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Hypoxic pulmonary vasoconstriction and the pharmacologically denervated lung
Author(s) -
OHMURA A.,
PACE N. L.,
WONG K. C.,
JOHANSEN R. K.
Publication year - 1982
Publication title -
anaesthesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.839
H-Index - 117
eISSN - 1365-2044
pISSN - 0003-2409
DOI - 10.1111/j.1365-2044.1982.tb01056.x
Subject(s) - medicine , anesthesia , hypoxic pulmonary vasoconstriction , hypoxia (environmental) , cardiac output , vascular resistance , saline , vasoconstriction , bupivacaine , hemodynamics , oxygen , chemistry , organic chemistry
Summary The roles of the autonomic nervous system and cardiac output on hypoxic pulmonary vasoconstriction were studied in 15 mongrel dogs anaesthetised with intravenous pentoharbitone (30 mg/kg) and the lungs mechanically ventilated to maintain normal arterial blood gases. After a hypoxic challenge in Group I (n = 6) and Group II (n = 3) animals, autonomic denervation was achieved by total spinal block with tetracaine (20 mg) injected into the cisterna magna. Group I animals received a large volume of intravenous fluid (80 ml/kg normal saline) before the block while Group II animals were given minimum fluid. When Group I animals were exposed to 10% inspired oxygen, mean pulmonary arterial pressure increased by 88 and by 72% before and after the block, respectively. The cardiac output increased by 27% with hypoxia before the block while it did not change significantly with hypoxia after the block. The pulmonary vascular resistance increased by 65 and by 152% with hypoxia before and after the block. Group II animals were also exposed to 10% inspired oxygen. They showed a similar response to Group I animals before the block. However, after the block irreversible hypotension developed with hypoxia.In Group III animals (n = 6), the same anaesthesia and hypoxic challenge protocol was used. Immediately after measurements at 10 minutes of hypoxia, the inferior vena cava was constricted to reduce the cardiac output to the control level and another set of measurements were made. The cardiac output increased by 30% with hypoxia and then was reduced to the control level with vena caval constriction. The mean pulmonary arterial pressure increased by 125% with hypoxia and then it decreased slightly with the inferior vena cava constriction. The pulmonary vascular resistance increased by 95% with hypoxia and then it further increased by 28% with the vena caval constriction. These results suggest that sympathectomy accentuates rather than attenuates the hypoxic pulmonary vasoconstriction and that an increase in cardiac output counteracts hypoxic pulmonary vasoconstriction. The results also suggest that adequate intravascular volume and oxygenation are extremely important for maintaining homeostasis when reflex sympathetic stimulation to the cardiovascular system has been eliminated.