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M Condorelli

Publications and source records attributed to M Condorelli.

At least 235 records · Page 13Linked to original sources
PubMed1982

Effects of combined alpha- and beta-blockade by labetalol in patients with coronary artery disease.

1 The effect of labetalol 100 mg orally twice daily on exercise tolerance has been compared with placebo in 19 normotensive subjects with angiographic evidence of coronary artery disease. 2 Labetalol, at the same work load as during placebo exercise, significantly reduced systolic and diastolic blood pressures, as well as heart rate and rate-pressure product. 3 Similarly, ST segment depression was reduced by labetalol from 2.0 +/- 0.4 to 1.36 +/- 0.6 mm (P less than 0.001), thus enabling an increase in exercise tolerance from a control value of 83.7 +/- 18 to 95.3 +/- 19 W (P less than 0.005). 4 In seven other patients, also with coronary artery disease, the haemodynamic effects of a single 0.6 mg/kg intravenous dose of the drug was evaluated during exercise. 5 Compared with conditions during control exercise, labetalol induced a significant reduction in rate-pressure product from 17228 +/- 2375 to 13445 +/- 2404 mmHg/min (P less than 0.005) and in peripheral vascular resistance from 612.0 +/- 61.2 to 512.7 +/- 36.2 dyn cm-5 m-2 (P less than 0.0025). These events were not accompanied by any change in cardiac index and in dP/dT left ventricular end-diastolic pressure (LVEDP) ratio. 6 These data suggest that labetalol may induce reduction in myocardial oxygen consumption, thereby increasing exercise tolerance in patients with coronary artery disease, without impairment of left ventricular performance.

Adult↗
PubMed1982

Renal function in borderline hypertensive first-degree relatives of essential hypertensives. Effects of sodium load.

Renal function in the basal state and after sodium load has been investigated in 21 borderline, hypertensive, first-degree relatives of established hypertensives and in 21 age- and sex-matched, normal subjects with no family history of hypertension. During intravenous infusion of inulin and p-aminohippurate in saline, both groups showed a decrease in plasma aldosterone levels (p less than 0.05) but renal plasma flow (595 +/- 48 vs. 750 +/- 59 ml/min, p less than 0.05), diuresis (1.4 +/- 0.2 vs. 2.2 +/- 0.5 ml/min, p less than 0.05), natriuresis (0.21 +/- 0.02 vs. 0.3 +/- 0.02 mEq/min, p less than 0.05) and sodium clearance (1.05 +/- 0.1 vs. 2.4 +/- 0.4 ml/min, p less than 0.05) in borderline hypertensives were higher than in the control group. After the salt load (NaCl, 1.35% i.v., 5 ml/min for 2 h) there was an increase in blood pressure and a decrease in plasma aldosterone and potassium levels in both groups. However, borderline hypertensives showed higher diuresis, natriuresis, sodium clearance and also kaliuresis compared to normotensives. These results suggest that borderline hypertensives already present the changes in renal function which are characteristics of established hypertensives.

Adolescent↗
PubMed1982

Further observations on the electrophysiologic effects of oral amiodarone therapy.

A case is presented of a reversible intra-Hisian block occurring under amiodarone treatment for atrial tachycardia in a patient without clear intraventricular conduction abnormalities. His bundle recordings showed an atrial tachycardia with intermittent exit block and greatly prolonged BH and HV intervals (40 and 100 msec, respectively). Thirty days after amiodarone discontinuation, His bundle electrograms showed atrial flutter without intra-Hisian or infra-Hisian delay. Amiodarone should be used with caution during long-term oral therapy in patients with or without clear intraventricular conduction defects.

Adult↗
PubMed1982

Quantitative assessment of infarct size in isoproterenol-infarcted rats.

The authors performed a number of experiments aiming at quantifying the infarct size in Sprague-Dawley male rats. The experimental model employed was isoproterenol (ISP) induced, infarctlike myocardial lesions. In quantifying the extent of the infarct area they compared the cross reliability of enzymatic and histological methods. ISP was administered in two subcutaneous injections (50 mg/100 Gm body weight) at a 24 hour interval. At the peak of the necrotic process (48 hrs after the first injection), the heart was subjected to enzymatic or histological studies. Thus, a group of infarcted animals (n = 25) and their controls (n = 15) underwent the assessment of creatine kinase (CK) content in the homogenate of the myocardium. Another group of animals (n = 15) was used for histological observations, including measurement of infarct size by planimetry from histological sections. A good relationship was observed between the percentage of necrotic tissue calculated on the basis of CK values (69.11 +/- 2.39%) and the infarction area assessed by planimetry (72.37 +/- 2.69%) (mean +/- standard error of the mean [SEM]). Thus, the present study confirms that ISP-induced myocardial lesions are a simple and reliable model for experimental infarct. Moreover, the assessment of the CK content in the heart is correlated with histological studies by planimetry, and is suggested as a direct enzymatic method to quantify the extent of myocardial necrosis.

Animals↗
PubMed1982

Activation of human basophils by staphylococcal protein A. I. The role of cyclic AMP, arachidonic acid metabolites, microtubules and microfilaments.

Protein A from Staphylococcus aureus (Staph A) induces histamine secretion from human basophil leucocytes in the concentration range 10(-4) - 10 micrograms/ml. This reaction has great similarities to that of antigen or anti-IgE-induced release. It is characterized by a two stage reaction, requires extracellular calcium and is optimal at 37 degrees C. The rate of release is similar to that of IgE-mediated reactions. Histamine release induced by Staph A is inhibited by metabolic inhibitors, drugs which increase intracellular cyclic AMP levels, inhibitors of lipoxygenase pathways and a phospholipase A2 inhibitor. D2O and cytochalasin B which affect microtubules and microfilaments respectively, enhance histamine release induced by Staph A. These results suggest that Staph A-induced release is modulated by intracellular cyclic AMP, arachidonic acid metabolites, requires energy and is enhanced by the disruption of microfilaments and stabilization of microtubules.

Arachidonic Acids↗
PubMed1982

[Closed chest interruption of A-V conduction in the treatment of refractory supraventricular tachyarrhythmias. A clinical contribution].

The AA. describe a technique for interrupting the A-V conduction using a direct-current shock delivered from a cardioversion unit to the A-V junctional tissue by means of a conventional electrode-catheter. The method was used in 2 patients with refractory supraventricular tachycardias. After the procedure both patients received a programmable A-V sequential pacemaker. The first patient, with cardiomyopathy and intermittent W-P-W syndrome, had a 2-year history of iterative reciprocating tachycardia and occasional episodes of atrial flutter-fibrillation. The second patient, with coronary heart disease, had recurrent episodes of atrial flutter for at least 2 years. In patient 1 the shock caused a suprahisian first-degree block. Atrial pacing at 580 ms cycle length provoked a 2:1 block and ventricular pacing showed no retrograde conduction. The patient, who is not pacemaker-dependent, is now free from reciprocating tachycardia and, during atrial flutter-fibrillation episodes, the ventricular rate varies from 62 to 75 bpm. In patient 2 the shock caused a persistent complete A-V block and neither antegrade nor retrograde conduction was observed during atrial and ventricular pacing. During a long episode of atrial flutter, there was a complete A-V block with a ventricular rate between 40 and 48 bpm. The follow-up is 9 months in both patients. We conclude that the technique used, which does not require open heart surgery, can be effectively used in patients with disabling supraventricular tachyarrhythmias resistant to drug treatment.

Amiodarone↗