Acta anaesth. scand. 1975, 19, 206-209
Influence of Glucagon on Systolic Time Intervals During Induction of Anaesthesia with Barbiturate M. IRLER and M. DALSGAARD Department of Anaesthesiology, Glostrup Hospital, Copenhagen, Denmark
The systolic time intervals and calculated parameters of PEPiLVET (pre-injection period/left ventricular ejection time-ratio) and 1/PEP2 before and after induction of anaesthesia with the barbiturate enibomal (Narcodorma) were studied noriinvasively in eight surgical patients after pretreatment with a bolus dose of glucagon. The mean difference between the PEP/LVET-ratio before and after induction was 0.06, and the mean difference between l/PEP’ before and after induction was -8. The corresponding values in the control group consisting of 12 patients wcre 0.09 and - 22, respectively, suggesting a somewhat greater depression of cardiac function in this group. However, no statistically significant difference at the 5% level was found betweenchanges in the glucagon group and controls. The influencc of barbiturates and glucagon on cardiac function is discussed.
Received 10 January, accepted for publication 4 E’rbruary 1975
The induction of anaesthesia with rapidly increase of cardiac output due to glucagon acting barbiturates is usually followed by a in dogs anaesthetized with pentobarbital. The interaction between glucagon and reduction of cardiac output (Lr 1964), which manifests itself as a transient decrease barbiturates has not yet been investigated in in blood pressure during the period immedi- man. The intention of the present investigaately after administration of the drug. tion was to evaluate the possible protective The reduction o f cardiac output is caused by effect of glucagon on the myocardial function an inhibition of the sympathetic nervous during induction of anaesthesia with thc activity (SKOVSTED et al. 1970) affecting barbiturate enibomal (Narcodorm’). both the heart and the peripheral vessels. However, barbiturates also elicit a direct negative inotropic action on the myocardium MATERIAL (KLARNER1962), which can be antagonised by digitalis (HAACKE& ZWIETEN1970). Patients Reduction of myocardial function was also The study comprised eight patients, five women and shown clinically by IBLER& DALSGAARDthree men admitted to hospital for elective abdominal (1975) after induction of anaesthesia with and orthopaedic surgery. None of the patients had anamnestic or clinical symptoms of heart-disease. the barbiturate enibomal. No abnormalities were present in the ECG’s. Recently, the positive inotropic action of After fasting for 8-10 h before the induction of glucagon has attracted interest also among anaesthesia, the patients were premedicated with 50anaesthesiologists. KATZet al. (1969) demon- 7.5 mg pethidine and 0.5 mg atropine subcutaneously. strated an increase of myocardial contractility Anaesthesia after the administration o f glucagon in dogs Lead I1 of the ECG, the phonocardiogram and thc and cats anaesthetized by halothane, while carotid pulse wave were recorded simultaneously with GILES & BURCH (1971) demonstrated an the patients in a supine position on the operating table
GLUCAGON, BARBITURATE AND SYSTOLIC TIME INTERVALS
Table 1 PEPjLVET quotient and l/PEPZ in s-‘ barbiturate. Glucagon group.
Patient
Age
Sex
no.
I1
~F M F
M F
F M F Mean s.e. mean
before and after administration of
1
PEPILVE?’ Before
I
After
I
(b-a)
I
l/PEPZ Before
I
After
I
(b-a)
-t19
0.41 0.50 0.47 0.31 0.39 0.42 0.23 0.36
0.39 0.52 0.43 0.45 0.45 0.35 0.35 0.44
-0.03 +0.02 - 0.04 +0.14 4-0.06 - 0.07 1-0.12 0.08
83 61 64 123 111 64 181 82
102 65 89 87 85 106 100 69
1 4 t25 - 36 - 26 4-42 -81 - 13
0.39 0.03
0.42 0.02
0.06 0.03
96 14
87 5
-8 13
a = before; b = after.
