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Effect of bronchospasm on hypoxic pulmonary vasoconstriction (HPV) in perfused cat lungs
WS6-J-I-05
EFFECT OF BRONCHOSPASM ON HYPOXIC PULMONARY VASOCONSTRICTION (HPV) IN PERFUSED CAT LUNGS Y. Nagasaka*, E. Fujita, R. Hazu, N. Nishimura, Y. Tohda, and S. Nakajima Fourth Department of Medicine, Kinki University School of Medicne, Osakasayama, Osaka, 589 Japan It has been believed that autonomic nerve plays little role in HPV. However, these studies were done in the conditions with normal bronchial tone. Little has been known about the role of autonomic nerve on HPV during broncho-spasm as in the case with bronchial asthma, in which autonomic nerves are involved in pathogenesis and the altered tone of autonomic nerve may affect pulmonary circulation. To clarify the role of autonomic nerves on HPV when there is bronchospasm, we induced hypoxia while provoking bronchospasm by intratracheal administration of histamine or acetylcholine in isolated cat lungs (n=36) perfused with diluted autologous blood (Ht=l 0%). We used 30% 0 2 and 5% CO2 for noormoxia and 2% 0 2 and 5% CO2 for hypoxia. Hexamethonium (C6) as a ganglion blockaer, tetrodotoxin (TTX) as a blockade of nerve conduction, atropine a muscarinic receptor antagonist, and also selective or non-selective adrenergic inhibitors (8: propranolol, 131;acebutolol, metoprolol, 13-2;butoxamine, alpha; phentolamine, alpha-1 ; prazosin, alpha-2; yohimbin) were administered before induction of bronchospasm following control HPV. C6 and TTX did not affect parameters of pulmonary circulation when HPV was not accompanied by bronchospasm or when bronchospasm was induced during normoxia. Nevertheless, these agents attenuated HPV when there was bronchospasm. Atropine almost completely abolished HPV during bronchospasm. Beta and selective 13-2 inhibitors also completely abolished HPV during bronchospasm. Alpha blockades did not affect HPV even when there was bronchospasm. We conclude that autonomic nerves, especially vagal nerves and 13adrenergic nerve play a crucial role in HPV when it occured during bronchospasm. These finding may indicate that many sympathetic agonist and anti-cholinergic drugs, used in the treatment of bronchial asthma, may affect ventilation-perfusion matching.
WS6-J-1-06 SYMPATHOADRENAL SYSTEM ATTENUATES HYPOXIC PULMONARY VASOCONSTRICTION DURING SYSTEMIC HYPOXIA IN CATS M. Shiral1, A. Shimouchi2, and I. Ninorniya3 1) Dept. of Cardiac Physiology and 2) Dept. of Cardiovascular Dynamics, National Cardiovascular Canter Research Institute, Sulta, Osaka 565; and 3) Dept. of Physiology, Institute of Health Sciences, Hiroshima University School of Medicine, Kasumi-cho, Hiroshima 734, Japan In this study, we examined how locally mediated hypoxic pulmonary vasoconstri¢~tion is modulated by autonomic nervous system activation dudng global alveolar hypoxia (GAH) accompanied by systemic hypoxemla. Using an X-ray television system on the in vlvo cat lung, we measured changes in the internal dlarneter (ID) during GAll and regional alveolar hypoxia (RAH) without systemic hypoxemia in identical small pulmonary artedes and veins (100-600 pm ID). We also analyzed the effects of the autonomic nervous system blockade on the hypoxic ID changes. Dudng GAH the ID of the artsdeo reduced by 5=1 and 3==1% with 10 and 5% O2 inhalations, respectively, whereas dudng RAH the artedal ID reduced 12:=1 and 18*1% with 10 and 5% 02 inhalations, respectively. The magnitude of the ID reduction was significantly smaller during GAH than dudng RAH. After pretreatment with propranolol, however, GAH induced large ID reductions (16=1 and 23±1% with 10 and 5% 02 inhalations) with patterns yew similar to those seen during RAH. Phentolamine and atropine had no effect on the response dudng GAH. The ID reductions dudng RAH, on the other hand, were unaffected by all the blockers. The results indicate that, in the cat, alveolar hypoxla per se acts Iocal.ly to constrict the small pulmonary vessels and that the hypoxic vasoconstriction is attenuated by a B-receptor-mediated vaeodllator effect during GAH with systemic hypoxemia. In addition, we found that after edranalectomy plus ganglion blockade with hexamathonium bromide, the GAH-induced ID reduction with 5% O2 inhalation was enhanced from 3 to 19%. The data suggest that the B-receptor-mediated vasodilator effect is caused chiefly by a reflex release of catecholamines from the adrenal glands and sympathetic nerves.
