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Biomedical subjects

M Condorelli

Publications and source records attributed to M Condorelli.

At least 73 records · Page 4Linked to original sources
PubMed1988

Atenolol and/or nifedipine in effort angina: which is the treatment of choice for exercise coronary protection?

The authors performed a long-term, double-blind, crossover, randomized study on the effects of two drugs (atenolol, 100 mg/day, or nifedipine, 10 mg t.i.d.) when administered alone or in combination on the exercise tolerance in 10 patients with stable angina on effort (mean age 52 +/- 4 years, 8 males and 2 females) and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. None of the drug treatments improved exercise duration or maximal sustained work load. Atenolol decreased significantly ST segment depression to -1 +/- 0.8 from -1.91 +/- 0.7, baseline and -2.05 +/- 0.5, placebo. Nifedipine was not better than placebo. The atenolol plus nifedipine treatment was better than placebo (p less than 0.001) or nifedipine alone (p less than 0.05) but was not more significantly efficacious than atenolol alone. Long-term management of exertional angina can be usefully performed using atenolol. The use of nifedipine at the present dose of 10 mg, although well tolerated, did not improve the ST signs of ischemia.

Adult↗
PubMed1987

[Mechanisms of regulation of arterial blood pressure: role of the sympathetic nervous system and of the renin-angiotensin system in patients on a low-sodium diet].

In order to discover more about the role of the sympathetic nervous and renin-angiotensin systems in the preservation of homeostasis during chronic reductions of salt intake, blood pressure, blood catecholamines and renin activity were measured in a group of healthy subjects in normal conditions and on a salt-free diet combined with blockade of the conversion enzyme by enalapril. The results confirmed the hypothesis advanced on an earlier occasion i.e. that both hormone systems contribute to pressure during salt depletion in the initial phase, while over the long term only the renin-angiotensin system is activated though when this is inhibited, the sympathetic nervous system will take over its function.

Adolescent↗
PubMed1987

[Regulation of coronary circulation in patients with hypertensive cardiopathy: role of ventricular mechanoreceptors].

In order to assess the involvement of the cardiopulmonary receptors in the regulation of the coronary circulation, changes in coronary resistance produced by the application of a -10 mmHg pressure to the lower body were studied in 6 healthy subjects and 6 patients with arterial hypertension and left ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy.

Adult↗
PubMed1987

Effects of intravenous verapamil administration on left ventricular diastolic function in systemic hypertension.

The effects of intravenous verapamil administration (0.1 mg/kg as a bolus followed by an infusion of 0.007 mg/kg/min) were studied using high-temporal-resolution radionuclide angiography in 27 patients with hypertension. Verapamil administration increased heart rate from 69 +/- 11 to 75 +/- 12 beats/min (p less than 0.001) and decreased systolic, diastolic and mean blood pressures (BPs) from 155 +/- 21/102 +/- 12 mm Hg (mean 119 +/- 14) to 142 +/- 19/95 +/- 12 mm Hg (mean 109 +/- 13) (p less than 0.001 for all). Ejection fraction decreased significantly (from 65 +/- 10% to 60 +/- 11%, p less than 0.005); peak filling rate, however, increased significantly only in patients in whom it was subnormal in the basal study (from 2.2 +/- 0.4 to 3.0 +/- 0.6 end-diastolic counts/s, p less than 0.001). These latter patients had significantly higher values of left ventricular (LV) mass index than patients with normal or increased peak filling rate (129 +/- 22 vs 112 +/- 22 g/m2, respectively, p less than 0.05). The isovolumic relaxation period changes were inversely related to the baseline values (r = 0.83, p less than 0.001). In the subgroup of patients in whom isovolumic relaxation period lengthened, time to end systole decreased (from 360 +/- 31 to 329 +/- 30 ms, p less than 0.025) and time to onset of rapid filling increased (from 420 +/- 31 to 451 +/- 34 ms, p less than 0.025), whereas these 2 intervals had opposite patterns in patients in whom isovolumic relaxation period decreased or did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Ventricular parasystole and ventricular couplets: a re-entry within the parasystolic focus?