PEPiLVET Patient no.
Age
1
45 48 29 40 30 33 53 37 43 49 42 53
2 3 4 5 6 7 8 9 10 11 12 Mean s.e. mean
Sex Before
F M F
hl F F
M F M F
M F
1
After
I
(b-a)
Before
I
l/PEPZ After
I
(b-a )
0.37 0.26 0.33 0.22 0.38 0.29 0.27 0.25 0.47 0.29 0.30 0.34
0.37 0.41 0.36 0.34 0.41 0.26 0.40 0.40 0.73 0.39 0.42 0.41
0.00 0.15 0.03 0.12 0.03 -0.03 0.13 0.15 0.26 0.10 0.12 0.07
120 152 113 187 102 192 173 192 60 120 149 92
118 104 115 113 118 260 96 96 50 73 108 62
-2 - 48 2 - 74 16 68 - 77 - 96 - 10 - 47 -41 - 30
0.31 0.02
0.41 0.03
0.09 0.02
137 12
109 15
-28 13
~~~
~~
a = before; b = aftcr.
207
208
M . IBLER AND M . DALSGAARD
mg/lO kg b.w. was administered slowly intravenously. 5-10 minutes later, a 5%-solution of enibomal (Naisopropyl-beta-bromallyl-N-methylbarbiturate)5 mg/ kg was given intravenously in the course of 3 0 4 0 s under spontaneous respiration with atmospheric air. 30-60 s after injection of the barbiturate, ECC: recordings were repeated, whereupon ventilation was started with N 2 0 and 0, and intubation was undertaken after a single dose of suxamethonium. Except for the administration of glucagon, the proredure in the control group, which comprised twelve clective abdominal and orthopaedic surgical patients without any cardiological or medical disorders was the same as mentioned above.
METHOD
group were 0.09 and -28, suggesting a somewhat greater depression of myocardial function in this group. Statistical analysis by means of Student's t-test showed significant changes of PEP/ LVET and 1/PEP2in both groups ( P < 0.01). However, no significant differencc at the 5% level was found between changes in the glucagon group and in the controls. KO remarkable difference in the blood prcssure decrease measured by the cuff method was observed between these two groups following induction of anaesthesia. A few patients experienced nausea for a duration of 1-2 min. This is a side effect of glucagon which can be prevcnted by prochlorperazine (LVOFF& WILCKEN 1972.
To evaluate an alteration in the contractility of the myocardium, a non-invasive method for measurement of the systolic time intervals: left ventricular ejection time (LVET), pre-ejection period (PEP) and their derivates PEP/LVET and 1/PEP2 was used (WEISSLER et al. 1969, REITANet al. 1972). Accordingly, the DISCUSSION application of negative inotropic agents should result in an increase of the pre-ejection periodileft ventricular The positive inotropic effect of glucagon is ejection time-ratio (PEP/LVET) and in a decrease of the result of a double mechanism of action I/PEPZ. I n our evaluations, we used a recorder, Multi- namely, beta-adrenergic stimulation and scriptor E K 26 (Hellige, Freiburg, West Germany) activation of the adenyl cyclase system. with a paper speed of 50 mm/s. The carotid pulse wave The first-mentioned mechanism which and heart sounds were recorded by means of a piezolasts 1 to 5 minutes can be inhibited by betaelectric amplified stethoscope and a microphone from blocking agents, while the second mechanism the same manufacturer. Each interval was calculated as a mean value of at least ten heart beats. The is not influenced by beta-blocking drugs and electromechanical time (EMT) was measured from the lasts about 20 minutes after a bolus dose of' beginning of the Q-wave in the electrocardiogram to glucagon 50 mg per kg body weight (LYDTIN the first deflection of the second heart sound. The left et al. 1971). As in the case of digitalis the ventricular ejection time (LVET) was measured from mechanism activating the adenyl cyclasc the beginning of the carotid pulse wave to the beginning system is followed by a rise of intracellular of the dicrotic elevation. The pre-ejection period (PEP) is calculated as the difference between E M T and calcium concentration in the myocardium. LVET. (NAYLER et al. 1970).
