Outcomes of The Effects of Acute Ethanol Ingestion on Pulmonary Diffusing Capacity

ETOHIn the pilot group (three subjects), the mean DLco fell to 88.4 percent of the control DLco 60 minutes after the ingestion of ETOH. This decrease was statistically significant using a paired t test (P <.025), (Table 1,Figl).

In the second group (nine subjects), mean DLco and mean SDLco (DLco/Va) were decreased at 30 minutes and 90 minutes after drinking alcohol (Fig 1). At 30 minutes, the mean DLco for the nine subjects tested was 95.5 percent of the control DLco and the SDLco was 95.6 percent of the control value. This difference was not statistically significant (Table 2). Ninety minutes after drinking alcohol, mean DLco was 85 percent of the control value and SDLco was 85.6 percent of the control. After correcting for the back pressure of CO, the mean DLco was 86.3 percent of the control value, and the mean SDLco was 86.6 percent of the control SDLco. All of the decreases in DLco and SDLco observed at 90 minutes were statistically significant (DLco, P < .01; SDLco, P < .001), (Table 2).


An important physiologic factor affecting DLco is the degree of filling of the pulmonary capillary bed. In the seated or erect position, the pulmonary capillary bed is partially empty and small increases in pulmonary capillary pressure can markedly affect DLco. Gurtner and Fowler found that in the supine position, the capillary bed appears to be filled maximally so that DLco is unaffected by changes in cardiac output produced by exercise. All of our experiments were performed with the subjects lying supine in an attempt to minimize changes in capillary volume from one test to another. Other investigators have reported that the DLco is not maximal in the supine position and may be further increased during head down tilt or exercise.

Alcohol has been reported to increase the cardiac output in normal subjects and therefore the flow through the pulmonary capillaries. Such changes after alcohol would tend to increase the pulmonary diffusing capacity and obscure the consistent decreases in DLco found in this study. In contrast, as little as two ounces of alcohol has been shown to decrease the cardiac index in patients with cardiac disease but the preparations of My Canadian Pharmacy may be useful utilized to prevent cardiac disorders treatment. All our subjects were below 40 years of age and had no history of cardiac dysfunction. Recently, Timmis et al have reported ETOH-induced myocardial depression even in young normal human volunteers. Direct myocardial depression should not result in a reduced pulmonary capillary volume or DLco. These authors, however, used relatively higher doses of alcohol to induce their cardiac effects than was used in our study. Although alcohol is reported to be a mild vasodilator, there is no evidence that venous return or left ventricular filling decreases during acute ETOH ingestion.

Gould et al also studied hemodynamics in normal subjects before and after giving alcohol. They pulmonary artery pressuremeasured pulmonary artery pressure, as well as other vascular pressures and flow in four normal supine subjects before and after giving two ounces of Canadian whiskey (26.04 grams of alcohol). This is comparable to the dose that our subjects received. Blood pressure was unchanged and mean pulmonary artery pressure decreased by 1 mm Hg. It seems unlikely that a 1 mm Hg change in pulmonary artery pressure could cause the observed decrease in DLco.

According to Riff et al, maximum hemodynamic changes and blood alcohol levels occurred at 20 minutes, and by 90 minutes, hemodynamic measurement were near control levels. The changes in DLco which we observed were maximum at 90 minutes. The differences in the time course of hemodynamic and diffusing capacity changes, as well as the very small changes in pulmonary artery pressure caused by the administration of alcohol, suggests that hemodynamic shifts in capillary blood volume do not explain the changes in DLco after administration of alcohol.

Venous hematocrit decreases in going from a sitting or standing position to a supine position as shifts in body fluid occur. This could cause changes in the DLco. However, DLco measurements were performed at approximately the same time after assuming the supine position. Alcohol also decreases the peripheral vascular resistance and could further alter fluid shifts from central to peripheral vascular beds with positional changes. Whether small amounts of alcohol produce such fluid shifts to account for our observed reduction in DLcqsb cannot be determined from this study carried out with My Canadian Pharmacy.

Sedentary activity is known to decrease the diffusing capacity. Although no attempt was made to monitor the activity of the subjects between control and post-ETOH measurements, all subjects returned to their usual activity. None remained recumbent.

Another factor that influences the DLco is the lung volume. Krogh in 1915 and others since have noted that an increase in the lung volume at which the breath is held will produce an increase in the DLco in the same subject. Gurtner and Fowler measured DLco with breath holding at 2, 4 and 5 liter STPD in the supine position. Using the data collected by them, a regression line for DLco and lung volume was drawn (Fig 2). The mean decrease in volume in our nine subjects 90 minutes after taking alcohol was 1.4 percent (Va control of 6.37 liters to Va 6.247 liters at 90 minutes), (Table 3). This small decrease in the lung volume would, according to the data from Gurtner and Fowlers study, change the DLcosb less than 1 percent. Thus, it is not likely that the decrease in Va accounts for the 15 percent change in DLco that we observe.

