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Left ventricular function during acute ethanol intoxication and hemodialysis
fOURNAL
OF
SURGICAL
RESEARCH
15, 207-211
(19%)
Left Ventricular Function During Acute Intoxication and Hemodialysis P.
N.
SYMBAS,
M.D.,
D.
H.
TYRAS,
M.D.,
IN ANESTHETIZED EXPERIMEKTAL ANIMALS, acute intravenous infusion of ethyl alcohol in moderately high concentrations has been shown to produce impairment in left ventricular function [2, 4, 5, 9, 111. Rapid detoxification of ethanol from blood passed through a single coil of a conventional twin-coil dialyzer has been effectively accomplished in experimental animals 131 and human subjects [lo]. The present study was undertaken to investigate the potential value of hemodialysis in reversing the adverse effects of acute ethanol intoxication on cardiac function in normal, nonanest.hetized dogs. METHODS
AND
MATERIAL
In 27 adult mongrel dogs, under general anesthesia, an electromagnetic ascending aortic flow probe was implanted and brought out through the skin of the back. After recovery from this procedure, 5-7 days after surgery, all dogs were anticoagulated with 3 mg/kg body weight of sodium heparin, and the aortic flow probe was connected to a Carolina ElectromagFrom the Joseph B. Whitehead Department of Surgery, Thoracic and Cardiovascular Surgery Division, and the Department of Medicine, Emory University School of Medicine, Atlanta, Georgia. This study was supported in part by United States Public Health Service Grants HE 05861 and HE 05731. Mailing address: Dr. P. N. Symbas, 69 Butler Street, S.E., Atlanta, Georgia 30303 Submitted for publication December 2, 1972.
@ 1973 by Academic Press. Inc. of reproduction in any form reserved.
B.
J.
BALDWIN,
M.D.
netic Flowmeter” and to an Electronics for Medicine Rec0rder.i A ?;io. 7 NIH catheter was also connected to the recorder after it was passed, under local anesthesia, through the carotid artery into the left ventricle. Baseline left ventricular pressures, it,s first derivative (dp/dt), aortic blood flow and its integral (stroke volume), and electrocardiogram were recorded. Baseline serum electrolytes (Sa, Cl, K, CO,) and arterial PO,, pH, and PCO, were obtained and ethanol (2.5 g/kg body wt) diluted in 50-80 ml 0.9% saline was infused intravenously over a 15-min period. The dogs were then divided into three groups. In group I (seven control dogs) after the ethanol infusion, all the above parameters were recorded every 15 min for l$i, hr, and simultaneous blood samples were obt.ained for serum ethanol determinations. In group II (13 experimental dogs) before the ethanol infusion, under only local anesthesia, the femoral artery and vein were exposed and connected to a membrane hemodialysis unit with a heat exchanger and a calibrated roller pump in t.he circuit (Fig. I). After the baseline and postethanol infusion parameters were recorded: the dogs were dialyzed for 1M hr; during this period, the same studies were obtained as in the group I dogs. Twenty-five Cuprophane membranesl framed in a Klung *Carolina Medical Electronics, P.O. Box 307, King, NC 27021. t Electronics for Medicine, 30 Virginia Road, V4’hite Plains, NY 10603. X Cobe Laboratories, Inc.. 1201 Oak Street, Lakewood, CO 80215.
207 Copyright All rights
AND
Ethanol
208
JOURNAL
OF
SURGICAL
1. Diagrammatic illustration group II dogs.
Fig.
RESEARCH,
15,
NO.
3,
SEPTEMBER
1973
of the preparation and the hemodialysis unit used in
Fig. 2. Diagrammatic illustration of the preparation and the arteriovenous fistula in group III dogs. Dialysis Frame were used for the hemodialysis. As dialysate, Hemotrate (Formula 33)” was used after it was diluted, adding 32 liters of water and 50 meq of KCL to 1000 ml of Hemotrate to give a final electrolyte concentration of Na 138, K 3.6, Cl * McCaw
VOL.