RESULTS Tables 1 and 2 show PEPiLVET and 1/PEP2 before and after induction of anaesthesia with barbiturate. I n the group of patients pretreated with glucagon, the mean difference between initial PEPiLVET and PEPiLVET measured after induction of anaesthesia was 0.06, whereas the mean difference between the initial l/PEP2 and 1/PEP2 after induction was - 8.
Reduced contractility of the myocardium and diminished calcium exchange after the administration of sodium hexobarbital has been demonstrated in vitro by HAACKE & ZWIETEN(1970), who also found that strophantin was capable of counterbalancing this hexobarbital clicited effect. However, the mechanism by which barbiturates influence the heart under clinical conditions is complicated by various factors, the most important of which is an inhibitory action on the sympathetic nervous system.
GLUCAGON, BARBITURATE AND SYSTOLIC 1 I M E INIERVALS
O u r results showed that a bolus dose of glucagon given 5 to 10 minutes before induction of anaesthesia was not able to protect the myocardium significantly from the inhibitory action of the barbiturate enibomal. As mentioned above, the beta stimulating action of glucagon is of short duration. I t is possible that the injection of a barbiturate within the interval of no more than 5 minutes after the administration of glucagon might lead to less myocardial depression than has been shown in the present study. If this is the case, some benefits of the administration of glucagon before the induction of anaesthesia might be expected under certain clinical conditions.
ACKNOWLEDGEMENT The authors are grateful to Nova Industry Ltd., Copenhagen, who provided glucagon and the apparatus used in this investigation.
ZUSAMMEIVFASSUNG Bei 8 chirurgischen Patienten wurden nach Vorbehandlung niit einer Bolus-Dosis von GIukagon die Systolen-Zeitintervalle und die berechneten Parameter PEPiLVET und l/PEP2 vor und nach Narkoseeinleitung mit dem Barbiturat Enibomal (Narcodorma) mittels einer nicht-invasiven Technik untersucht. Der mittlere Unterschied zwischen den PEP/LVETVerhaltnissen vor und nach Narkosecinleitung war 0,06, die mittlere Differenz zwischen den l/PEPZWerten vor und nach der Einleitung -8. Die korrespondierenden Werte in der Kontrollgruppe waren 0,09 bzw. - 28, was auf eine etwas starkere Depression der Herzfunktion in dieser Gruppe hinweist. Ein statistisch gesicherter Unterschied von p i 0,05 zwischen den Veranderungen in der Glukagongruppe und denen der Kontrollgruppe wurde allerdings nicht gefunden. Der EinfluB von Barbituraten und von Glukagon auf die Herzfunktion wird diskutiert.
