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Biomedical subjects

M Condorelli

Publications and source records attributed to M Condorelli.

At least 145 records · Page 8Linked to original sources
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↗
PubMed1984

Postural changes and isosorbide dinitrate. A polygraphic study in patients with coronary artery disease.

Sitting or orthostatic positions and trinitrine-like drugs reduce venous return. We focused on the non-invasive assessment of postural-induced cardiovascular stress and isosorbide dinitrate (IDN) induced changes in 8 male patients with coronary artery disease (CAD), using polygraphic recordings by means of a Thermistor Pulse Transducer. The pre-ejection period (PEP) is sensitive to reduced preload and to the positive inotropic state of the myocardium. In addition, the % diastole (RR interval--electromechanical systole/RR interval) has been recently demonstrated to be correlated to coronary perfusion in CAD patients. We observed that IDN in clinostatism and the sitting position reduced preload (longer PEP) with increased heart rate (HR) and did not affect % diastole. In orthostatism, while controls showed an increased HR and prolonged PEP, the HR was higher after IDN, with a fall in PEP and a significant decrease in % diastole. We ascribed this change to adrenergic stimulation by the hypotensive actions of IDN (lowered mean blood pressure) in orthostatism and with a fall in coronary perfusion. Caution should be taken in CAD patients when postural stress could occur during IDN treatment. Moreover, polygraphic studies can be useful to detect individual responses to nitrates and serial recordings could be employed to assess late responses to chronic management with IDN.

Analysis of Variance↗
PubMed1984

The mechanism of basophil histamine release induced by pepstatin A.

Pepstatin A, a natural pentapeptide isolated from cultures of actinomycetes, induced histamine secretion from human basophils in the concentration range of 3 X 10(-7) to 10(-4) M. The characteristics of this reaction were similar to those of f-met-peptide-induced histamine release: pepstatin A-induced release required Ca2+, and the release reaction was complete within 2 min at 22 or 37 degrees C but did not occur at 4 degrees C. There was excellent correlation (r = 0.93; p less than 0.001) between the maximal histamine release induced by pepstatin A and f-met-peptide, but there was no relationship to the capacity of basophils to release with anti-IgE (r = -0.03) or the Ca2+ ionophore A23187 (r = -0.22). Release by pepstatin A was reversibly inhibited by two nonreleasing analogs of f-met-peptide, CBZ-Phe-Met and BOC-Met-Leu-Phe. BOC-Met-Leu-Phe competitively inhibited the effect of both f-met-peptide and pepstatin A on histamine release from basophils. The dissociation constant (Kd) for the BOC-Met-Leu-Phe-receptor complex in both conditions was approximately 10(-6) M. Furthermore, there was complete cross-desensitization between pepstatin A and f-met-peptide, whereas cells desensitized to pepstatin A released normally with anti-IgE and vice versa. A variety of pharmacologic agents had similar effects on both pepstatin A- and f-met-peptide-induced release (e.g., slight inhibition with cyclic AMP-active agents, no enhancement with D2O, and marked enhancement with cytochalasin B). We suggest that the natural pentapeptide pepstatin A induces histamine release from human basophils by activating a cell surface receptor(s) also activated by the synthetic tripeptide f-met-peptide.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Effect of beta-blockade on thallium-201 dipyridamole myocardial scintigraphy.

The effect of beta-blockade on dipyridamole thallium-201 images was assessed in 8 patients with coronary artery disease and positive dipyridamole test. Three dipyridamole thallium-201 tests were performed, the first in basal conditions, the second 30' after propranolol and the third with propranolol and atrial pacing. After dipyridamole heart rate and double product increased respectively from 75 +/- 7 to 98 +/- 15 b/min (p less than 0.01 vs starting values) and from 10 551 +/- 1255 to 11 740 +/- 4542 mmHg X b/min (p less than 0.05 vs starting values). Propranolol reduced heart rate to 64 +/- 6 b/min (p less than 0.05 vs basal conditions), systolic blood pressure to 136 +/- 13 and double product to 8733 +/- 1248 (p less than 0.05 vs basal conditions). Dipyridamole when infused after propranolol, induced an increase in heart rate to 70 +/- 5 b/min (p less than 0.05 vs starting values) while double product was 9133 +/- 1189 mmHg X b/min (p = NS vs starting values). Atrial pacing prevented the fall in heart rate and double product induced by propranolol so during dipyridamole infusion double product increased to 13 271 +/- 1868 (p less than 0.05 vs propranolol treatment; p less than 0.05 vs starting values). Segmental score calculated after dipyridamole was 5.2 +/- 2.0 in basal conditions, 5.1 +/- 1.3 after propranolol (p = NS) and 4.8 +/- 1.3 after propranolol plus atrial pacing (p = NS). Thus the results of the study show that beta-blockade does not worsen dipyridamole thallium-201 images. Furthermore the steal phenomenon seems to be the main mechanism of the dipyridamole induced ischemia. In fact, also when the increase, oxygen consumption is blunted with beta-blockade the disparity in myocardial blood flow resulted unaffected.

