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Biomedical subjects

M Condorelli

Publications and source records attributed to M Condorelli.

At least 127 records · Page 7Linked to original sources
PubMed1984

Effect of acebutolol on left ventricular hemodynamics and anatomy in systemic hypertension.

In 18 patients with mild or moderate essential hypertension who responded favorably to acebutolol antihypertensive therapy, echocardiography (echo) was performed in the basal condition and after 6 and 12 months of follow-up. Acebutolol induced a significant decrease in blood pressure (BP), from a basal value of 167 +/- 3/105 +/- 2 mm Hg to 138 +/- 5/90 +/- 2 mm Hg after 6 months (p less than 0.01) and to 134 +/- 3/91 +/- 3 mm Hg after 1 year (p less than 0.01), and in heart rate, from 75 +/- 3 to 63 +/- 2 beats/min after 6 months (p less than 0.01) and to 63 +/- 2 beats/min after 1 year (p less than 0.01). The decrease in BP was achieved through a decrease in cardiac output from 6.3 +/- 0.28 to 5.3 +/- 0.25 liters/min after 6 months (p less than 0.05) and to 5.32 +/- 0.2 liters/min after 1 year (p less than 0.05), which resulted from a reduction in heart rate; stroke volume did not show significant change during the treatment and left ventricular (LV) performance was improved. There was a parallel decrease in LV posterior wall and ventricular septal thicknesses and estimated LV mass. In patients with LV hypertrophy, the change in mass was significantly correlated with the change in heart rate both after 6 and 12 months of therapy (r = 0.6234, p less than 0.05 and r = 0.7121, p less than 0.05 after 6 and 12 months, respectively).

Acebutolol↗
PubMed1984

Evaluation of noninvasive tests for identifying patients with preexcitation syndrome at risk of rapid ventricular response.

Intermittent preexcitation, block in the accessory pathway after intravenous injection of ajmaline or procainamide, and block in the accessory pathway during exercise usually exclude a short antegrade refractory period of an accessory pathway in patients with the Wolff-Parkinson-White syndrome. This report describes three patients with these findings suggestive of a relatively long antegrade effective refractory period of the accessory pathway in whom life-threatening ventricular response occurred during atrial fibrillation. In the first patient with a pattern of intermittent preexcitation, rapid ventricular response with wide QRS was present during atrial fibrillation. In the second patient in whom preexcitation disappeared after intravenous injection of ajmaline or procainamide as well as during exercise testing, atrial pacing showed 1:1 conduction over the accessory pathway at a cycle length of 220 msec and the shortest R-R interval during induced atrial fibrillation was 190 msec. The third patient, with no evidence of preexcitation during sinus rhythm, presented antidromic reciprocating tachycardia and atrial fibrillation with life-threatening ventricular response, the minimal R-R interval being 220 msec. Noninvasive tests in the preexcitation syndrome lack sufficient prognostic sensitivity. The evaluation of ventricular response during induced atrial fibrillation represents the most reliable means of identifying such patients at risk.

Adult↗
PubMed1984

Adrenergic activity as a modulating factor in the genesis of myocardial hypertrophy in the rat.

Sprague Dawley male rats (200-220 g) were subjected to a long-term treatment with low doses of catecholamines in an attempt to assess the effect of the adrenergic stimulation on ventricular weights, hemodynamics, and hydroxyproline content in the myocardium. Data are presented indicating that both exogenous catecholamines (i.e., isoproterenol) and endogenous catecholamines (released from tyramine) are able to bring about a degree of myocardial hypertrophy associated with a significant increase in the ventricular concentrations of hydroxyproline, without affecting hemodynamic parameters (blood pressures and heart rate). Thus the modulation of sympathetic tone in the genesis of cardiac hypertrophy is demonstrated, and a direct effect of the catecholamines on cardiac cells is postulated which is independent of hemodynamic changes.

Animals↗
PubMed1984

Sick sinus syndrome: the role of hypervagotonia.

A 58-year-old man with persistent symptomatic sinus bradycardia (52 beats/min) showed a markedly prolonged postpacing pause (3240 msec) after atrial pacing at a cycle of 840 msec. In addition, Wenckebach block occurred following atrial pacing at a cycle length of 700 msec. After atropine (2 mg) postpacing pauses returned to normal value and type 1 second-degree AV block completely reversed to 1:1 AV conduction until paced rates greater than 140/min. It may be that in some patients marked and persistent vagal overactivity may predispose to "intrinsic" sinus node dysfunction; in later stages, sinus node function may paradoxically result unaffected by changes in autonomic tone.

Heart Block↗
PubMed1984

Long-term protection of ischaemic myocardium by nitroglycerin ointment.