HAACKE, H . & ZWIETEN,VAN 1'. A. (1970) Die gegensinnige Wirkung von Hexobarbital-Na und g-Strophantin auf die Konttraktionskraft und den Calciumstoffwechseldes Herzmuskels. Anaesthesirl19, 301. IBLER, M . & DALSGAARI), M. (1973) The effect of the short-acting barbiturate enibomal (Narcodorm@) on systolic time intcrvals. Acta nnaesth. scand. 19, 44. KArz, R. L., HINDS, I,. & MILLS,C . J. (1969) Ability of glucagon to produce cardiac stimulation without arrhythmias in halothane-anaesthetized animals. Brit. 3. Anaesth. 41, 574. KLARNER,P. (1962) The influence of barbiturates, thiobarbiturates, and barbituric acid on cellular potentials and contractility of thc guinea pig atria ~aunyn-Schnieidelberg'sarch. exp. Path. Pilannahol. 243, 269. LI, TSUNG-HAN (1964) Effectso f Anesthetics on the Circnlation. Charles C. Thomas, Springfield, Ill., p. 166. LVOPF, R . & WILCKEN, E. L. D. (1972) Glucagon in heart failure and in cardiogcnic shock. Experience in 50 patients. Circulation 45, 534. LYIITIN, H., LOHMOLLER, G., DANIEL, W., SCHIBRL, W., SCIIEWE, ST., KEMPEK, H . , LOIIMOLLER,R., WALTER,I., & Kusus, T. (1971) Kardiovasculire Wirkungen von Glucagon vor und nach Propranololgabe. Verh. dtsch. Ges. inn. Med. 77, 1000. NAYLER,W. G., MCINNES,I., CHIPPERFIELD, D., CARSON,V., & DAILE, P. (1970) The effect of glucagon on calcium exchangeability, coronary blood flow, myocardial function and high energy phosphate stores. 3. Pharmacol. ex/). Ther. 171, 265. REITAN,.J. A,, TY SMITH,N., SCOTTBORIsnN, V. Bi KADIS,L. B. (1972) The cardiac prc-ejection period: A correlate of peak ascending aortic blood-flow acceleration. Anesthesiology 36, 76. SKOVSTED, P., PRICE,M. L. & PRICE,H. L. (1970) The effects of short-acting barbiturates on arterial pressure, preganglionic sympathetic activity and barostatic reflexes. Anesthesiology 33, 10. WEISSIZR, A. M., HARRIS, E. S. & SCIIOENFELD, C. D. (1969) Bedside technics for the evaluation of ventricullar function in man. Anzer. 3. Curdiol. 23, 577.
Address : Mluden Ibler, M.D.
REFERENCES GILES,T . D. & BURGH,G. E. (1971) The influence of anesthesia on hemodynamic responses to glucagon in intact dog (35964). Proc. Soc. exfi. Biol. (N.Y.) 138, 66.5.
209
Department of Anaesthesiology Glostrup Hospital Nordre Ringvej 2600 Glostrup Denmark
Influence of Glucagon on Systolic Time Intervals During Induction of Anaesthesia with Barbiturate M. IRLER and M. DALSGAARD Department of Anaesthesiology, Glostrup Hospital, Copenhagen, Denmark
The systolic time intervals and calculated parameters of PEPiLVET (pre-injection period/left ventricular ejection time-ratio) and 1/PEP2 before and after induction of anaesthesia with the barbiturate enibomal (Narcodorma) were studied noriinvasively in eight surgical patients after pretreatment with a bolus dose of glucagon. The mean difference between the PEP/LVET-ratio before and after induction was 0.06, and the mean difference between l/PEP’ before and after induction was -8. The corresponding values in the control group consisting of 12 patients wcre 0.09 and - 22, respectively, suggesting a somewhat greater depression of cardiac function in this group. However, no statistically significant difference at the 5% level was found betweenchanges in the glucagon group and controls. The influencc of barbiturates and glucagon on cardiac function is discussed.
