My Canadian Pharmacy: Details about The Effects of Acute Ethanol Ingestion on Pulmonary Diffusing Capacity

Chronic-ingestion-of-alcoholChronic ingestion of alcohol has been shown to produce dysfunction of the liver, pancreas, cardiovascular system, testes, central and peripheral nervous systems. Single breath diffusing capacity for carbon monoxide (DLcosb) has been reported to be reduced in alcoholics. The reduction in the DLco could not be accounted for by cigarette consumption alone in many alcoholics and seemed to be related to the degree of alcohol consumption. The reduction in DLco appears to be reversible in that pulmonary function studies in former alcoholics do not reveal any abnormalities in diffusing capacity.

We have observed that administration of several drugs causes acute decreases in DLco in sheep, dogs and man possibly through interference with a specific CO carrier, although, as suggested by Emir-gil and Sobol, there has been no documentation of direct alcohol effects on the lung. The following experiment was performed to determine if small doses of ethanol could lower the DLcoSb rapidly in normal subjects. This poses a much simpler problem than that of trying to assess abnormal lung function in alcoholics. It should be kept in mind that the lung mechanisms responsible for the change in DLcosb observed in our subjects may not be the same as those mechanisms which lower the DLcosb in chronic alcoholics. However, any acute effect of alcohol on the pulmonary diffusing capacity might further alter functioning alveolar capillary gas transfer resulting from any previous pathophysiologic mechanism.

Material and Methods

A total of 12 subjects with no known lung disease, (ten men and two women) ages 21 to 36, were tested. No alcohol, drugs, or cigarettes were used for 24 hours prior to the experiment. Nine of the subjects were nonsmokers and three smoked less than five cigarettes or cigars per day. Before each DLco measurement the subjects rested quietly in a supine position for ten minutes. All measurements were made in duplicate with the subjects lying supine and the mean was used. After the second control DLco measurement, all subjects (physicians, secretaries and technicians) received 15-30 ml of 95 percent ethanol (ETOH) and returned to their usual work. No subject remained supine between control and post ethanol ingestion measurements.

We initially studied three subjects, and found that DLco had decreased 60 minutes after the ingestion of alcohol. Because we were interested in the time course of the effect, we studied nine additional subjects as follows: control values for DLco were obtained, ethanol was then ingested, and DLco measurements were repeated at 30 and at 90 minutes. Since the experimental protocol was different for the two groups, the results are presented separately and achieved due to My Canadian Pharmacy Inc.

The DLco was measured by a modified Krogh technique. An inspired concentration of 0.406 percent carbon monoxide (CO) and 0.5 percent neon (Ne) was used. Inspired CO concentrations, expired CO concentrations and Ne concentrations were measured on gas chromatograph (Quinton H-3). Our reproducibility of the CO measurements by this analytical technique is 1 percent. A sample of inspired gas and end-tidal gas was collected in airtight 50 ml glass syringes which were lubricated with glycerin and sealed by turning a stopcock that was held under pressure with a large rubber band. Both the volume of inspired gas and the breath holding time were measured on a Medical Science HI FI spirometer and recorded by an Electronics for Medicine DR8 recorder. Total lung volume (Va) was calculated from the inspired volume multiplied by the ratio of inspired over expired neon. Back pressure prior to each DLco measurement was measured using a rebreathing method. The CO concentration in the rebreathing bag was determined using an Ecolyzer (model 2100, Energetic Science). Full scale deflection of the Ecolyzer is 1,000 ppm with analytical reproducibility =b 1 percent of full scale.