THE EFFECTS OF INTRAVENOUSLY ADMINISTERED AMINOPHYLLINE ON CEREBRAL CIRCULATION AND METABOLISM IN MAN 1

Open Access
Publisher Website
Google Scholar
Abstract
The effects of admn. of clinically therapeutic doses of aminophylline (0.5 g. in 250 cc. of physiol. saline soln.) were studied on the blood gases, blood pH, cerebral blood flow (CBF), cerebral O2 consumption (CMRO2), and cerebrovascular resistance (CVR) in 10 hospitalized patients without any obvious cerebral depression. These studies showed a statistically significant decrease in CBF from 59.4 to 44.4 cc/100 g./ min. (p<0.01) due to an increase in CVR from 1.7 to 2.1 mm. Hg. (p<0.001). Other results include a decrease in arterial CO2 tension and an increase in arterial pH (reflecting an expected hyperventilation), a decrease in internal jugular O2 content from 8.2 to 6.2 vols. % (p<0.001) and an increased cerebral arteriovenous O2 difference from 6.7 to 8.7 vols.% (p<0.01). There was no significant change in the internal jugular CO2 content, pH, CO2 tension, arterial O2 content, or CMR02 in the group as a whole. Although a drop in arterial CO2 tension is known to cause constriction of cerebral vessels, the decrease in CBF which occurred in these patients after aminophylline, seemed greater than that expected from comparable degrees of hyperventilation alone. It is perhaps more probable that aminophylline constricts the cerebral vessels and thus causes the decrease in CBF, which would be expected to increase the CO2 tension of the brain. Since increased CO2 tension is a known respiratory stimulant, it may be postulated as the cause of the hyperventilation, which diminished arterial CO2 tension and resulted in a drop of the brain and internal jugular CO2 tension to normal. With the decrease in CBF and the constant overall O2 consumption, the internal jugular O2 content, of course, falls. Since the internal jugular O2 content is a reflection of the brain O2 content, aminophylline causes anoxia of cerebral tissue. Four of the patients reacted to the drug with pronounced anxiety, associated symptoms, and a statistically significant increase in CMRO2 from 3.7 to 4.6 cc/ 100 g./min. None of the other 6 patients showed this increase, their mean showing a statistically significant decrease. In those patients with anxiety, aminophylline, by its effect on the heart, blood pressure, and kidneys, may have caused the associated symptoms, which could lead to the anxiety and thus the increase in CMRO2. It is also possible that the aminophylline increased CMR02 which resulted in the anxiety and associated symptoms.