Laboratories, Milledgeville, GA.
107, acetate 37, Mg 1.6, and Ca 3.2 meq per liter. A 1:2 blood to dialysate flow ratio was maintained through the membrane during the period of dialysis and blood flow rate was kept at 200 ml/min. In group III (seven AVF dogs) before the ethanol infusion, under local anesthesia, a same-size fistula as in group II dogs was created between the femoral artery and vein (Fig. 2). After the baseline and postethanol infusion parameters were rethe arteriovenous fistula was corded, opened, and the same studies obtained as in the two previous groups. The blood flow through the fistula was kept at 200 ml/min with a calibrated roller pump. Gas chromatography was used to determine blood ethanol levels according to the method of Roach and Creaven [7]. All obtained data were statistically analyzed using an F test. RESULTS The blood gases, serum electrolytes, and heart rate were not sienificantlv altered
SYMBAS,
TYRAS,
AND
BALDWIN:
either during the study period of each dog or between groups of dogs. The serum ethanol level immediately aft.er the ethanol infusion in the control dogs was 334 (2192)) in the hemodialyzed dogs 310 (290) and in the AVF dogs 350 (4 160). During the study period, the ethanol level decreased in all three groups but the decrease of its level in the hemodialyeed dogs was more rapid and of greater magnitude (Fig. 3). The absolute decrease of the ethanol level in the hemodialyzed dogs was significantly greater than that observed in the control and in the AVF dogs (P < 0.05). All the hemodynamic parameters except the heart rate were found to be significantly impaired immediately after the ethanol infusion (Figs. 47). Fifteen minmes later, the mean stroke volume and the aortic blood flow returned to control level and remained at that level during the rest of the study period (Figs. 4 and 5). The left ventricular end-diastolic pressure (LVEDP) 15 min after the ethanol infusion, in the hemodialyzed dogs, returned to almost baseline levels and stayed at that or even lower levels during the study period, whereas, the decline of t,he LVEDP in the control and AVF dogs was slower and of lesser magnifude (Fig. 6). The difference of the decrease of the LVEDP in the hemodialyzed dogs was statistically significant compared with that observed in the control and in the AVF dogs (P < 0.005). The dp/dt markedly decreased in all three groups of dogs immediately after the ethanol infusion, but progressively returned to t’he prealcohol infusion level. The return of the dp/dt to the preethanol infusion level was more rapid in the hemodialyzed dogs (Fig. 7). This increase of the dp/dt in hemodialyzed dogs was statistically significant compared with that in the control and AVF dogs (P < 0.05). DISCIBSION Although the mechanism of impairment of left ventricular function produced by
ACUTE
ETHANOL
209
INTOXICATION C.&OH
BLOOD LEVELS
5d
400 1 350 300
1 z 250 z3 2200 I 150 100 50 1
0L control
30’ after ethyl olcohot Infusion
I
Fig. 3. Mean of all three period.
values groups
of ethyl alcohol of dogs during
STROKE
35
I
blood the
level study
VOWME
30 25
0
control
immed.
Fi3. 4. Mean of dogs
15’ 30’ 45’ 60’ after ethyl alcohol mfusion
stroke vo!ume of all the study period.
during
MEAN
7r
AORTIC
BLOOD
three
90
groups
FLOW
.z 4 :3 2 I 0
I
after ethyl alcohol infusion
Fig. 5. Mean aortic blood flow of dogs during the study period.