403
EFFECT OF BRONCHOSPASM ON HYPOXIC PULMONARY VASOCONSTRICTION (HPV) IN PERFUSED CAT LUNGS Y. Nagasaka*, E. Fujita, R. Hazu, N. Nishimura, Y. Tohda, and S. Nakajima Fourth Department of Medicine, Kinki University School of Medicne, Osakasayama, Osaka, 589 Japan It has been believed that autonomic nerve plays little role in HPV. However, these studies were done in the conditions with normal bronchial tone. Little has been known about the role of autonomic nerve on HPV during broncho-spasm as in the case with bronchial asthma, in which autonomic nerves are involved in pathogenesis and the altered tone of autonomic nerve may affect pulmonary circulation. To clarify the role of autonomic nerves on HPV when there is bronchospasm, we induced hypoxia while provoking bronchospasm by intratracheal administration of histamine or acetylcholine in isolated cat lungs (n=36) perfused with diluted autologous blood (Ht=l 0%). We used 30% 0 2 and 5% CO2 for noormoxia and 2% 0 2 and 5% CO2 for hypoxia. Hexamethonium (C6) as a ganglion blockaer, tetrodotoxin (TTX) as a blockade of nerve conduction, atropine a muscarinic receptor antagonist, and also selective or non-selective adrenergic inhibitors (8: propranolol, 131;acebutolol, metoprolol, 13-2;butoxamine, alpha; phentolamine, alpha-1 ; prazosin, alpha-2; yohimbin) were administered before induction of bronchospasm following control HPV. C6 and TTX did not affect parameters of pulmonary circulation when HPV was not accompanied by bronchospasm or when bronchospasm was induced during normoxia. Nevertheless, these agents attenuated HPV when there was bronchospasm. Atropine almost completely abolished HPV during bronchospasm. Beta and selective 13-2 inhibitors also completely abolished HPV during bronchospasm. Alpha blockades did not affect HPV even when there was bronchospasm. We conclude that autonomic nerves, especially vagal nerves and 13adrenergic nerve play a crucial role in HPV when it occured during bronchospasm. These finding may indicate that many sympathetic agonist and anti-cholinergic drugs, used in the treatment of bronchial asthma, may affect ventilation-perfusion matching.
WS6-J-1-06 SYMPATHOADRENAL SYSTEM ATTENUATES HYPOXIC PULMONARY VASOCONSTRICTION DURING SYSTEMIC HYPOXIA IN CATS M. Shiral1, A. Shimouchi2, and I. Ninorniya3 1) Dept. of Cardiac Physiology and 2) Dept. of Cardiovascular Dynamics, National Cardiovascular Canter Research Institute, Sulta, Osaka 565; and 3) Dept. of Physiology, Institute of Health Sciences, Hiroshima University School of Medicine, Kasumi-cho, Hiroshima 734, Japan In this study, we examined how locally mediated hypoxic pulmonary vasoconstri¢~tion is modulated by autonomic nervous system activation dudng global alveolar hypoxia (GAH) accompanied by systemic hypoxemla. Using an X-ray television system on the in vlvo cat lung, we measured changes in the internal dlarneter (ID) during GAll and regional alveolar hypoxia (RAH) without systemic hypoxemia in identical small pulmonary artedes and veins (100-600 pm ID). We also analyzed the effects of the autonomic nervous system blockade on the hypoxic ID changes. Dudng GAH the ID of the artsdeo reduced by 5=1 and 3==1% with 10 and 5% O2 inhalations, respectively, whereas dudng RAH the artedal ID reduced 12:=1 and 18*1% with 10 and 5% 02 inhalations, respectively. The magnitude of the ID reduction was significantly smaller during GAH than dudng RAH. After pretreatment with propranolol, however, GAH induced large ID reductions (16=1 and 23±1% with 10 and 5% 02 inhalations) with patterns yew similar to those seen during RAH. Phentolamine and atropine had no effect on the response dudng GAH. The ID reductions dudng RAH, on the other hand, were unaffected by all the blockers. The results indicate that, in the cat, alveolar hypoxla per se acts Iocal.ly to constrict the small pulmonary vessels and that the hypoxic vasoconstriction is attenuated by a B-receptor-mediated vaeodllator effect during GAH with systemic hypoxemia. In addition, we found that after edranalectomy plus ganglion blockade with hexamathonium bromide, the GAH-induced ID reduction with 5% O2 inhalation was enhanced from 3 to 19%. The data suggest that the B-receptor-mediated vasodilator effect is caused chiefly by a reflex release of catecholamines from the adrenal glands and sympathetic nerves.
403