Blood Pressure↗
PubMed1984

Possible role of calmodulin in the control of lysosomal enzyme release from human polymorphonuclear leukocytes.

Human polymorphonuclear leukocytes (PMNs) were found to contain a mean +/- S.E.M. of 21.7 +/- 7.9 ng of immunoreactive calmodulin (CaM)/10(6) PMNs, which represents 0.032 +/- 0.001% of the total cellular protein. The functional role of CaM in the control of lysosomal enzyme release from human PMNs was investigated using several CaM antagonists. Trifluoperazine (TFP) (10(-6)-2 X 10(-5) M), pimozide (10(-6)-1.5 X 10(-5) M), chlorpromazine (CPZ) (10(-5)-10(-4) M) and promethazine (2 X 10(-5)-10(-4) M) inhibited in vitro lysosomal enzyme release from human PMNs induced by immunological (serum-treated zymosan, concanavalin A and formyl-L-methionyl-L-leucyl-L-phenylalanine) and nonimmunological (Ca++ ionophore A23187) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity for CaM, had practically no inhibitory effect on lysosomal enzyme release. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, W-7, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of lysosomal enzymes from PMNs. In contrast, the chloride-deficient analog, W-5, N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride, which interacts only weakly with CaM, had practically no inhibiting effect. The IC50 for enzyme release by a series of eight CaM antagonists was closely correlated (r = 0.89; P less than .001) with their affinity for binding to CaM, supporting the concept that these agents act by binding to CaM and thereby inhibiting lysosomal enzyme release.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1984

[Closed-chest interruption of abnormal bundles of His. Its use in a case of "incessant" tachycardia guided by an experimental model].

The usefulness and safety of intracardiac discharge of a synchronized DC shock through a catheter-electrode to ablate the His bundle has led the Authors to evaluate the use of this technique to interrupt bypass tracts located near the coronary sinus. Acute experiments were performed in 10 open chest dogs. A tripolar 6F catheter-electrode was placed in the coronary sinus and 2 or 3 unipolar shocks of 80-120 joules were delivered to each electrode. After the procedure the coronary sulcus was inspected and a lesion 2-3 cm wide and 2-4 mm deep with edema and haemorrhage was found in all cases. On the basis of the data obtained in dogs, the technique was successfully used in a woman with "incessant" supraventricular tachycardia due to reentry through a concealed anomalous pathway located in the posterior septum. A careful mapping of the coronary sinus allowed the localization of the earliest retrograde atrial activation. Two shocks of 120 joules were delivered in the coronary sinus at the site suggested by the electrophysiologic mapping. The patient has remained free from tachycardia since the time of the discharge (follow-up: three weeks).

Adult↗
PubMed1983

Prajmalium bitartrate in chronic ventricular arrhythmias: comparison with disopyramide.

24-h ECG recordings were used to assess the efficacy of prajmalium bitartrate (PB) in reducing the incidence and the severity of premature ventricular complexes (PVCs), and to compare its antiarrhythmic action with that of Disopyramide. 13 patients with frequent PVCs were distributed randomly into 2 groups. The first group of 7 patients received PB 80 mg/day for 4 days as their first treatment, and disopyramide 400 mg/day for a further 4 days as the second therapy. The succession of the drugs was reversed in the other group of 6 patients. Analysis of the Holter recordings showed that PB and disopyramide reduced PVC frequency to a similar extent as compared to the corresponding wash-out period, viz. by 56.7% (p less than 0.05) and 62.1% (p less than 0.01), respectively. Thus, PB appears to be an effective antiarrhythmic drug and comparable to disopyramide. It may be used to prevent premature ventricular complexes and runs of ventricular tachycardia.

Adult↗