of all three
I
groups
210
JOURNAL
OF
SURGICAL
RESEARCH,
ethanol infusion or intake is unclear and somewhat controversial, there is relative agreement that significant elevation of the blood ethanol level results in reduction of left vent,ricular function in experimental animals. In the normal papillary muscle preparation, an ethanol concentraticn of 100 mg/lOO ml caused a 9% decrease in the contractile element velocity at a constant load of 0.5 mg/mm 181. Webb et rrb. [ 121 observed an increased work load of the heart and reduction of its functional capacity after acute ethanol infusion in lightly anesthetized dogs. In other studies, he and his associates [13] found no depression of ventricular contractility in isolated heart-lung preparation even when the alcohol concentration was increased to 900 mg/lOO ml and suggested that the previously reported decreased left ventricular contra&lity after alcohol administration in intact animals was due to secondary effects of alcohol upon blood pH, heart rate, stroke volume, and other variables that affect ventricular performance. Regan et al. [5] found diminished left ventricular function manifested by decline of stroke output, rise of LVEDP, and significant myocardial damage with significant elevation of the coronary sinus concentration of potassium and phosphate ions as well as of serum glutamie oxaloacetic transaminase after intravenous infusion of 0.1 ml/kg body weight per minute of 15% ethanol for 2 hr. Similar hemodynamic findings were observed by Regan and associates in eight subjects with chronic alcoholism under 42 years of age [6]. In normal human subjects, however, with blood alcohol levels of ‘90-209 mg/lOO ml, the cardiac capacity at maximal oxygen uptake level of physical activity was not affected by the alcohol ingestion [ 11. In general, it appears that the adverse effects of ethanol upon left vent,ricular function are the result of the direct effect of the ethanol upon the myocardium and that they are in direct relation to the blood ethanol level [4, 5, 111.
VOL.
15,
NO.
3,
SEPTEJIBER
1973
L.V E. D. I?
18-
1
1614-
IL?I”E
IO-
~8 6 4 2 0
COM
afler ethyl alcohol infusion
Fig. 6. Mean of all three period.
left ventricular end-diastolic groups of dogs during
I
the
pressure stud)
4039 $500
0
control
Immed.
15’ 30’ 45’ 60’ after ethyl alcohol infusion
Fig. 7’. Mean dp/dt of all during the study period.
three
groups
90
of
dogs
In vitro and in viva experiments [3] have shown that the removal of ethanol from the blood was 4.1 times (meani faster in the hemodialyzed dogs utilizing a single coil of the conventional twin-coil dialyzer than the physiological metabolic degradation by the control dogs. The control dogs remained unconscious and unresponsive during the lo-hr study in contrast to the dialyzed dogs that awoke by the second hour of the procedure. In our study, the decrease of the serum ethanol level in the hemodialyzed dogs was also faster and greater than the control
SYkU3AS,
TYRAS,
AND
BALDWIN:
and the AVF groups of dogs. Coincident with the blood-ethanol level decrease in the hemodialyzed dogs, there was return of t’hc LVEDP and ot.her hemodynamie parameters to normal levels within the first 15 min of hemodialysis. In these dogs the alteration of the LVEDP does not appear to be relat’ed to the arteriovenous shunting through the hemodialysis unit since similar alteration of the LVEDP did not occur in the AVF group of dogs. Our control and AVF dogs remained unconscious and unresponsive during the study period, whereas, the hemodialyzed animals were a$vake within 60-90 min of hemodialysis. SUMMARY Acute intravenous infusion of ethanol 2.5 g/kg body wt, over 15 min in nonanesthetized dogs resulted in impairment of left ventricular function. The blood concentration of alcohol declined more rapidly in dogs treated by hemodialysis than in control dogs or in dogs with a temporary l:eripheral arteriovenous fistulae. Hemodialysis caused a rapid reversal of the adverse effects of ethanol upon left ventricular function and expedited recovery of consciousnessin intoxicated dogs. REFERENCES 1. Blomqvist, G., Saltin, B., and Mitchell, J. H. Acute effects of ethanol ingestion on the response to submaximal and maximal exercise in man. Cited by Mitchell, J. H., and Cohen, L. S. Alcohol and the heart. Mod. Concepts Cardiovasc. Dis. 39: 109, 1970.
