Role of the Central Nervous System on Adrenaline Pulmonary Edema (1) : Influence of Blocking of Central Nervous System on Adrenaline Pulmonary Edema.

Abstract

Large doses of adrenaline result in death accompanied by an acute pulmonary edema in rabbit. Luisada claimed that adrenaline pulmonary edema was mediated via the central nervous system controlling the permeability of the pulmonary capillaries. But there is no evidence of the nervous control of capillary permeability. To investigate the role of central nervous system on adrenaline pulmonary edema in rabbit, an experiment was performed with blockage at various part of central nervous system. Material and Method : Male as well as female rabbits weighing about 2 kg were used. Anesthesia was induced by the intraperitoneal injection of 1 gm of urethan per kilogram of body weight. In all cases artificial respiration was maintained through a tracheal cannula, and arterial pressure was measured from the left femoral artery by a mercury manometer. In some cases venous pressure was measured from the jugular vein and electrocardiogram was recorded. 1.0 mg/kg of adrenaline was injected through the right auricular vein.The thorax was opened immediatly after death, then lung and heart were dissected off. The lung and heart were weighed and lung body ratio and lung heart ratio were calculated as follows, Lung Body Ratio (L/B)=(Lung Weight)/(Body Weight)×100 Lung Heart Ratio (L/H)=(Lung Weight)/(Heart Weight) The grade of pulmonary edema in macroscopic finding was evaluated according to Jordan's classification and histological examination was made. To investigate the influence of the central and autonomic nervous system blockage on adrenaline pulmonary edema several procedures were carried out prior to adrenaline injection as follows : I Control II Decerebration or Labonal anesthesia III Incision of diencephalon IV Cervical spinal transection or high spinal anesthesia VI Hexamethonium (C6) administration VII Vagotomy or atropine administration VIII Dextran transfusion after cervical spinal transection IX Dextran transfusion after C6 administration Result : In control group massive pulmonary edema was induced by 1.0mg/kg of adrenaline in all cases. No pulmonary edema occurred after neither transection of diencephalon, high spinal transection and anesthesia nor C6 administration. Decerebration, low spinal transection and anesthesia had no influence on adrenaline pulmonary edema. Vagotomy or atropine administration seems to tend to accelerate the development of adrenaline pulmonary edema. By the transfusion of dextran solution after high spinal transection or C6 administration, pulmonary edema developed with adrenaline injection. Blood pressure decreased remarkably after high spinal blocking or C6 administration and very instable after transection of diencephalon, but no remarkable change after other procedures. In case of development of pulmonary edema, lung body ratio was 0.96±0.75, peak, level of elevated blood pressure 182±20 mmHg, change of venous pressure +46±9.4 mmH20 ; in case of no pulmonary edema, lung body ratio was 0.41±0.03, lung heart ratio 1.60±9.16, peak level of elevated blood pressure 111±26 mmHg and change of venous pressure +21±10 mmH2O.Discussion : The intravenous injection of adrenaline provoked marked hypertension without exception. The evidence suggests that the left ventricle may be greatly burdened from the hypertension induced by adrenaline. Under these conditions, adequate performance of the right ventricle leads to a pulmonary engorgement and edema. Adrenaline pulmonary edema was prevented by transection of diencephalon or high spinal blocking. It is obvious that central nervous system does not control the permeability of the pulmonary capillaries, because pulmonary edema occured when dextran solution was transfused after the high spinal transection. [the rest omitted]