J.Jpn. Surg. Soc.. 59(4): 642-656, 1958
EXPERIMENTAL STUDY ON THE CHANGES OF THE RESPIRATION, BLOOD PRESSURE AND ELECTROCARDIOGRAM PRODUCED BY ANOXIC ANOXIA
II. CHANGE AFTER THE BLOCKADE OF THE AUTONOMIC NERVES
|
Second Surgical Clinic, Faculty of Medicine, Kyushu University, Fukuoka (Director: Prof. Masanobu TOMODA) Yukio MIZUNOE |
1. In dogs in progressive anoxic anoxia after th vagus cut on the both icle of the neck or intravenous injection of atropine 0.25 mg/kg, the blood pressure rose by degree after the beginning of the experiment. It showed neither sudden decrease, nor the pulse pressure rose, after a crisis. In ECG the crisis was not followed by any serious bradycardia or by any abnormal heart rhythm.
2. In dogs with their vagus cut on the both side of the neck after crisis, the crisis was followed by a rise of the blood pressure, a fall of the pulse pressure and a rise of the heart rate. There was a sinus rhythm noted, but not any nodal rhythm or any ventricular automatism persisting.
3. From the fact described above, in dogs with their vagus left intact there occurred after the crisis a blood pressure fall, an exaggerated bradycardia, an increased pulse pressure, and a nodal rhythm or a ventricular automatism, each result of the downward shift of the pacemaker, appears to be ascribable to the vagus being excited in an extreme degree.
4. Progressive anoxic anoxia induced after the intravenous administration of a sympathicolytic agent-Dibenamine in a dose of 10 mg/kg or Dibenzyline in a dose of 2.5 mg/kg- left the blood pressur in pre-crisis unaltered in some cases and brought it down below the level befor the experiment in others. The heart rate was not raised, too. The changes produced by the vagal excitement in the blood pressure and in the ECG were the same in dogs given a sympathicolytic agent and in those not given the drug in post-crisis.
5. In dogs given the autonomic ganglionic blocking agent, TEAB, intravenously in a dose of 30 mg/kg and then placed in a state of progressive anoxic anoxia, the blood pressure was either kept constant or brought down before respiratory standstill, and was either brought up or kept for two minutes or so at or about its pre-experimental level after the cessation of respiration. The respiratory standstill was not preceded by any increased heart rate, nor was it followed by any bradycardia, by an increased puls pressure or by any abnormal rhythm.
6. The results of the experimients described above make it coneivable that a sympathicolytic agent administered Dibenamine, Dibenzyline or TEAB- has an inhibitory action on the blood pressure and heart rate rising before a crisis, and that an excitation of the sympathetic may reasonably be held responsible for the changes occurring before a crisis in the blood pressure and in the ECG.
7. It appears, in other words, that the changes produced in the blood pressure and in ECG in the process of progressive anoxic anoxia may be attributed to an excitation of the sympathetic when they are caused before a crisis, and to that of the parasympathetic when they are produced after a crisis.
(author 's abstract)
To read the PDF file you will need Adobe Reader installed on your computer.