Received 10 January, accepted for publication 4 E’rbruary 1975
The induction of anaesthesia with rapidly increase of cardiac output due to glucagon acting barbiturates is usually followed by a in dogs anaesthetized with pentobarbital. The interaction between glucagon and reduction of cardiac output (Lr 1964), which manifests itself as a transient decrease barbiturates has not yet been investigated in in blood pressure during the period immedi- man. The intention of the present investigaately after administration of the drug. tion was to evaluate the possible protective The reduction o f cardiac output is caused by effect of glucagon on the myocardial function an inhibition of the sympathetic nervous during induction of anaesthesia with thc activity (SKOVSTED et al. 1970) affecting barbiturate enibomal (Narcodorm’). both the heart and the peripheral vessels. However, barbiturates also elicit a direct negative inotropic action on the myocardium MATERIAL (KLARNER1962), which can be antagonised by digitalis (HAACKE& ZWIETEN1970). Patients Reduction of myocardial function was also The study comprised eight patients, five women and shown clinically by IBLER& DALSGAARDthree men admitted to hospital for elective abdominal (1975) after induction of anaesthesia with and orthopaedic surgery. None of the patients had anamnestic or clinical symptoms of heart-disease. the barbiturate enibomal. No abnormalities were present in the ECG’s. Recently, the positive inotropic action of After fasting for 8-10 h before the induction of glucagon has attracted interest also among anaesthesia, the patients were premedicated with 50anaesthesiologists. KATZet al. (1969) demon- 7.5 mg pethidine and 0.5 mg atropine subcutaneously. strated an increase of myocardial contractility Anaesthesia after the administration o f glucagon in dogs Lead I1 of the ECG, the phonocardiogram and thc and cats anaesthetized by halothane, while carotid pulse wave were recorded simultaneously with GILES & BURCH (1971) demonstrated an the patients in a supine position on the operating table
GLUCAGON, BARBITURATE AND SYSTOLIC TIME INTERVALS
Table 1 PEPjLVET quotient and l/PEPZ in s-‘ barbiturate. Glucagon group.
Patient
Age
Sex
no.
I1
~F M F
M F
F M F Mean s.e. mean
before and after administration of
1
PEPILVE?’ Before
I
After
I
(b-a)
I
l/PEPZ Before
I
After
I
(b-a)
-t19
0.41 0.50 0.47 0.31 0.39 0.42 0.23 0.36
0.39 0.52 0.43 0.45 0.45 0.35 0.35 0.44
-0.03 +0.02 - 0.04 +0.14 4-0.06 - 0.07 1-0.12 0.08
83 61 64 123 111 64 181 82
102 65 89 87 85 106 100 69
1 4 t25 - 36 - 26 4-42 -81 - 13
0.39 0.03
0.42 0.02
0.06 0.03
96 14
87 5
-8 13
a = before; b = after.
PEPiLVET Patient no.
Age
1
45 48 29 40 30 33 53 37 43 49 42 53
2 3 4 5 6 7 8 9 10 11 12 Mean s.e. mean
Sex Before
F M F
hl F F
M F M F
M F
1
After
I
(b-a)
Before
I
l/PEPZ After
I
(b-a )
0.37 0.26 0.33 0.22 0.38 0.29 0.27 0.25 0.47 0.29 0.30 0.34
0.37 0.41 0.36 0.34 0.41 0.26 0.40 0.40 0.73 0.39 0.42 0.41
0.00 0.15 0.03 0.12 0.03 -0.03 0.13 0.15 0.26 0.10 0.12 0.07
120 152 113 187 102 192 173 192 60 120 149 92
118 104 115 113 118 260 96 96 50 73 108 62
-2 - 48 2 - 74 16 68 - 77 - 96 - 10 - 47 -41 - 30
0.31 0.02
0.41 0.03
0.09 0.02
137 12
109 15
-28 13
~~~
~~
a = before; b = aftcr.
207
208
M . IBLER AND M . DALSGAARD
mg/lO kg b.w. was administered slowly intravenously. 5-10 minutes later, a 5%-solution of enibomal (Naisopropyl-beta-bromallyl-N-methylbarbiturate)5 mg/ kg was given intravenously in the course of 3 0 4 0 s under spontaneous respiration with atmospheric air. 30-60 s after injection of the barbiturate, ECC: recordings were repeated, whereupon ventilation was started with N 2 0 and 0, and intubation was undertaken after a single dose of suxamethonium. Except for the administration of glucagon, the proredure in the control group, which comprised twelve clective abdominal and orthopaedic surgical patients without any cardiological or medical disorders was the same as mentioned above.
