Simultaneous Determination of the Blood Sugar Content, and the Gas Content and Alkalinity of the Arterial Blood during Carbon Monoxide Poisoning

Abstract

I. In rabbits poisoned by carbon monoxide gas the content of CO2 and O2 in the arterial blood was determined simultaneously with the blood sugar content. When CO was hypodermically administered in a moderate quantity the tachypnoea did not occur infrequently. When it happened, it lasted only transitorily or for some ten minutes, it seldom exceeded one hour. In cases of an excessive dose, such as 250-450-600-900 c. c. CO per animal, the tachypnoea was seen invariably, and sometimes continued for longer, say one to two hours. The subcutaneous injection of CO called forth definitely the diminution in the O2 content as well as the CO2 content of the arterial blood. The minimum of the former was attained at 1-2 hours after the injection, sometimes a little earlier, sometimes a little later. The minimum of CO2 content in the arterial blood was reached usually at 2-3 hours, that is somewhat later than the O2 reduction. When an excessive amount of CO was given, the increase in CO content and the reduction of O2 content did not reach the climax in the early stage of the experiment, but progressed further. Roughly speaking, the reduction in the O2 and the CO2 content of the arterial blood and the augmentation of the blood sugar content run parallel, the greater the former the greater the hyperglycaemia. In the experiments in which CO was given to breath for 20 minutes or somewhat longer, the time relation between the changes of CO, O2 and CO2 content in the arterial blood and the blood sugar content became noticeably clearer. The change (reduction and then recovery) in CO2 content was far slower than that in CO and in O2 content. The latter ran parallel with each other, but as a matter of course in the reverse direction. The blocd sugar content also increased slowly, somewhat similarly to the CO2 reduction, but it recovered the initial value almost at the same time as the recovery of O2 content, that is distinctly earlier than that of CO2 content. The CO2 content at the moment when the hyperglycaemia became clearly manifest was invariably unmistakably larger than that at the time when it completely disappeared. The magnitudes of O2 reduction, CO2 reduction and blood sugar increase, however, ran parallel as a whole, comparing experiment with experiment. In the majority of cases the tachypnoea-in the present investigations the ventilation volume was not measured-resulted, but it was too short to account for the CO2 reduction in the arterial blood, which further progressed for 1-2 hours after discontinuation of CO inhalation. In some instances the respiration rate directly tended to become slow, without indicating any sign of acceleration. In the blood samples collected almost immediately prior to death caused by inhalation of CO mixture for a short time as 6-50′ the content of CO and CO2 in the arterial blood did not materially differ from that of the surviving cases, but the O2 reduction was highly remarkable. In delving into the cause of death stress must be laid on the O2 reduction, rather than on the CO2 reduction. The doubly vagotomized rabbits showed no particular features concerning the respiration rate and the CO2 reduction towards the CO poisoning. That is, the tachypnoea resulted also in the vagotomized ones, and the CO2 reduction occurred in the usual manner. Only it was noted that the recovery of the O2 content underwent distinct retardment, and the hyperglycaemia was often of a somewhat higher degree and much longer.