ACUTE
ETHANOL
INTOXICATION
211
2. Ganz, V. The acute effect of alcohol on the circulat,ion and on the oxygen metabolism of the heart. Am. Herrrt d. 66:494, 1963. 3. Marc-Aurele, J., and Schreiner, G. E. The dialysance of ethanol and methanol: A proposed method for t!rc treatment of massive intoxication by ethyl and methyl alcohol. J. Clin. Invest. 39:892. 1960. 4. Mirrzwiak, D. S., Wildcnthal, K., and Mitchell, J. H. Effect of ethanol on the canine left ventricle. C/in. Res. 15:215, 1967. 5 Regan, T. J., Koroxendis, G., Moschos, C. B., Oldewurtel H. A., Lehan, P. H., and Hellems, H. K. The acute metabolic and hemodynamic responses of the left ventricle to ethanol. 1. Cl& Invest. 45:270, 1966. 6. Regan, T. J., Levinson, G. E., Oldewurtel, II. A., Ventricular fnnetion in noncardiacs with alcoholic fatty liver: Role of ethanol in the production of cardiomyopathy. J. C’lin. Itcvext. 48:397,
1969.
7. Roach, M. K., and Creavrn, P. J. A micro method for the determination of acetaldehyde and ethanol in blood. Clir~. Chim. Acta 21:275, 1968. 8. Spann, J. F., Jr., Mason, D. T., Belser, G. D., et al. Actions of ethanol on the contractile state of the normal and failing cat papillary muscle. (abstr.) Clin. Res. l&249, 1968. 9. Unal, M., Webb, W. R., and Cook, W. A. Alcohol and myocardial metabolism. Sung. Forum 16:61, 1965. 10. Walder, A. I., Redding, J. S., Faillance, L., and Steenburg, R. W. Rapid detoxification of acute alcoholic with hemodialysis. Surgery 66:201,
1969.
11. Webb, W. R., and Degerli, I. U. Ethyl alcohol and the cardiovascular system: Effects on coronary blood flow. JAMA 191:1055, 1965. 12. Webb, W. R., Degerli, 1. U., Cook, W. A., et al. Alcohol, digitalis, and cortisol, and myocardial contractility. Ann. Surg. 163:811, 1966. 13. Webb, W. R., Gupta. D. N., Cook, W. A., et al. Effects of nlrohol on myocardial conizractility. Dis. Chest 52:602, 1967.
OF
SURGICAL
RESEARCH
15, 207-211
(19%)
Left Ventricular Function During Acute Intoxication and Hemodialysis P.
N.
SYMBAS,
M.D.,
D.
H.
TYRAS,
M.D.,
IN ANESTHETIZED EXPERIMEKTAL ANIMALS, acute intravenous infusion of ethyl alcohol in moderately high concentrations has been shown to produce impairment in left ventricular function [2, 4, 5, 9, 111. Rapid detoxification of ethanol from blood passed through a single coil of a conventional twin-coil dialyzer has been effectively accomplished in experimental animals 131 and human subjects [lo]. The present study was undertaken to investigate the potential value of hemodialysis in reversing the adverse effects of acute ethanol intoxication on cardiac function in normal, nonanest.hetized dogs. METHODS
AND
MATERIAL
In 27 adult mongrel dogs, under general anesthesia, an electromagnetic ascending aortic flow probe was implanted and brought out through the skin of the back. After recovery from this procedure, 5-7 days after surgery, all dogs were anticoagulated with 3 mg/kg body weight of sodium heparin, and the aortic flow probe was connected to a Carolina ElectromagFrom the Joseph B. Whitehead Department of Surgery, Thoracic and Cardiovascular Surgery Division, and the Department of Medicine, Emory University School of Medicine, Atlanta, Georgia. This study was supported in part by United States Public Health Service Grants HE 05861 and HE 05731. Mailing address: Dr. P. N. Symbas, 69 Butler Street, S.E., Atlanta, Georgia 30303 Submitted for publication December 2, 1972.
@ 1973 by Academic Press. Inc. of reproduction in any form reserved.
B.
J.
