Maximal Rate of the Left Ventricular Pressure Fall (Peak Negative dP/dt) in Early Stage of Myocardial Ischemia Following Experimental Coronary Occlusion

We determined the effects of vagal stimulation on the time constant (tau) of left ventricular isovolumic pressure decay and on the maximum rates of left ventricular pressure change (dP/dt) during contraction and relaxation in anesthetized dogs. In each dog, the atria were paced at a constant rate of 150 beats/min. We recorded left ventricular pressure waveforms in the absence (control) and in the presence of vagal stimulation at frequencies of 1, 2, and 3 Hz. During the control periods and during vagal stimulation at each frequency, we determined tau, the maximal rate of contraction, and the maximal rate of relaxation from left ventricular pressure waveforms recorded at medium (100 mmHg), high (130 mmHg), and low (73 mmHg) afterloads. Vagal stimulation at a frequency of 3 Hz increased tau by 23%. This effect of vagal stimulation on tau was most pronounced at the high afterload. Vagal stimulation at 3 Hz decreased the maximal rate of relaxation by 19%, but it decreased the maximal rate of contraction by only 8%. Thus vagal stimulation significantly decreased the rate of left ventricular relaxation and had a greater depressant effect on ventricular relaxation than on contraction.

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Effects of a coronary alpha 1-constriction on transmural left ventricular flow and contractile function

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.4.h965 ◽

1992 ◽

Vol 262 (4) ◽

pp. H965-H972 ◽

Cited By ~ 4

Author(s):

P. A. Gwirtz ◽

J. M. Dodd-O ◽

H. F. Downey ◽

H. J. Mass ◽

B. A. Barron ◽

...

Keyword(s):

Contractile Function ◽

Stellate Ganglion ◽

Systolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Maximal Rate ◽

Circumflex Artery ◽

Ventricular Systolic Pressure ◽

Adrenergic Antagonist

Modulation of myocardial contractile function and perfusion by alpha 1-adrenergic receptors were examined in anesthetized dogs during left stellate ganglion stimulation. In 11 dogs, stellate stimulation significantly increased heart rate, mean arterial pressure, left ventricular systolic pressure, maximal rate of left ventricular pressure generation, segmental shortening and rate of shortening in anterior and posterior ventricular regions, and myocardial oxygen extraction. Myocardial lactate extraction decreased. The selective alpha 1-adrenergic antagonist prazosin (0.5 mg) injected into the circumflex artery during stellate stimulation caused significant additional increases in maximal rate of left ventricular pressure generation by 19 +/- 5% and in rate of shortening in posterior subendocardium by 20 +/- 6%. No changes were observed in posterior subepicardial or anterior subendocardial segmental contractile function. Myocardial oxygen and lactate extractions returned to their control values following prazosin injection. Regional left ventricular perfusion was measured using tracer microspheres in five additional dogs. Stellate stimulation increased subepicardial and subendocardial perfusion by 30%. Prazosin increased both subepicardial and subendocardial perfusion by an additional 36%. Stellate stimulation increased norepinephrine concentration in the coronary sinus, but no further increase was noted after blockage of alpha 1-receptors by prazosin. Thus, during sympathetic stimulation, an alpha 1-vasoconstriction existed uniformly across the left ventricular wall. However, blockade of this vasoconstriction was associated with an increase in contractile function only in the deeper muscle layers.

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Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

Circulation ◽

10.1161/01.cir.48.4.775 ◽

1973 ◽

Vol 48 (4) ◽

pp. 775-785 ◽

Cited By ~ 42

Author(s):

JOHN L. McCANS ◽

JOHN O. PARKER

Keyword(s):

Myocardial Ischemia ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure

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Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.205.1.30 ◽

1963 ◽

Vol 205 (1) ◽

pp. 30-36 ◽

Cited By ~ 252

Author(s):

Andrew G. Wallace ◽

N. Sheldon Skinner ◽

Jere H. Mitchell

Keyword(s):

Heart Rate ◽

Diastolic Pressure ◽

Complex Function ◽

Left Ventricular Pressure ◽

Aortic Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Maximal Rate ◽

Pressure Development ◽

Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

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