Pulmonary hemodynamics in respiratory acidosis in dogs

¹ Departments of Pediatrics, Medicine, and Physiology, School of Medicine, University of California, and Mount Sinai Hospital, Los Angeles, California

Pulmonary vascular resistance of intact anesthetized dogs rose during constant ventilation with 5–8% CO₂. This rise was not due to mechanical effects of decreased pulmonary artery or left atrial pressures or to decreased cardiac output, but appeared to be due to active pulmonary vasoconstriction. The increased pulmonary vascular resistance during CO₂ breathing was eliminated by either adrenalectomy or sham operation, but not by acute hemorrhage, indicating that some mechanism other than blood loss accounted for the failure of response. This effect of operation may explain the variation in results previously reported. The mechanism is not known, but may be related to altering adrenal medullary secretions, which are known to cause pulmonary vasoconstriction. The response to CO₂ was not restored in adrenalectomized animals by administration of maintenance or extra hydrocortisone, suggesting that the failure of pulmonary vascular resistance to rise in laparotomized animals was not due to adrenocortical depletion following surgery.

Note:
With the Technical Assistance of Robert Powell

Key Words: pulmonary circulation • CO₂ breathing • pulmonary vascular resistance • acid-base disturbances • blood gases • cardiac output • catecholamine effects

Submitted on April 3, 1963

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