BALDWIN,
M.D.
netic Flowmeter” and to an Electronics for Medicine Rec0rder.i A ?;io. 7 NIH catheter was also connected to the recorder after it was passed, under local anesthesia, through the carotid artery into the left ventricle. Baseline left ventricular pressures, it,s first derivative (dp/dt), aortic blood flow and its integral (stroke volume), and electrocardiogram were recorded. Baseline serum electrolytes (Sa, Cl, K, CO,) and arterial PO,, pH, and PCO, were obtained and ethanol (2.5 g/kg body wt) diluted in 50-80 ml 0.9% saline was infused intravenously over a 15-min period. The dogs were then divided into three groups. In group I (seven control dogs) after the ethanol infusion, all the above parameters were recorded every 15 min for l$i, hr, and simultaneous blood samples were obt.ained for serum ethanol determinations. In group II (13 experimental dogs) before the ethanol infusion, under only local anesthesia, the femoral artery and vein were exposed and connected to a membrane hemodialysis unit with a heat exchanger and a calibrated roller pump in t.he circuit (Fig. I). After the baseline and postethanol infusion parameters were recorded: the dogs were dialyzed for 1M hr; during this period, the same studies were obtained as in the group I dogs. Twenty-five Cuprophane membranesl framed in a Klung *Carolina Medical Electronics, P.O. Box 307, King, NC 27021. t Electronics for Medicine, 30 Virginia Road, V4’hite Plains, NY 10603. X Cobe Laboratories, Inc.. 1201 Oak Street, Lakewood, CO 80215.
207 Copyright All rights
AND
Ethanol
208
JOURNAL
OF
SURGICAL
1. Diagrammatic illustration group II dogs.
Fig.
RESEARCH,
15,
NO.
3,
SEPTEMBER
1973
of the preparation and the hemodialysis unit used in
Fig. 2. Diagrammatic illustration of the preparation and the arteriovenous fistula in group III dogs. Dialysis Frame were used for the hemodialysis. As dialysate, Hemotrate (Formula 33)” was used after it was diluted, adding 32 liters of water and 50 meq of KCL to 1000 ml of Hemotrate to give a final electrolyte concentration of Na 138, K 3.6, Cl * McCaw
VOL.
Laboratories, Milledgeville, GA.
107, acetate 37, Mg 1.6, and Ca 3.2 meq per liter. A 1:2 blood to dialysate flow ratio was maintained through the membrane during the period of dialysis and blood flow rate was kept at 200 ml/min. In group III (seven AVF dogs) before the ethanol infusion, under local anesthesia, a same-size fistula as in group II dogs was created between the femoral artery and vein (Fig. 2). After the baseline and postethanol infusion parameters were rethe arteriovenous fistula was corded, opened, and the same studies obtained as in the two previous groups. The blood flow through the fistula was kept at 200 ml/min with a calibrated roller pump. Gas chromatography was used to determine blood ethanol levels according to the method of Roach and Creaven [7]. All obtained data were statistically analyzed using an F test. RESULTS The blood gases, serum electrolytes, and heart rate were not sienificantlv altered
SYMBAS,
TYRAS,
AND
BALDWIN:
either during the study period of each dog or between groups of dogs. The serum ethanol level immediately aft.er the ethanol infusion in the control dogs was 334 (2192)) in the hemodialyzed dogs 310 (290) and in the AVF dogs 350 (4 160). During the study period, the ethanol level decreased in all three groups but the decrease of its level in the hemodialyeed dogs was more rapid and of greater magnitude (Fig. 3). The absolute decrease of the ethanol level in the hemodialyzed dogs was significantly greater than that observed in the control and in the AVF dogs (P < 0.05). All the hemodynamic parameters except the heart rate were found to be significantly impaired immediately after the ethanol infusion (Figs. 47). Fifteen minmes later, the mean stroke volume and the aortic blood flow returned to control level and remained at that level during the rest of the study period (Figs. 4 and 5). The left ventricular end-diastolic pressure (LVEDP) 15 min after the ethanol infusion, in the hemodialyzed dogs, returned to almost baseline levels and stayed at that or even lower levels during the study period, whereas, the decline of t,he LVEDP in the control and AVF dogs was slower and of lesser magnifude (Fig. 6). The difference of the decrease of the LVEDP in the hemodialyzed dogs was statistically significant compared with that observed in the control and in the AVF dogs (P < 0.005). The dp/dt markedly decreased in all three groups of dogs immediately after the ethanol infusion, but progressively returned to t’he prealcohol infusion level. The return of the dp/dt to the preethanol infusion level was more rapid in the hemodialyzed dogs (Fig. 7). This increase of the dp/dt in hemodialyzed dogs was statistically significant compared with that in the control and AVF dogs (P < 0.05). DISCIBSION Although the mechanism of impairment of left ventricular function produced by
ACUTE
ETHANOL
209
INTOXICATION C.&OH
BLOOD LEVELS
5d
400 1 350 300
1 z 250 z3 2200 I 150 100 50 1
0L control
30’ after ethyl olcohot Infusion
I
Fig. 3. Mean of all three period.