We report a 62-year-old man with a persistent ventricular rhythm originating in a parasystolic focus associated with frequent ventricular couplets with fixed coupling. Both intravenous (IV) procainamide (1 g) and propafenone (70 mg IV) promptly suppressed only the second component of ventricular couplets, suggesting that re-entry rather than enhanced automaticity was the mechanism of ventricular couplets. On the contrary, the nonresponse of ventricular rhythm and ventricular couplets to verapamil (10 mg IV) suggested that triggered activity should not play a role in the genesis of this ventricular rhythm. The mechanisms of the ventricular couplets (rapidly discharging parasystolic focus vs. re-entry) are discussed.

Arrhythmias, Cardiac↗
PubMed1987

Early diastolic time intervals during hypertensive pregnancy.

Early diastolic time intervals have been assessed by means of the echopolycardiographic method in 17 pregnant women who developed hypertension during pregnancy (HP) and in 14 normal pregnant women (N). Systolic time intervals (STI), stroke volume (SV), ejection fraction (EF), and mean velocity of myocardial fiber shortening (VCF) were also evaluated. Recordings were performed in the left lateral decubitus (LLD) and then in the supine decubitus (SD). In LLD, isovolumic relaxation period (IRP) was prolonged in the hypertensive pregnant women compared with normal pregnant women (HP 51 +/- 12.5 ms, N 32.4 +/- 15 ms p less than 0.05), whereas time of the mitral valve maximum opening (DE) was not different in the groups. There was no difference in SV, EF, and mean VCF, whereas STI showed only a significant (p less than 0.05) lengthening of pre-ejection period (PEP) in HP. When the subjects shifted from the left lateral to the supine decubitus position, left ventricular ejection time index (LVETi) and SV decreased significantly (p less than 0.05) in both normotensive hypertensive pregnant women. IRP and PEP lengthened significantly (p less than 0.05) only in normals, whereas they were unchanged in HP. DE time did not vary in either group. In conclusion, hypertension superimposed on pregnancy induces lengthening of IRP, as well as of PEP, and minimizes the effects of the postural changes in preload on the above-mentioned time intervals.

Adolescent↗
PubMed1987

Effects of celiprolol on systemic and forearm circulation in hypertensive patients: a double-blind cross-over study versus metoprolol.

The antihypertensive efficacy of a new beta-receptor blocking agent, celiprolol, was compared with that of a well-established antihypertensive drug, metoprolol. Their systemic and forearm hemodynamic effects were investigated using echocardiography and two-dimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive patients completed a double-blind, cross-over, randomized study using celiprolol and metoprolol. Two six-week courses with celiprolol or metoprolol were preceded and followed by a two-week placebo period; the total duration of the study was 18 weeks. In spite of a comparable efficacy in reducing systolic and diastolic blood pressure (about 10% of the basal value), the two drugs showed quite different systemic and regional hemodynamic effects. Celiprolol induced a significant decrease in forearm vascular resistance (from 157 +/- 17 to 113 +/- 13 mm Hg/mL/s, P less than .01) and total peripheral resistance (from 1596 +/- 90 to 1398 +/- 91 dyne.s.cm-5, P less than .05) whereas cardiac output remained unchanged and forearm blood flow increased. Metoprolol reduced cardiac output (from 6.5 +/- 3 to 5.7 +/- 3 L/min, P less than .05), through a reduction in heart rate, since stroke volume was unchanged. Both drugs did not significantly modify cardiac performance, as evaluated by left ventricle fractional shortening and ejection fraction. Thus, the two drugs seem to reduce blood pressure through different hemodynamic mechanisms.

Adrenergic beta-Antagonists↗
PubMed1987

Hemodynamic and hormonal effects of atrial natriuretic factor in patients with essential hypertension.

