Effect of the Alpha-Adrenergic Blockade in Experimental Neurogenic Pulmonary Edema in Cats.

Kang, Joon Ki; Chang, Sang Kun; Kim, Moon Chan; Ha, Young Soo; Song, Jin Un

Original Article

Journal of Korean Neurosurgical Society 1981;10(1): 53-70.

Joon Ki Kang, Sang Kun Chang, Moon Chan Kim, Young Soo Ha, Jin Un Song

Department of Neurological Surgery, Catholic Medical School, Seoul, Korea.

ABSTRACT

An experimental neurogenic pulmonary edema model in cats is described in which we have attempted to produce a neurogenically mediated hemodynamic storm. This experimental study was done to better define the hemodynamic responses to the elevated intracranial pressure and the effect and role of the alpha-adrenergic blockade in the neurogenic pulmonary edema. 50 adult cats weighing 2.5 to 4.0kg, were used in this study. The components of the pathophysiological hemodynamic responses, systemic changes, lung weight, and histopathological changes of lung in experimental models were studied in groups of animals when intracranial pressure(ICP) was raised for 2 hours by intraventricular infusion with normal saline to 200mmH2O and 300mmH2O. We have also observed the effect of the alpha-adrenergic blockade(pentolamin) in the neurogenic pulmonary edema which was produced by elevated intracranial pressure. The animals were divided into 5 groups: The normal control group was comprised of 10 normal cats. Control and pentolamin treated animal groups which had an elevated ICP of up to 200mmH2O consisted of 10 cats each. Control and pentolamin, treated animal groups which had an elevated ICP of up to 300mmH2O consisted of 10 cats each but in addition they had a neurogenically mediated pulmonary edema. 1) In the animal groups of elevated ICP to 200mmH2O and 300mmH2O, there were hemodynamic systemic changes which were neurogenically mediated and resulted in an immediate elevation in blood pressure from 30mmHg to 60mmHg. There was also bradycardia, a slight elevation of central venous pressure, and reduction of PaO2 during the controlling of the elevated ICP. The hemodynamic responses of the animals that had an elevated ICP of up to 300mmH2O were significantly more changed than the 20mmHO ICP group. The hemodynamic responses of the pentolamin treated animals with elevated ICP to up to 200 and 300mmH2O were less changed and nearly approached the normal limit. 2) This animal model allows quantitative measurement of the neurogenically mediated pulmonary edema of the lungs by weighing. The lung weights of the animals with an elevated ICP of up to 200 and 300mmH2O were significantly greater then the normal control value(P<0.05) and the lung weights of the animals with an elevated ICP of 300mmH2O were significantly greater than those with an ICP of 200mmH2O(P<0.01). The lung weights of the pentolamin treated animal groups with the elevated ICP were significantly less 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 200mmH2O in the experimental animals we have confirmed gross and micropic appearances of hemorrhagic pulmonary edema. Partial destruction and congestion appeared along with hemorrhage in the alveolar and alveolar wall in the groups with an ICP of 300mmH2O. Histopathological changes of the pentolamin treated animals with the elevated ICP were significantly less severe than in the control groups and also had a tendency of returning to to a normal state. 4) This experimental model may facilitate clarification of the pathophysiolagical pathogenesis of neurogenic pulmonary edema. The authors defined the concept of neurogenic pulmonary edema as resulting from an increase in pulmonary capillary permeability mediated by massive symphathetic discharges to those vessels. Blockade of the sympathetic innervation to the systemic and pulmonary vascular beds lower the vascular pressures and brings the pulmonary capillary pressures back to normal.