values groups
of ethyl alcohol of dogs during
STROKE
35
I
blood the
level study
VOWME
30 25
0
control
immed.
Fi3. 4. Mean of dogs
15’ 30’ 45’ 60’ after ethyl alcohol mfusion
stroke vo!ume of all the study period.
during
MEAN
7r
AORTIC
BLOOD
three
90
groups
FLOW
.z 4 :3 2 I 0
I
after ethyl alcohol infusion
Fig. 5. Mean aortic blood flow of dogs during the study period.
of all three
I
groups
210
JOURNAL
OF
SURGICAL
RESEARCH,
ethanol infusion or intake is unclear and somewhat controversial, there is relative agreement that significant elevation of the blood ethanol level results in reduction of left vent,ricular function in experimental animals. In the normal papillary muscle preparation, an ethanol concentraticn of 100 mg/lOO ml caused a 9% decrease in the contractile element velocity at a constant load of 0.5 mg/mm 181. Webb et rrb. [ 121 observed an increased work load of the heart and reduction of its functional capacity after acute ethanol infusion in lightly anesthetized dogs. In other studies, he and his associates [13] found no depression of ventricular contractility in isolated heart-lung preparation even when the alcohol concentration was increased to 900 mg/lOO ml and suggested that the previously reported decreased left ventricular contra&lity after alcohol administration in intact animals was due to secondary effects of alcohol upon blood pH, heart rate, stroke volume, and other variables that affect ventricular performance. Regan et al. [5] found diminished left ventricular function manifested by decline of stroke output, rise of LVEDP, and significant myocardial damage with significant elevation of the coronary sinus concentration of potassium and phosphate ions as well as of serum glutamie oxaloacetic transaminase after intravenous infusion of 0.1 ml/kg body weight per minute of 15% ethanol for 2 hr. Similar hemodynamic findings were observed by Regan and associates in eight subjects with chronic alcoholism under 42 years of age [6]. In normal human subjects, however, with blood alcohol levels of ‘90-209 mg/lOO ml, the cardiac capacity at maximal oxygen uptake level of physical activity was not affected by the alcohol ingestion [ 11. In general, it appears that the adverse effects of ethanol upon left vent,ricular function are the result of the direct effect of the ethanol upon the myocardium and that they are in direct relation to the blood ethanol level [4, 5, 111.
VOL.
15,
NO.
3,
SEPTEJIBER
1973
L.V E. D. I?
18-
1
1614-
IL?I”E
IO-
~8 6 4 2 0
COM
afler ethyl alcohol infusion
Fig. 6. Mean of all three period.
left ventricular end-diastolic groups of dogs during
I
the
pressure stud)
4039 $500
0
control
Immed.
