1995 Fiscal Year Final Research Report Summary
The role of sympathetic nervous system in the genesis of pulmonary edema
| Project/Area Number |
05454420
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Shinshu University School of Medicine |
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Principal Investigator |
SHIBAMOTO Toshishige Shinshu Univ. Sch. Med. Associate professor, 医学部, 助教授 (90178921)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Yoshihiro Shinshu Univ. Sch. Med. Instructor, 助手 (10210379)
KOYAMA Shozo Shinshu Univ. Sch. Med. Professor, 教授 (00115346)
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| Project Period (FY) |
1993 – 1995
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| Keywords | pulmonary edema / vascular permeability / catecholamines / symapathetic nerve / norepinephrine / filatration coefficient / epinephrine / ノルエピネフリン |
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| Research Abstract |
We studied the role of sympathetic nervous system in the genesis of pulmonary edema. One of the purpose of this study was to determine the mechanism for neurogenic pulmonary edema, which is caused by massive sympathetic activation and has been demonstrated to be due to increased vascular permeability. We determined the effects of large doses of catecholamines on pulmonary vascular permeability. Epinephrine or norepinephrine (100,300 mug) was infused into isolated dog lungs perfused with heparinized blood at constant pressure. Both catecholamines increased the pulmonary capillary pressure but reduced the lung weights. The pulmonary vascular permeability, assessed by the capillary filtration coefficient (Kfc) and the isogravimetric capillary pressure, did not change significantly at 30 and 60 min after infusion of either catecholamine. These results suggest that large doses of catecholamines do not increase the pulmonary vascular permeability in isolated dog lungs. Indeed, the lung weigh
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t response to adrenaline contrasted with the responses to platelet-activating factor (PAF) and the stable thromboxane A_2 analogue (TxA_2). In lungs treated with PAF or TxA_2, capillary pressure similarly increased to the level equivalent to that in the adrenaline-treated lungs, but lung weight progressively increased. This comparison indicates that pulmonary vascular permeability of adrenaline-treated lungs is apparently smaller than that of lungs treated with either PAF or TxA_2, and may reinforce the conclusion that catecholamines do not increase pulmonary microvascular permeability. Another major purpose of this study was to determine whether activation of sympathetic nerve innervating lung causes an increase in pulmonary vascular permeability. No changes were found in pulmonary vascular permeability as evaluated by Kfc of either isolated canine or rabbit lungs, whose postganglionic fibers of stellate ganglions were electrically stimulated. These findings suggest that sympathetic nervous system may not play a crucial role in the integrity of pulmonary circulation. Less
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Research Products
(13 results)
