2 to hemoglobin, the distribution of protons across the erythrocyte membrane, the equilibrium constants for the reactions between CO2 and H2O, and CO2 and oxyhemoglobin, the buffer capacity of oxygenated erythrolysate, and the buffer capacity of plasma. ⋯ Furthermore, the coefficient depends on the hemoglobin O2 saturation and the erythrocyte volume fraction. The dependency of the Haldane coefficient on the O2 saturation and the PCO2 causes an increase in the O2-linked CO2 flux across the alveolar membrane by more than 30% in patients with respiratory insufficiency.