METHOD
group were 0.09 and -28, suggesting a somewhat greater depression of myocardial function in this group. Statistical analysis by means of Student's t-test showed significant changes of PEP/ LVET and 1/PEP2in both groups ( P < 0.01). However, no significant differencc at the 5% level was found between changes in the glucagon group and in the controls. KO remarkable difference in the blood prcssure decrease measured by the cuff method was observed between these two groups following induction of anaesthesia. A few patients experienced nausea for a duration of 1-2 min. This is a side effect of glucagon which can be prevcnted by prochlorperazine (LVOFF& WILCKEN 1972.
To evaluate an alteration in the contractility of the myocardium, a non-invasive method for measurement of the systolic time intervals: left ventricular ejection time (LVET), pre-ejection period (PEP) and their derivates PEP/LVET and 1/PEP2 was used (WEISSLER et al. 1969, REITANet al. 1972). Accordingly, the DISCUSSION application of negative inotropic agents should result in an increase of the pre-ejection periodileft ventricular The positive inotropic effect of glucagon is ejection time-ratio (PEP/LVET) and in a decrease of the result of a double mechanism of action I/PEPZ. I n our evaluations, we used a recorder, Multi- namely, beta-adrenergic stimulation and scriptor E K 26 (Hellige, Freiburg, West Germany) activation of the adenyl cyclase system. with a paper speed of 50 mm/s. The carotid pulse wave The first-mentioned mechanism which and heart sounds were recorded by means of a piezolasts 1 to 5 minutes can be inhibited by betaelectric amplified stethoscope and a microphone from blocking agents, while the second mechanism the same manufacturer. Each interval was calculated as a mean value of at least ten heart beats. The is not influenced by beta-blocking drugs and electromechanical time (EMT) was measured from the lasts about 20 minutes after a bolus dose of' beginning of the Q-wave in the electrocardiogram to glucagon 50 mg per kg body weight (LYDTIN the first deflection of the second heart sound. The left et al. 1971). As in the case of digitalis the ventricular ejection time (LVET) was measured from mechanism activating the adenyl cyclasc the beginning of the carotid pulse wave to the beginning system is followed by a rise of intracellular of the dicrotic elevation. The pre-ejection period (PEP) is calculated as the difference between E M T and calcium concentration in the myocardium. LVET. (NAYLER et al. 1970).
RESULTS Tables 1 and 2 show PEPiLVET and 1/PEP2 before and after induction of anaesthesia with barbiturate. I n the group of patients pretreated with glucagon, the mean difference between initial PEPiLVET and PEPiLVET measured after induction of anaesthesia was 0.06, whereas the mean difference between the initial l/PEP2 and 1/PEP2 after induction was - 8.
Reduced contractility of the myocardium and diminished calcium exchange after the administration of sodium hexobarbital has been demonstrated in vitro by HAACKE & ZWIETEN(1970), who also found that strophantin was capable of counterbalancing this hexobarbital clicited effect. However, the mechanism by which barbiturates influence the heart under clinical conditions is complicated by various factors, the most important of which is an inhibitory action on the sympathetic nervous system.
GLUCAGON, BARBITURATE AND SYSTOLIC 1 I M E INIERVALS
O u r results showed that a bolus dose of glucagon given 5 to 10 minutes before induction of anaesthesia was not able to protect the myocardium significantly from the inhibitory action of the barbiturate enibomal. As mentioned above, the beta stimulating action of glucagon is of short duration. I t is possible that the injection of a barbiturate within the interval of no more than 5 minutes after the administration of glucagon might lead to less myocardial depression than has been shown in the present study. If this is the case, some benefits of the administration of glucagon before the induction of anaesthesia might be expected under certain clinical conditions.
ACKNOWLEDGEMENT The authors are grateful to Nova Industry Ltd., Copenhagen, who provided glucagon and the apparatus used in this investigation.