Hemodynamic and hormonal effects of two graded infusions of alpha-human-(1-28)-atrial natriuretic factor (0.5 microgram/kg prime followed by 0.05 microgram/kg per min for 20 minutes and by 0.1 microgram/kg per min for 20 minutes) were evaluated in 13 patients with mild to moderate essential hypertension. The lower dose of atrial natriuretic factor did not change significantly any of the considered variables, although it tended to reduce aortic mean blood pressure (from 132.6 +/- 5.3 to 125.5 +/- 4.6 mm Hg), cardiac index (from 3.67 +/- 0.2 to 3.54 +/- 0.18 liters/min per m2) and forearm vascular resistance (from 178.6 +/- 15 to 148.3 +/- 10 mm Hg/ml per s). The higher dose of atrial natriuretic factor significantly reduced mean aortic pressure (118.6 +/- 5 mm Hg), cardiac index (3.29 +/- 0.16 liters/min per m2) and stroke volume index (from 45.9 +/- 2.6 to 38.9 +/- 3 ml/m2) and slightly decreased pulmonary wedge pressure, whereas both total peripheral resistance and forearm vascular resistance were not modified. With this latter dose a reduction in aortic pressure was observed in all patients at the steady state, and this was associated with a fall in stroke volume index in 10 of the 13 patients and with a reduction in total peripheral resistance in only 6 patients. Heart rate and right atrial and pulmonary pressures did not change during infusion of atrial natriuretic factor. Plasma renin activity was only slightly reduced by atrial natriuretic factor, whereas plasma norepinephrine rose significantly (from 233 +/- 34 to 330 +/- 58 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Effects of coronary occlusion on arterial baroreflex control of heart rate and vascular resistance.

This study was planned to assess whether circumflex coronary occlusion (CO) impairs the arterial baroreflex control of heart rate (HR) and hindlimb vascular resistance (HVR), and to determine the mechanisms involved in the mediation of these phenomena. Increasing doses of phenylephrine and nitroglycerin were given intravenously to anesthetized dogs with a constant flow-perfused hindlimb before and during 30-s CO. The reflex responses were assessed by the changes in HR and hindlimb perfusion pressure evoked by changes in arterial pressure following phenylephrine and nitroglycerin administration. During CO, there was an attenuation of the reflex control of HR and HVR as compared with control conditions. The application of lidocaine on the left ventricular epicardial surface was able to prevent the effect of CO on both the baroreflex responses. The intravenous administration of atropine prevented only the impairment in arterial baroreflex control of HR induced by CO. After the injection of phentolamine into the perfused hindlimb, the baroreflex had no effect on HVR either before or during CO. Finally, intravenous administration of propranolol failed to modify the effect of CO on both the baroreflex responses. These data indicate that CO attenuates the arterial baroreflex control of both HR and HVR through the stimulation of left ventricular receptors. The effect on HR is mediated by the parasympathetic system, whereas the effect on HVR is due to sympathetic efferents.

Animals↗
PubMed1987

Betamethasone modulates the biological function of human polymorphonuclear leukocytes.

We have examined the influence of betamethasone (BT) on cyclic AMP (cAMP) metabolism and lysosomal enzyme release from highly purified (approximately equal to 99%) human polymorphonuclear leukocytes (PMNs). Preincubation (1-24 h) of human PMNs with BT (10(-9)-10(-5) M) had no effect on either cAMP content or on beta-glucuronidase release induced by formyl-containing tripeptide (f-met peptide). Preincubation (16-24 h) of PMNs with BT (10(-8)-10(-7) M) dose-dependently potentiated the cAMP accumulation caused by beta-agonists (isoproterenol), adenosine A2/Ra agonist (NECA), prostaglandin E1 (PGE1) and histamine in PMNs. Similarly, BT potentiated the inhibition of f-met peptide-induced beta-glucuronidase release from human PMNs caused by PGE1 (10(-6) M), histamine (2 X 10(-5) M), NECA (10(-4) M) and isoproterenol (10(-6) M).

Adenylyl Cyclases↗
PubMed1987

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 +/- 0.1 to 2.0 +/- 0.1 pg/ml; p less than 0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors.

Adult↗
PubMed1987

Vagal mediation of the effects of atrial natriuretic factor on blood pressure and arterial baroreflexes in the rabbit.

