Effect of Phentolamine on the Lung and Hypothalamic Lesions in the Experimental Neurogenic Ulmonary Edema in Cats.
- Author:
Choon Jang LEE
1
;
Min Woo PAIK
;
Dal Soo KIM
;
Choon Wong HUH
;
Young Soo HA
;
Joon Ki KANG
;
Jin Un SONG
Author Information
1. Department of Neurosurgery, Catholic Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Neurogenic pulmonary edema;
Intracranial pressure;
Sympathetic discharge;
Phentolamine;
Hypothalamic lesion
- MeSH:
Adult;
Animals;
Blood Pressure;
Cats*;
Edema*;
Hemodynamics;
Humans;
Hypothalamus;
Hypothalamus, Anterior;
Infusions, Intraventricular;
Intracranial Pressure;
Lung*;
Models, Theoretical;
Phentolamine*;
Pulmonary Edema;
Reference Values;
Weights and Measures
- From:Journal of Korean Neurosurgical Society
1982;11(3):283-297
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This experiment was performed to define the paricipation of a discrete hypothalamic neural structure in the genesis of pulmonary edema and the effect of alpha adrenergic blockade. Fifty adult cats weighing 2.5 to 4.0 Kg, were used in this study. The components of the pathophysiological systemic changes, lung weight, and histopathological changes of lung and hypothalamus were studied in groups of animals when intracranial pressure(ICP) was raised to 200 mmH2O of 300 mmH2O for 2 hours by intraventricular infusion with normal saline. The animals were divided into 5 groups : The normal control group was comprised in 10 normal cats. Control and phentolamine treated animal groups which had an elevated ICP of up 200 mmH2O consisted of 10 cats each. Control and phentolamine treated animal groups which had an elevated ICP of up to 300 mmH2O consisted of 10 cats each. The results obtained were as follows : 1) In the animal groups of elevated ICP to 200 mmH2O or 300 mmH2O, there were hemodynamic systemic changes which were neurogenically mediated and caused an immediate elevation in blood pressure of 30 mmHg to 60 mmHg. The hemodynamic data of the animals that had an elevated ICP of up to 300 mmH2O were significantly more deviated from normal control values than the 200 mmH2O ICP groups. The hemodynamic responses of the phentolamine treated animal with elevated ICP of up to 200 and 300 mmH2O were less deviated from normal control values. 2) The lung weights of the animals with an elevated ICP of up to 200 and 300 mmH2O were significantly heavier than the normal control value(p<0.05) and the lung weights of the animals with an elevated ICP of 300 mmH2O were significantly heavier than those with an ICP of 200 mmH2O(p<0.01). The lung weights of the phentolamine treated animal groups were significantly lighter than the control group but showed little increase in the lung weight when compared to the normal value. 3) By controlling the elevated ICP above 200 mmH2O in the experimental animals we have confirmed gross and microscopic appearances of hemorrhagic pulmonary edema. Histopathological changes of the phentolamine treated animals were significantly less sever than in the control groups. 4) By elevating ICP above 200 mmH2O in the experimental animals, we have confirmed discrete bilateral hemorrhagic spots of the anterior hypothalamus, preoptic region induced by increased intracranial pressure. Histopathological changes of the phentolamine treated animals with the elevated ICP were significantly less severe than of the control groups. 5) This experimental model may define the specific particification of the hypothalamus in the pathophysiological pathogenesis of neurogenic pulmonary edema. These results suggest that the lungs are directly affected by the intense sympathetic discharge evoked by release phenomenon from the sympathoinhibitory influence of the hypothalamus, and pulmonary edema was effectively eliminated by alpha adrenergic blockade.
