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J Spadaro

Publications and source records attributed to J Spadaro.

At least 37 records · Page 2Linked to original sources
PubMed1982

Effects of perfusion pressure on myocardial performance, metabolism, wall thickness, and compliance: comparison of the beating and fibrillating heart.

The effects of brief periods of graded reductions in perfusion pressure on normally beating and fibrillating hearts were examined. Mechanical and metabolic parameters were studied in the isolated, isovolumic (balloon in left ventricle), blood-perfused dog heart preparation. Experiments were carried out at perfusion pressures of 100, 75, 50, and 25 mm Hg, and comparisons of performance were made at the same ventricular volumes in the beating and fibrillating heart. A fall in perfusion pressure significantly decreased systolic performance in the beating heart. Diastolic pressure-volume relations were not altered by changes in perfusion pressure in the beating heart, but the fibrillating heart became significantly more compliant as perfusion pressure declined. Coronary blood flow and myocardial oxygen consumption were consistently higher during fibrillation than during sinus rhythm, and both parameters declined significantly at decreasing perfusion pressures. The fibrillating heart produced lactate at a perfusion pressure below 65 mm Hg, while the beating heart produced lactate at a perfusion pressure below 35 mm Hg. These studies demonstrate that brief periods of relatively modest decreases in perfusion pressure during ventricular fibrillation alter myocardial energy demand-supply relationships to result in ischemia of the fibrillating heart.

Animals↗
PubMed1981

Pericardial modulation of right and left ventricular diastolic interaction.

We studied the effects of the right ventricle (RV) and pericardium on left ventricular (LV) diastolic pressure-volume (P-V) relations in the normothermic isolated blood-perfused dog heart. Studies were performed at a constant heart rate (atrial pacing at 120 beats/min) with a coronary perfusion pressure of 100 mm Hg. LV volume was directly controlled by an intraventricular balloon, whereas RV filling pressure was increased stepwise from zero to 20 mm Hg. During progressive increases in RV filling pressure, with the pericardium intact, the LV diastolic P-V relations were shifted up and to the left; this leftward shift of the LV diastolic P-V relation was associated with an increase in the modulus of LV chamber stiffness. Closing the small pericardial incisions with sutures significantly increased this effect. In the absence of the pericardium, progressive filling of the RV resulted in minor changes in LV diastolic P-V relations. Only when the RV filling pressure was markedly elevated (20 mm Hg) was there a significant effect on LV diastolic pressure. The pericardium has a small but significant effect on LV diastolic P-V relations at physiological RV filling pressures, and this effect becomes considerable at high RV filling pressures. The RV influence on LV diastolic P-V relations is significantly modulated by the presence of tightness of the pericardium.

Animals↗
PubMed1980

Characterization of myocardial infarcts in the rat.

In 42 male Sprague-Dawley rats, the distribution of coronary arteries, the geometry of myocardial infarcts (MIs) and the involvement of the left ventricular papillary and trabecular muscles, after left coronary occlusion, were investigated. The septal branch was found to be responsible for the blood supply to the septum and, thus, occlusion of the left coronary artery, which spares the septal branch, results in an infarct that does not include the interventricular wall. Myocardial infarct size was measured by planimetry of histologic sections of serial slices of the left ventricle. There was no difference between the average percent of subepicardial (43% +/- 1%) and subendocardial (44% +/- 3%) infarction when the whole left ventricle was considered. Analysis of individual slices had shown that the infarcts comprised a greater percentage of left ventricular circumference at the apex than at the base in both layers of the myocardium. Toward the apex, more subendocardium was infarcted than subepicardium. The papillary and trabecular muscles are minimally involved in 75% of infarcts.

Animals↗
PubMed1980

Inversion of cardiac inotropism response to carotid arteries occlusion in dogs treated with propranolol.

The effect of beta-adrenergic blockade achieved by propranolol (0.5-1.0 mg/kg) on the inotropic alterations induced by adrenergic hyperactivity resulting from bilateral carotid occlusion (BCO) was analysed in 25 dogs anesthetized with morphine (2 mg/kg) and sodium pentobarbital (20 mg/kg). The heart rate was kept unchanged by means of a pace-maker. The first derivative of ventricular pressure (dp/dt) was considered as contractility index. Because BCO is followed by increase of left ventricle end-diastolic pressure (LVEDP) and of blood pressure (BP), to avoid the influence of these variables on dp/dt, we have reduced preload and afterload by means of hemorrhage (group A) and alpha-adrenergic blocker administration--phentolamine (group B). The carotid occlusion promoted similar variations in hemodynamic parameters in the two groups--there was a significant increase of blood pressure and LVEDP. BCO did not produce alteration in dp/dt values in both groups; when BP and LVEDP in group A were reduced, there was a significant reduction of dp/dt (2 927 +/- 139 to 2 066 +/- 95 mmHg/s; p less than 0.01). However there was no dp/dt alteration in group B (2 559 +/- 239 to 2 512 +/- 285 mmHg/s). These results suggest that during increase of sympathetic activity, anesthetized dogs under beta-adrenergic blockade show contractility depression. This could be related to secondary myocardic hypoxia and coronary vasoconstriction due to coronary alpha-adrenergic hyperactivity, once cardiac inotropism response can be alleviated by alpha-adrenergic blockers.

Animals↗
PubMed1979

Myocardial infarct size and ventricular function in rats.

To define the relationship between infarct size and ventricular performance, we performed hemodynamic studies in rats 21 days after left coronary artery occlusion. Ventricular performance was assessed under ether anesthesia by measurements of baseline hemodynamics and stressed performance as determined by the peak cardiac output and stroke volume obtained during intravenous volume loading and by the peak left ventricular developed pressure obtained during occlusion of the ascending aorta. Infarct size was determined by planimetry of the endocardial circumference of each of four histological slices of the left ventricle. Rats with small (4-30%) myocardial infarctions had no discernible impairment in either baseline hemodynamics or peak indices of pumping and pressure-generating ability when compared to the sham-operated, noninfarcted rats. Rats with moderate (31-46%) infarctions had normal baseline hemodynamics but reduced peak flow indices and developed pressure. Rats with infarctions greater than 46% had congestive heart failure, with elevated filling pressures, reduced cardiac output, and a minimal capacity to respond to pre- and after load stresses. The entire spectrum of postinfarction ventricular function was observed, from no detectable impairment to congestive failure. In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium.

Animals↗
PubMed1976

Evaluation of V max TP as an index of myocardial contractility during afterload and preload elevations.

In order to test if the maximal velocity of shortening (V max TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V max TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V max TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.

Angiotensin II↗