ZUSAMMEIVFASSUNG Bei 8 chirurgischen Patienten wurden nach Vorbehandlung niit einer Bolus-Dosis von GIukagon die Systolen-Zeitintervalle und die berechneten Parameter PEPiLVET und l/PEP2 vor und nach Narkoseeinleitung mit dem Barbiturat Enibomal (Narcodorma) mittels einer nicht-invasiven Technik untersucht. Der mittlere Unterschied zwischen den PEP/LVETVerhaltnissen vor und nach Narkosecinleitung war 0,06, die mittlere Differenz zwischen den l/PEPZWerten vor und nach der Einleitung -8. Die korrespondierenden Werte in der Kontrollgruppe waren 0,09 bzw. - 28, was auf eine etwas starkere Depression der Herzfunktion in dieser Gruppe hinweist. Ein statistisch gesicherter Unterschied von p i 0,05 zwischen den Veranderungen in der Glukagongruppe und denen der Kontrollgruppe wurde allerdings nicht gefunden. Der EinfluB von Barbituraten und von Glukagon auf die Herzfunktion wird diskutiert.
HAACKE, H . & ZWIETEN,VAN 1'. A. (1970) Die gegensinnige Wirkung von Hexobarbital-Na und g-Strophantin auf die Konttraktionskraft und den Calciumstoffwechseldes Herzmuskels. Anaesthesirl19, 301. IBLER, M . & DALSGAARI), M. (1973) The effect of the short-acting barbiturate enibomal (Narcodorm@) on systolic time intcrvals. Acta nnaesth. scand. 19, 44. KArz, R. L., HINDS, I,. & MILLS,C . J. (1969) Ability of glucagon to produce cardiac stimulation without arrhythmias in halothane-anaesthetized animals. Brit. 3. Anaesth. 41, 574. KLARNER,P. (1962) The influence of barbiturates, thiobarbiturates, and barbituric acid on cellular potentials and contractility of thc guinea pig atria ~aunyn-Schnieidelberg'sarch. exp. Path. Pilannahol. 243, 269. LI, TSUNG-HAN (1964) Effectso f Anesthetics on the Circnlation. Charles C. Thomas, Springfield, Ill., p. 166. LVOPF, R . & WILCKEN, E. L. D. (1972) Glucagon in heart failure and in cardiogcnic shock. Experience in 50 patients. Circulation 45, 534. LYIITIN, H., LOHMOLLER, G., DANIEL, W., SCHIBRL, W., SCIIEWE, ST., KEMPEK, H . , LOIIMOLLER,R., WALTER,I., & Kusus, T. (1971) Kardiovasculire Wirkungen von Glucagon vor und nach Propranololgabe. Verh. dtsch. Ges. inn. Med. 77, 1000. NAYLER,W. G., MCINNES,I., CHIPPERFIELD, D., CARSON,V., & DAILE, P. (1970) The effect of glucagon on calcium exchangeability, coronary blood flow, myocardial function and high energy phosphate stores. 3. Pharmacol. ex/). Ther. 171, 265. REITAN,.J. A,, TY SMITH,N., SCOTTBORIsnN, V. Bi KADIS,L. B. (1972) The cardiac prc-ejection period: A correlate of peak ascending aortic blood-flow acceleration. Anesthesiology 36, 76. SKOVSTED, P., PRICE,M. L. & PRICE,H. L. (1970) The effects of short-acting barbiturates on arterial pressure, preganglionic sympathetic activity and barostatic reflexes. Anesthesiology 33, 10. WEISSIZR, A. M., HARRIS, E. S. & SCIIOENFELD, C. D. (1969) Bedside technics for the evaluation of ventricullar function in man. Anzer. 3. Curdiol. 23, 577.
Address : Mluden Ibler, M.D.
REFERENCES GILES,T . D. & BURGH,G. E. (1971) The influence of anesthesia on hemodynamic responses to glucagon in intact dog (35964). Proc. Soc. exfi. Biol. (N.Y.) 138, 66.5.
209
Department of Anaesthesiology Glostrup Hospital Nordre Ringvej 2600 Glostrup Denmark