To assess whether the reduction in ischaemic injury during acute myocardial infarction induced by nitroglycerin (NTG) results in a decrease in tissue necrosis, 96 rats were assigned to two groups. The first group (n = 34) was sham-operated. The second group of 62 rats was randomised in a ratio of 2:1 into control (n = 43) and treated (n = 19) subgroups following coronary artery occlusion. Treated animals received an application of 2% NTG ointment every 8 h immediately post-occlusion. All rats were killed 48 h after coronary artery occlusion and total creatine kinase activity (CK) of the left ventricle (LV) was measured. Infarct size calculated by CK depletion was 65.2 +/- 14.3% (mean +/- SD) of LV in control rats, and 51.6 +/- 14.0% of LV in NTG-treated (p less than 0.02). In a further series of 46 rats with coronary occlusion, the area of infarcted myocardium 21 days post-occlusion was assessed by planimetry on histological sections. In rats with control occlusion (n = 22), the extent of infarction was 30.6 +/- 4.8% of LV, and in NTG-treated rats (n = 24) it was 16.2 +/- 5.8% of LV (p less than 0.001). The amount of scar tissue in the infarcted myocardium 21 days post-occlusion was also determined by measuring LV hydroxyproline and collagen content in an additional 32 rats randomly assigned to a control (n = 11), a NTG-treated (n = 9) and a sham-operated group (n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Nonparoxysmal atrioventricular junctional rhythm. A clinical and electrophysiologic study.

The patient, a 74-year-old man, developed a persistent nonparoxysmal junctional accelerated rhythm at rate of 60-75 beats min-1 because of chronic depressed sinus node function. Intravenous atropine resulted in no change of junctional pacemaker rate but i.v. isoproterenol significantly accelerated it suggesting that autonomic neural imbalance might underlie the mechanism of nonparoxysmal junctional rhythm. Intravenous verapamil (10 mg) induced no change in the junctional pacemaker rate and postpacing pauses suggesting that the slow inward current did not play an important role in the nonparoxysmal junctional rhythm.

Aged↗
PubMed1984

Ouabain-induced reflex coronary vasodilatation mediated by cardiac receptors.

Experiments were performed to determine the effects of digitalis-induced stimulation of cardiac receptors on the coronary circulation. In chloralose-anesthetized dogs, left circumflex coronary artery was perfused at constant flow, and heart rate was maintained constant by electric pacing. Ouabain injection in the perfused coronary artery produced a significant decrease in coronary perfusion pressure. Epicardial application of lidocaine completely blocked the reflex response. Vagotomy also prevented this reflex response. Sympathetic blockade with intravenous guanethidine or intracoronary phentolamine partially reduced the reflex coronary vasodilatation. Intracoronary atropine also partially reduced the coronary vasodilator response to ouabain. The combined administration of guanethidine and atropine completely abolished the coronary reflex response. These data demonstrate that ouabain can evoke reflex coronary vasodilation by stimulating cardiac receptors. This reflex response is mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.

Animals↗
PubMed1984

Relationships between left ventricular mass and clinical, biohumoral and hemodynamic parameters in human hypertension.

The relationships between left ventricular mass (LVM), assessed by echocardiography, and several biohumoral and hemodynamic parameters were studied in 63 mild or moderate hypertensive patients and in an age-matched group of 23 normotensive subjects. In hypertensive patients, but not in normotensives, LVM index was significantly correlated with beta-adrenoceptor responsiveness, as evaluated by the chronotropic response to isoproterenol ( CD25 ) (r = 0.525, p less than 0.001) and with the 24-hour catecholamine urinary output (r = 0.485, p less than 0.001). Both CD25 and the catecholamine urinary output were significantly higher in the hypertensives as compared with the normotensive subjects. Moreover, left ventricular wall thickness (septum + posterior wall) was significantly correlated with CD25 and urinary catecholamines only in hypertensive patients. No significant correlation was found between LVM or wall thickness and body surface area, age, blood pressure, heart rate, cardiac output, total peripheral resistance and left ventricular systolic wall stress, whereas CD25 was correlated with urinary catecholamines only in hypertensive patients (r = 0.606, p less than 0.001). These results seem to support the hypothesis that an elevated adrenergic tone may exert a permissive role in the development of left ventricular hypertrophy in human hypertension.

Adolescent↗
PubMed1984

Inhibition of IgE-mediated histamine release from human basophils and mast cells by fenoterol.

Fenoterol, a beta 2-adrenergic agonist recently introduced to treat asthmatic disorders, inhibits antigen-induced histamine release from human basophil leukocytes and lung mast cells in a dose-dependent fashion. The dose-response inhibition curve is paralleled by a fenoterol-induced increase in the cAMP levels of human leukocyte preparations. The relationship between the effect of fenoterol and cAMP level is supported by the finding that the beta 2-adrenergic agonist only inhibits the first stage of antigen-induced histamine release and not the release caused by the Ca2+ ionophore, A23187. Propranolol, a competitive antagonist of beta 2-adrenergic receptor, blocks the inhibition of release and the cAMP accumulation caused by fenoterol. Finally, theophylline, a cAMP phosphodiesterase inhibitor, synergistically potentiates the inhibitory effect of fenoterol on histamine release and the accumulation of cAMP. These data suggest that fenoterol may modulate the in vivo release of the mediators of immediate hypersensitivity reactions via the activation of beta 2-adrenergic receptor linked to adenylate cyclase on human basophils and mast cells.

Adolescent↗