Inotropic Index Research Articles

Alterations in alpha 1-adrenoceptor stimulation of isolated atria from experimental diabetic rats.

This purpose of this investigation was to determine the influence of experimental diabetes (3 months) on the responsiveness of rat isolated atria to alpha 1-adrenoceptor stimulation by phenylephrine. Diabetes was chemically induced with streptozotocin (65 mg/kg i.v.) in 42- to 43-day-old, nonfasted male Sprague-Dawley derived rats. Chronotropic (right atria) and inotropic (left atria) indices were recorded in response to alpha 1-adrenoceptor stimulation by phenylephrine. These experiments were performed in the presence of beta-adrenoceptor antagonism (timolol). Isolated right atria from diabetic rats demonstrated a greater increase in heart rate in response to phenylephrine than did corresponding control atria. Left atria were supersensitive (decrease in EC50 values) and hyperresponsive to alpha 1-adrenoceptor stimulation by phenylephrine when compared with stimulation of control left atria. Diabetic left atria in response to phenylephrine were observed to exchange more radioactive calcium (45Ca2+) than control left atria, whereas both diabetic and control left atria exchanged the same amount of 45Ca2+ during basal contractile conditions. Phenylephrine had no effect on 45Ca2+ efflux from either diabetic or control atria. These results indicate that 3 months of uncontrolled experimental diabetes in the rat produces an enhancement of alpha 1-adrenoceptor activation of isolated atria, and that there is an alteration in Ca2+ mobilization which may contribute to the enhanced receptor activation.

Preload dependence of dP/dt max, VCE max and calculated V max compared to the inotropic sensitivity of these indices of cardiac contractility.

In five canine heart-lung preparations the preload dependence of dP/dt max, V max, VCE max and (dP/dt:P-EDP + C) max was related to the inotropic sensitivity of these indices. V max and (dP/dt:P-EDP + C) max are less affected by preload changes than dP/dt max and therefore should be more suitable for inotropic measurements. But even if the preload changes caused by inotropic interventions are not taken into account, V max shows the same inotropic sensitivity as dP/dt max when the contractile state is reduced and an even lower sensitivity when the contractile state is enhanced. The sensitivity of (dP/dt:P-EDP + C) max, however, is much lower over the whole range of tested inotropic states. If enddiastolic pressure is kept constant during inotropic interventions, dP/dt max is a much more sensitive inotropic index than V max. VCE max usually shows a negative correlation to the diastolic filling of the heart. In the improved inotropic state this correlation can become positive, thus making it impossible to evaluate the influence of the preload dependence on the result. None of the tested parameters shows a higher inotropic sensitivity than dP/dt max, though the preload dependence of dP/dt max is more evident. Therefore, none of these more complicated parameters has any advantage over the simple measure dP/dt max for evaluation of acute changes in contractility.

Regulation of cardiac performance in clinical heart disease: Interactions between contractile state mechanical abnormalities and ventricular compensatory mechanisms

Cardiac function in clinical heart disease is governed by ventricular (1) preload, (2) contractility, (3) afterload, (4) heart rate, and (5) dyssynergy. The major types of pathophysiologic abnormalities include inotropic disturbances, systolic mechanical pressure and volume overloads and diastolic mechanical ventricular underloading. In contractility and systolic mechanical disorders, the cardiac compensatory mechanisms of (1) Frank-Starling principle, (2) ventricular hypertrophy, and (3) sympathetic nervous system furnish substantial but limited protective reserve for maintaining cardiac output. Assessment of cardiac performance by pump (hemodynamics) and muscle (isovolumic and ejection mechanics) characteristics, including measurements of inotropic indexes of contractile force and velocity properties, provides quantitative analysis of ventricular function determinants and compensatory system interactions in heart disease. Congestive heart failure is compensated when resting cardiac output is maintained at normal levels by the adaptive reserves with their deleterious early effects: dyspnea (preload rise), angina pectoris (increased mass) and tachycardia (adrenergic activity). Decompensated congestive heart failure is the inability of the heart to deliver normal basal cardiac output with attendant late symptoms of fatigue at rest and body organ failure despite maximal use of protective reserves. The compensatory responses utilized and the critical level of depressed contractility causing decompensation are dependent on the specific pathophysiologic condition. Thus, the fundamental variable in congestive heart failure is inotropic integrity of which its abnormal degree determines decompensation in chronic heart disease. Compensation can be sustained by reserve mechanisms at a lower inotropic state in cardiomyopathy than in systolic mechanical disorders in which volume overload can be compensated for at a more depressed level of contractility than pressure overload. The standard classification of clinical function in congestive heart failure is based more on early symptoms consequent to secondary adjustments (compensatory mechanisms) than on disturbances of the primary factors of decompensation: cardiac output (crucial hemodynamic variable) and contractility (the fundamental determinant).

Pa CO2 and the pre-ejection period: the pa CO2 inotropy response curve.

The squared reciprocal of the pre-ejection period (1/PEP2) is an inotropic index which may be measured without catheterization of the left ventricle. Changes in 1/PEP2 in response to changes in arterial carbon dioxide tension have been studied. The character of the Paco2/myocardial inotropy response