Hydrocortamate Hydrochloride

Among the various methods proposed for the treatment of acute pulmonary edema, there has been known no definitive method to inhibit permeability of the pulmonary capillaries. On the basis of abilities of adrenocorticoids- to inhibit capillary permeability and to reduce capillary fragility, the author conducted a series of clinical investigations and proved their efficacy. Hydrocortisone was tested for its therapeutic value in experimental pulmonary edema of different pathophysiology produced by three different techniques. A) Materials and Methods 1) Nerogenic pulmonary edema by Reilly phenomenon. (Stimulation of cervical sympathetics in rabbits.) 2) ANTU pulmonary edema in rats. 3) Post-operative acute pulmonary edema produced by the sequence of pneumonectomy, anoxia then intravenous infusion in dogs. B) Methods of administering hydrocortisone. In groups 1 and 2, hydrocortisone 3 mgm per kilogram of body weight was given prophylactically one hour prior to the start of the procedure to produce pulmonary edema. In group 3, hydrocortisone 3 mgm per kilogram of body weight was given by intravenous infusion together with IPPB/i O2 at the establishment of pulmonary edema. A group of dogs was treated with IPPB/i O2 alone as a control. C) Evaluation of therapeutic efficacy. Therapeutic efficacy was compared among the groups mainly on the basis of pathological findings, macroscopically, histologically and by water content of the lungs, upon sacrificing. In addition. prolonged survival time was taken into account in group 2. In group 3, such parameters as respiratory and circulatory functions (pulse rate, femoral arterial pressure, central venous pressure, pulmonary arterial pressure, pulmonary capillary pressure, oxygen saturation and microscopic observation of the omental capillary vessels) as well as X-ray findings of the chest were also considered. Result and Conclusion 1) Excessive stimulation of the cervical sympathetic nerves caused marked congestion in the pulmonary capillaries, hemorrhage and edema into alveoli in rabbits. Hydrocortisone given prophylactically in a dose of 3 mgm. per kilogram of body weight prevented these changes almost completely. 2) The lung of rats given ANTU appeared like liver in consistency, with intense hemorrhage and edema, and all the animals died within four hours. Hydrocortisone given prophylactically in a dose of 3 mgm per kilogram of body weight suppressed those changes and prolonged the survival period to 16 hours or more. 3) Many of the dogs subjected to the sequence of pneumonectomy, anoxia and intravenous infusion developed in typical pulmonary edema. Although improvements in respiratory and circulatory dynamics were noted in the group treated solely with IPPB/i O2, improvements in oxygen saturation, and blood flow in omental capillaries were better in the group treated with hydrocortisone in addition to IPPB/i O2. This was reflected in pathohistological findings and JORDAN II-IV changes still persisted in the control group (IPPB only) whereas in the group treated with hydrocortisone and IPPB only JORDAN C-II changes were noted, and water content of lungs returned to the value noted before edema developed.