The Effect of Glucagon Infusion on Cardiovascular Function in the Critically Ill

Jh, Siegel; Levine, Micah; McConn, Rita; Guercio, Louis R. M. Del

doi:10.1097/00132586-197112000-00008

Cited by 4 publications

(4 citation statements)

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“…Kinin activation may sustain both the vascular changes and the impairment in 02 extraction. The infusion of bradikinin into an isolated perfused limb produced a reduction in vascular tone as well as a lowering in O2 consumption [29].…”

Section: Discussionmentioning

confidence: 97%

Hemodynamic and metabolic impairment in acute pancreatitis

et al. 1981

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Twenty-one patients with acute pancreatitis underwent evaluation of cardiovascular function and oxygen consumption; 5 of those who were critically ill had a further study of hormonal metabolism. The evaluation of hemodynamic parameters was made using a computer-based cardiovascular program developed by Siegel et ai. During the initial phase of the disease a reduction in vascular tone (relating cardiac index with total peripheral resistance) represented the basic abnormality seen in all patients, while a depression in ventricular function (relating left ventricular stroke work with central venous pressure) was observed in more than 40% of patients. With the progression of pancreatitis, cardiovascular monitoring identified a time, 5 days after admission, in which a clear deterioration of the hemodynamic parameters occurred. Beyond 5 days, all patients developed a hyperdynamic state with mild to severe deficiency of oxygen extraction. In the most seriously ill patients, oxygen consumption fell and peripheral shunting increased in a similar manner to that observed in septic and cirrhotic patients. At this time a Survival Index permitted recognition of those patients at high risk of rapid deterioration who might benefit from emergency surgical therapy. In 5 patients who developed a hyperdynamic unbalanced state, a marked reduction in oxygen consumption was associated with significantly increased serum levels of insulin, glucagon, aromatic amino acids, octopamine, and phenylethanolamine. While false neurotransmitters may be invoked in explanation of peripheral vascular abnormalities, the cause of impairment in oxygen extraction remains unclear.

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Section: Discussionmentioning

confidence: 97%

Hemodynamic and metabolic impairment in acute pancreatitis

et al. 1981

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“…Large doses of exogenous glucagon exert positive inotropic and chronotropic effects on the heart. [18][19][20][21] In humans, glucagon's inotropic effects are more pronounced than its chronotropic effects, an advantage that minimizes myocardial oxygen consumption and irritability. 18,20 Glucagon increases the movement of calcium ions into myocardial cells 22 and increases intracellular cyclic adenosine monophosphate (cAMP) levels.…”

Section: Glucagonmentioning

confidence: 99%

“…25 Glucagon's cardiotonic effects are additive to that of beta-adrenergic agonists such as dopamine, epinephrine, and isoproterenol. 21,23 Glucagon has been used effectively in the treatment of heart failure and cardiogenic shock 20,[26][27][28] (Table 5). Its major advantages include its synergism with beta-adrenergic agonists and its low dysrhythmogenic properties.…”

Section: Glucagonmentioning

confidence: 99%

The Use of Hormones as Therapeutic Agents

Zaloga¹,

Chernow²

1985

Semin Respir Crit Care Med

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“…The polypeptide hormone, glucagon, has been reported to possess a marked positive inotropic effect on isolated cardiac muscle (Farah and Tuttle, 1960;Glick et al, 1968;Lucchesi, 1968), in intact animals (Glick et al, 1968;Lucchesi, 1968) and in patients with impaired cardiac function (Brogan et al, 1969;Vaughn et al, 1970;Wilcken and Lvoff, 1970;Siegel et al, 1970;Lvoff and Wilcken, 1972). There is some uncertainty, however, concerning the effectiveness of glucagon in the management of patients with chronic cardiac decom-pensation (Williams et al, 1969;Greenberg et al, 1970;Smithen et al, 1972).…”

Section: Introductionmentioning

confidence: 99%

The positive inotropic effect of glucagon in the chronically failed right ventricle as demonstrated in the isolated cat heart

Winokur

Nobel-Allen

Lucchesi

1975

European Journal of Pharmacology

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Previous in vitro studies had provided evidence to show that papillary muscles obtained from cats with chronic right ventricular failure had lost their ability to develop a positive inotropic response to glucagon. Since it is difficult to extrapolate from the isolated papillary muscle to the intact heart, studies were done to assess the effects of glucagon in the perfused isovolumically beating heart obtained from cats four months after surgical banding of the pulmonary artery for the experimental production of chronic right ventricular failure (CRVF). At the peak of the dose-response curve, glucagon increased right ventricular isovolumic pressure 25% (39.00 +/- 4.37 to 49.67 +/- 5.15 mm Hg; p less than 0.001) and right ventricular dP/dt 63% (522.2 +/- 93.9 to 852.6 +/- 159.9 mm Hg/sec; p less than 0.001) in 6 normal hearts. Similar dose related increases in right ventricular isovolumic pressure and dP/dt were obtained in 6 hearts taken from cats with chronic right ventricular failure. The respective increases in right ventricular isovolumic pressure and dP/dt were 43% (30.33 +/- 4.01 to 43.67 +/- 6.25 mm Hg; p less than 0.025) and 73% (317.50 +/- 30.29 to 550.83 +/- 89.04 mm Hg/sec; p less than 0.025). These results provide evidence that glucagon possesses the capacity to augment myocardial contractility in the heart with experimentally induced chronic right ventricular failure.

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The Effect of Glucagon Infusion on Cardiovascular Function in the Critically Ill

Cited by 4 publications

References 0 publications

Hemodynamic and metabolic impairment in acute pancreatitis

Hemodynamic and metabolic impairment in acute pancreatitis

The Use of Hormones as Therapeutic Agents

The positive inotropic effect of glucagon in the chronically failed right ventricle as demonstrated in the isolated cat heart

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