15’ 30’ 45’ 60’ after ethyl alcohol infusion
Fig. 7’. Mean dp/dt of all during the study period.
three
groups
90
of
dogs
In vitro and in viva experiments [3] have shown that the removal of ethanol from the blood was 4.1 times (meani faster in the hemodialyzed dogs utilizing a single coil of the conventional twin-coil dialyzer than the physiological metabolic degradation by the control dogs. The control dogs remained unconscious and unresponsive during the lo-hr study in contrast to the dialyzed dogs that awoke by the second hour of the procedure. In our study, the decrease of the serum ethanol level in the hemodialyzed dogs was also faster and greater than the control
SYkU3AS,
TYRAS,
AND
BALDWIN:
and the AVF groups of dogs. Coincident with the blood-ethanol level decrease in the hemodialyzed dogs, there was return of t’hc LVEDP and ot.her hemodynamie parameters to normal levels within the first 15 min of hemodialysis. In these dogs the alteration of the LVEDP does not appear to be relat’ed to the arteriovenous shunting through the hemodialysis unit since similar alteration of the LVEDP did not occur in the AVF group of dogs. Our control and AVF dogs remained unconscious and unresponsive during the study period, whereas, the hemodialyzed animals were a$vake within 60-90 min of hemodialysis. SUMMARY Acute intravenous infusion of ethanol 2.5 g/kg body wt, over 15 min in nonanesthetized dogs resulted in impairment of left ventricular function. The blood concentration of alcohol declined more rapidly in dogs treated by hemodialysis than in control dogs or in dogs with a temporary l:eripheral arteriovenous fistulae. Hemodialysis caused a rapid reversal of the adverse effects of ethanol upon left ventricular function and expedited recovery of consciousnessin intoxicated dogs. REFERENCES 1. Blomqvist, G., Saltin, B., and Mitchell, J. H. Acute effects of ethanol ingestion on the response to submaximal and maximal exercise in man. Cited by Mitchell, J. H., and Cohen, L. S. Alcohol and the heart. Mod. Concepts Cardiovasc. Dis. 39: 109, 1970.
ACUTE
ETHANOL
INTOXICATION
211
2. Ganz, V. The acute effect of alcohol on the circulat,ion and on the oxygen metabolism of the heart. Am. Herrrt d. 66:494, 1963. 3. Marc-Aurele, J., and Schreiner, G. E. The dialysance of ethanol and methanol: A proposed method for t!rc treatment of massive intoxication by ethyl and methyl alcohol. J. Clin. Invest. 39:892. 1960. 4. Mirrzwiak, D. S., Wildcnthal, K., and Mitchell, J. H. Effect of ethanol on the canine left ventricle. C/in. Res. 15:215, 1967. 5 Regan, T. J., Koroxendis, G., Moschos, C. B., Oldewurtel H. A., Lehan, P. H., and Hellems, H. K. The acute metabolic and hemodynamic responses of the left ventricle to ethanol. 1. Cl& Invest. 45:270, 1966. 6. Regan, T. J., Levinson, G. E., Oldewurtel, II. A., Ventricular fnnetion in noncardiacs with alcoholic fatty liver: Role of ethanol in the production of cardiomyopathy. J. C’lin. Itcvext. 48:397,
1969.
7. Roach, M. K., and Creavrn, P. J. A micro method for the determination of acetaldehyde and ethanol in blood. Clir~. Chim. Acta 21:275, 1968. 8. Spann, J. F., Jr., Mason, D. T., Belser, G. D., et al. Actions of ethanol on the contractile state of the normal and failing cat papillary muscle. (abstr.) Clin. Res. l&249, 1968. 9. Unal, M., Webb, W. R., and Cook, W. A. Alcohol and myocardial metabolism. Sung. Forum 16:61, 1965. 10. Walder, A. I., Redding, J. S., Faillance, L., and Steenburg, R. W. Rapid detoxification of acute alcoholic with hemodialysis. Surgery 66:201,
1969.
11. Webb, W. R., and Degerli, I. U. Ethyl alcohol and the cardiovascular system: Effects on coronary blood flow. JAMA 191:1055, 1965. 12. Webb, W. R., Degerli, 1. U., Cook, W. A., et al. Alcohol, digitalis, and cortisol, and myocardial contractility. Ann. Surg. 163:811, 1966. 13. Webb, W. R., Gupta. D. N., Cook, W. A., et al. Effects of nlrohol on myocardial conizractility. Dis. Chest 52:602, 1967.