Cardiovascular Effects of Glucagon in Man

Parmley, William W.; Glick, Gerald; Sonnenblick, Edmund H.

doi:10.1056/nejm196807042790103

Cited by 232 publications

(74 citation statements)

References 9 publications

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“…The lungs were clear to auscultation, and chest X-ray revealed no definite evidence of congestion. Group lb (patients [15][16][17][18][19][20][21][22][23][24][25][26] presented with clinical evidence of heart failure manifested by persistent rales usually accompanied by X-ray evidence of pulmonary venous engorgement or interstitial edema. Several of these latter patients had no pulmonary symptoms, but most were aware of mild to moderate shortness of breath.…”

Section: Resultsmentioning

confidence: 99%

“…The need for improved management of cardiac and circulatory failure after myocardial infarction has led to the introduction of new drugs (14,15), mechanical cardiac assist devices (16), and aggressive surgical procedures (17) for the emergency treatment of myocardial infarction. The availability of these techniques has increased the requirement for an understanding of the functional disturbance associated with acute myocardial infarction and of means for detecting early signs of impending pump failure (18).…”

Section: Introductionmentioning

confidence: 99%

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Left ventricular function in acute myocardial infarction

Hamosh¹,

Cohn

1971

J. Clin. Invest.

125

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A B S T R A C T Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m'), stroke volume (38.3 ml/m'), and stroke work (49.2 g-m/m') were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m'), but stroke volume (31.6 ml/m') and stroke work (37.3 g-m/m') were reduced.In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/ m'), stroke volume (16.5 ml/m'), and stroke work (11.1 g-m/m') were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure.These data show the following: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some indiThis work was presented in part at the meeting of The

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Left ventricular function in acute myocardial infarction

Hamosh¹,

Cohn

1971

J. Clin. Invest.

125

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“…Mean changes were tion were comparable with respect to body weight and compiled for all eight animals receiving glucagon, since left ventricular weight per kilogram body weight. Heart the changes in the two receiving 20 .sg/kg were not difrate and systemic blood flow, i.e. cardiac output, were ferent from those in the six given 40 meg/kg.…”

Section: Methodsmentioning

confidence: 69%

“…Digitalis preparations have occasionally been found to aggravate cardiac failure in patients with myocardial infarction (4,6) or hypertensive cardiovascular disease (5), presumably because of their vasopressor effect and perhaps particularly because this effect may preceed the inotropic effect (6,9,11,17). Although the vasopressor response to the glycosides may be attenuated or reversed in the presence of cardiac failure, at least in some circumstances, (10,12,13 (20)(21)(22)(23)(24)(25), perhaps because of failure to stimulate the enzyme, adenyl cyclase, in the presence of cardiac failure (26), reports of its use in acute myocardial infarction are generally more optomistic (27)(28)(29)(30). In view of these points, the effects observed with glucagon suggest that it and other agents with similar hemodynamic effects, such as isoproterenol, could be useful in the emergency management of acute severe aortic regurgitation.…”

Section: Discussionmentioning

confidence: 99%

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Digitalis-Induced Increase in Aortic Regurgitation and the Contrasting Effects of Glucagon in the Sedated Dog

Hopkins¹,

Taylor²

1974

J. Clin. Invest.

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A B S T R A C T The hemodynamic and phasic ascending aortic flow changes induced by acetylstrophanthidin and glucagon were studied in closed-chest sedated dogs with aortic regurgitation. While the positive inotropic effect of both agents was reflected in an increase in peak rate of rise of left ventricular pressure, acetylstrophanthidin increased aortic regurgitation, while glucagon decreased it. With the former, left ventricular end-diastolic pressure rose from 20±6 to 27+6 mm Hg (P < 0.005), but fell from 18+4 to 11±3 mm Hg (P < 0.001) with glucagon. Acetylstrophanthidin increased systemic vascular resistance, aortic diastolic pressure, and diastolic regurgitant flow rate, and, heart rate and the duration of regurgitation per beat and per minute being unchanged, regurgitant flow per beat increased 32±15% (P <0.001). Glucagon decreased regurgitant flow per beat 27±14% (P < 0.001) because of abbreviation of diastole associated with tachycardia, and because of reduction in regurgitant flow rate. Despite tachycardia, the duration of regurgitation per minute was unchanged, and the small fall in regurgitant blood flow per minute was not significant, but this pertained in the face of 47% increase in effective cardiac output (P < 0.001). In contrast, acetylstrophanthidin increased regurgitant flow per minute 28±14% (P < 0.001) without change in effective cardiac output. The increase in cardiac contractility, tachycardia, and systemic vasodilatation induced by glucagon preferentially enhanced forward blood flow, which led to reduction in left ventricular volume overload, while it increased cardiac output. Contrarily, acetylstrophanthidin increased aortic regurgitation and, despite its inotropic effect, increased left ventricular volume overload without an increase in cardiac output.

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