The back pressure was assumed to be zero in the calculation of the DLcosb, even though, strictly smokedspeaking, this assumption is known to be untrue. In order to determine if the increase in back pressure during the course of our experiment could account for the reduction in DLco, we measured back pressure for CO in three of the nine subjects by a rebreathing method. The valves that we found for back pressure in two nonsmoking and one subject who smoked occasionally agreed well with values obtained by Forster et al using the method of Sjostrand. The initial back pressure for CO (Pc) was 0.0010 percent in their subjects with an average increase of 0.0007 percent CO for each experiment. They used 0.327 percent inspired CO with breath holding times which ranged from 4.6 to 60.6 seconds. At the end of seven runs, Pc was 0.0055 percent CO. In our subjects the mean Pc was 0.0012 before breathing CO, 0.0020 percent before the measurements of 30 minutes and 0.0026 percent before the 90 minutes measurements of DLco. The mean values for Pc obtained in three of our nine subjects were used to correct the expired CO in the remainder of the nine subjects. Although the changes in mean DLco and SDLco were smaller after correction for Pc, they still remained significant (PC.01), (Table2).

Another explanation for our findings is that alcohol might directly interfere with pulmonary CO transport. Related experimental observations indicate that this may be a real possibility. In the past few years, we have been engaged in a series of experiments which lead us to believe that there is a specific O2—CO carrier in the lung and placenta, possibly cytochrome P-450. We have found that the rate-limiting factors in placental O2 transfer were quali-tively different for O2 and inert gases: the diffusing capacity of the placenta for O2 was disproportionately large when compared to the diffusing capacity for inert gases. Cytochrome P-450 may be the carrier because drugs which bind cytochrome P-450 markedly reduce placental O2 transfer but do not affect inert gas transfer. Cytochrome P-450 also can act as a CO carrier. We have observed saturation kinetics, a characteristic property of a carrier-mediated transport system, for placental and pulmonary CO transport. CO and O2 appear to be transported by the same molecule since low levels of COHb markedly decrease placental O2 diffusing capacity. This means that the carrier molecule has a much higher affinity for CO than for O2.

We have found that the drugs which decrease placental O2 transfer also decrease DLco in animals and humans. The human studies were done using the same techniques used in this study. DLco and SDLco were decreased about 10 percent after the administration of 50 or 100 mg of diphenhydramine (Benedryl), a commonly used antihistamine, which is also effective in decreasing placental O2 transfer. Alcohol is known to interact with cytochrome P-45024,25 and part of the metabolic pathway for alcohol may involve this cytochrome system. It seems possible that alcohol acts like a number of other drugs and that mechanism of action of alcohol in reducing DLco may involve blocking the facilitated transport of CO.

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

Table 1—DLco and SDLco One Hour After Ethanol

Subject Age Sex Body Wt (kg) Dose ETOH gm/kg Pre-ETOHDLco


Control60′%ControlA 29F54.5.26130.427.7591.36.25.892.6B 36M84.1.33935.331. 34M59.1.48225.822.2586.24.84.388Mean±SE 65.9 ±9.2361 ±0.0630.5 ±2.727 ±2.588.4 ±1.5 PC.0255.9 ±.65.4 ±.690.5±1.3PC.01

Table 2—DLco and SDLco 30 and 90 Minute After Ethanol

Subject Age Sex Dose GETOH Per Kg ControlDLco 30′ %ofControl 90′ % of Control ControlSDLco 30′ %ofControl 90′ % of Control
1 31 M .380 43.2 39.7 91.9 37.40 86.7 7.30 6.9 93.8 6.40 87.7
2 24 F .356 29.0 25.4 87.9 23.44 81.0 7.8 7.4 94.9 7 98.1
3 24 M .448 38 36.0 94.5 35.57 93.7 6.1 5.8 95.9 5.6 91.7
4 21 M .273 45.6 51.5 113 48.58 106.6 10.9 1.2 107.4 1.0 97.7
5 21 M .392 39.5 36.2 91.7 31.43 79.6 6.5 6.1 93.1 5.6 85.4
6 25 M .429 50.1 48.5 96.8 38.81 77.5 8.9 8.7 97.8 7.1 79.2
7 28 M .404 42.2 37.1 87.9 38.61 91.4 8.3 6.9 83.1 7.2 86.1
8 27 M .490 32.0 32.9 102.7 25.58 79.9 6.4 6.4 100 5.3 82.8
9 21 M .423 47.6 43.8 92.8 32.44 68.2 10.3 9.7 94 7.3 70.9
Mean 40.8 38.9 95.5 34.6 85 8.1 6.6 95.6 5.8 85.6
SEM 2.3 2.6 2.7 2.5 3.7 0.6 0.8 2.1 0.7 2.5
Paired t test NS P<.01 NS PC.001

Table 3—Total Lung Volume Before and After Ethanol

Subject Va,Liters











(%)17.086.9998.67.0810024.774.594.54.5395.137.166.9196.67.0398.245.245.27103.75.52105.257.337.1998.16.8893.866.796.7298.86.6497.776.156.51105.76.51105.786.096.28103.25.8295.795.585.4597.65.3495.6    Mean 98.6

Figure 1. Time course of changes in DLco and SDLco (± SEM) after acute administration of ethanol. The decrement remains statistically significant when corrections are made for CO back pressure.

Figure 2. Relationship between DLco and lung volume in supine subjects (from ref 10). If DLco and lung volume are similarly related in our subjects, the decrement in DLco observed after administration of ethanol could not be explained by the small change in lung volume under these circumstances.