We investigated the hemodynamic effect of synthetic atrial natriuretic factor Auriculin A (ANF) and its influence on arterial baroreflex control of heart rate, systemic blood pressure, and perfusion pressure in the hind limb (perfused at constant flow) in rabbits anesthetized with alpha-chloralose and urethane. The neural mechanisms underlying these effects were also studied. In the intact animal, a 45-minute constant infusion of ANF (2 micrograms/kg prime, 0.2 microgram/kg/min) significantly reduced mean blood pressure and increased mean perfusion pressure, while heart rate did not change. Comparable data were obtained with lower (0.5 microgram/kg + 0.05 microgram/kg/min; 1 microgram/kg + 0.1 microgram/kg/min) or higher (4 micrograms/kg + 0.4 microgram/kg/min; 8 micrograms/kg + 0.8 microgram/kg/min) doses of ANF. In addition, ANF enhanced bradycardic reflex responses to phenylephrine i.v. bolus administration, while it did not change baroreflex-mediated responses to nitroglycerin i.v. bolus administration and to 30-second bilateral carotid occlusion. The specificity of the influence of ANF on arterial baroreflex responses was confirmed by the observation that no significant change in reflex responses to phenylephrine or carotid occlusion was detectable during a comparable decrease in blood pressure induced by a constant infusion of nitroglycerin. Bilateral vagotomy prevented both the fall in blood pressure and the increase in perfusion pressure induced by ANF, while cholinergic blockade (atropine, 0.5 mg/kg i.v.) or adrenergic blockade (propranolol, 0.3 mg/kg i.v. + phentolamine, 0.3 mg/kg i.v.) did not modify the hemodynamic response to ANF observed in the intact animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Influence of atrial natriuretic factor on forearm reflex vasoconstriction induced by cardiopulmonary or arterial receptor unloading.

We studied the influence of atrial natriuretic factor (ANF) infusion on the reflex increase in forearm vascular resistance in normotensive subjects. Reflex vasoconstriction was induced by cardiopulmonary receptor unloading [lower body negative pressure (LBNP), -20 mmHg for 15 min] or by carotid baroreceptor deactivation (+60 mmHg increase in external neck pressure by a pneumatic neck-chamber). Atrial natriuretic factor induced a significant increase in the reflex forearm vasoconstriction to LBNP, but did not modify systemic and regional reflex haemodynamic responses to carotid baroreceptor deactivation. These results suggest that ANF has important interactions with the neural control of peripheral circulation. In addition, the study shows that the peptide causes a selective potentiation of the reflex vasoconstrictor response evoked by cardiopulmonary receptor unloading.

Adult↗
PubMed1987

Inhibition of ischemia-induced phospholipase activation by quinacrine protects jeopardized myocardium in rats with coronary artery occlusion.

Phospholipase activation has been proposed as one relevant biochemical step toward irreversible myocardial injury during ischemia. Accordingly, after coronary artery occlusion, the time course of myocardial phospholipid degradation was studied in 83 control rats and 84 rats treated with quinacrine (75 mg/kg s.c. every 8 hr), a phospholipase inhibitor. Animals were sacrificed at different times ranging from 2 to 48 hr postocclusion. In controls a rapid fall in left ventricular phospholipid concentration (from 1.33 +/- 0.12 to 0.67 +/- 0.05 micrograms of P/mg of protein) and creatinkinase (CK) activity (from 9.84 +/- 0.49 to 6.93 +/- 0.60 I.U./mg of protein) was observed within 4 hr postocclusion. In quinacrine-treated animals phospholipids and CK also fell initially; however, 24 and 48 hr after occlusion they were higher than in controls (phospholipids: 0.99 +/- 0.05 vs. 0.62 +/- 0.04 micrograms of P/mg of protein, P less than .001; CK: 7.76 +/- 0.54 vs. 4.99 +/- 0.37 I.U./mg of protein, P less than .001, at 48 hr). Additional rats surviving coronary occlusion were divided randomly into a control (n = 14) and three treated groups receiving quinacrine every 8 hr at the dose of 5 (n = 13), 20 (n = 13) or 75 mg/kg (n = 15); 13 rats were sham-operated. Forty-eight hours postocclusion myocardial phospholipids were measured and infarct size calculated by CK depletion. Infarct size was significantly smaller in high dose quinacrine-treated than in control rats (16.6 +/- 5.7 vs. 42.1 +/- 4.4% of left ventricle, P less than .001). In treated animals, myocardial phospholipid concentration was also significantly higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