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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
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↗
PubMed1986

Possible role of calmodulin in the control of histamine release from human basophil leukocytes.

We investigated the possible role of calmodulin (CaM) in the control of histamine release from human basophil leukocytes 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 (PMZ) (2 X 10(-5)-10(-4) M) inhibited in vitro histamine secretion from human basophils induced by several immunological (antigen, anti-IgE, and formyl-L-methionyl-L-leucyl-L-phenylalanine: f-met peptide) and nonimmunological (Ca2+ ionophore A23187 and the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate: TPA) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity to CaM, had practically no inhibitory effect on histamine release from human basophils. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, the compound N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) (2.5 X 10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of histamine from basophils. In contrast, the chloride deficient analogue, W-5, 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 = 0.91; p less than 0.001) with the CaM specific binding, supporting the concept that these agents act by binding to CaM and thereby inhibiting histamine release. TFP and W-7 inhibited histamine release in the absence and in the presence of increasing concentrations of extracellular Ca2+. These results emphasize the possible role of CaM in the control of histamine secretion from human basophils.

Basophils↗
PubMed1986

Effect of nifedipine on dipyridamole thallium-201 myocardial scintigraphy.

The effect of a calcium antagonist drug, nifedipine, on dipyridamole thallium-201 images was assessed in 10 angina patients with positive dipyridamole test. Two dipyridamole thallium-201 tests were performed, the first in basal conditions, the second after administration of 20 mg nifedipine. After dipyridamole, heart rate and double product increased respectively from 68.0 +/- 8.2 to 94.7 +/- 11.5 beats/min (p less than 0.01) and from 9459.5 +/- 1800.2 to 12,770.0 +/- 1864.7 mmHg X beats/min (p less than 0.01). Dipyridamole when infused after nifedipine induced an increase in heart rate from 74.2 +/- 7.16 to 88.8 +/- 5.6 beats/min (p less than 0.01) and in double product from 9650.5 +/- 1348.0 to 11,399.0 +/- 1146 mmHg X beats/min (p less than 0.05). Systolic and diastolic blood pressures were unmodified during the two studies. Segment scores were comparable before and after nifedipine. Thus, nifedipine does not worsen thallium-201 myocardial images obtained during dipyridamole infusion, therefore, this test could provide an alternative to exercise thallium-201 in patients receiving calcium antagonist drugs.

Coronary Circulation↗
PubMed1986

Exercise-induced changes of left ventricular ejection time in noninvasive evaluation of chest pain.

Significance and clinical usefulness of exercise-induced changes of noninvasive left ventricular ejection time, recorded by mechanocardiography, in detecting coronary artery disease is still controversial. We investigated the changes of the left ventricular ejection time (LVET), corrected for heart rate as ETI (LVET/square root RR), after a standard 4-min exercise by bicycle ergometer (50 W/min for 2 min, increased by 20 W after 2 min) in 56 male volunteers. They were invasively studied for typical or atypical chest pain. Thirty-four had coronary artery disease (CAD) and the others served as controls. Immediately after exercise LVET shortened according to the rise in heart rate in both groups. ETI increased similarly. After 2 minutes from exercise ETI increased only in the CAD group, according to a longer LVET, in spite of the rise in heart rate. In contrast, ETI was unchanged in controls, according to a shortened LVET. Totally, 27/34 CAD patients and 9/22 controls had a greater ETI than at rest. Employing this delta ETI as a "marker" of CAD we found a predictive accuracy of 74%. We suggest postexercise ETI could be a simple and inexpensive support to electrocardiogram in basic evaluation of subjects with chest pain.

Angina Pectoris↗
PubMed1986

Physiological concentrations of zinc inhibit the release of histamine from human basophils and lung mast cells.

We have previously shown that physiological concentrations of zinc (congruent to 7 X 10(-6) M) inhibit the release of histamine from human basophil leukocytes (Marone et al., J. Pharmacol. Exp. Ther. 217: 292, 1981). In these experiments we compared the effect of zinc chloride on the release of chemical mediators from human basophils and mast cells isolated from human lung. Preincubation (5 min, 37 degrees C) of human basophils and lung mast cells with zinc chloride (10(-6)-3 X 10(-5) M) caused dose-related inhibition of histamine and peptide leukotriene C4 (LTC4) release induced by anti-IgE. Increase Ca2+ concentrations (0.3 to 6 mM) in the extracellular medium completely reversed the inhibitory effect of zinc on anti-IgE-mediated histamine secretion. Zinc chloride was a competitive antagonist of the action of Ca2+ in histamine secretion induced by anti-IgE with a dissociation constant (Kd) of about 10(-5) M in both the basophil and mast cell systems. Thus physiological concentrations of zinc inhibit the release of histamine from human basophils and lung mast cells, presumably by blocking Ca2+ uptake induced by anti-IgE activation.

Basophils↗
PubMed1986

IgE-mediated activation of human heart in vitro.

We used human cardiac tissue from the right atrial appendages of patients undergoing corrective heart surgery to study content and de novo synthesis of mediators in the human heart. Human heart tissue contained 1.7 +/- 0.1 micrograms/g wet weight of histamine (mean +/- S.E.M.) and spontaneously produced 6-keto-PGF1 alpha (38.4 ng/g wet weight/min), PGF1 alpha (1.9 ng/g wet weight/min), PGE (1.7 ng/g wet weight/min) and thromboxane B2 (TxB2) (1.7 ng/g wet weight/min). Spontaneous release of PGD2, leukotriene C4 and histamine was negligible. Rabbit anti-human IgE (1-10 micrograms/ml) dose-dependently induced the release of histamine (5 to 15% of the total histamine content) and of PGD2 (5 to 100 ng/g of wet tissue). The effect of anti-IgE was dose-related and reached a maximum after 30-45 min of incubation. A significant linear correlation (rs = 0.90; p less than 0.001) was found between de novo synthesis of PGD2 and the secretion of histamine induced by anti-IgE challenge of human heart. These results support the concept that PGI2 is the main, but not the sole, product of arachidonic acid metabolism synthesized by human heart in vitro. Additionally, anti-IgE challenge of human heart in vitro induces the release of histamine and PGD2. The local concentrations of these mediators appear high enough to play some role in the modulation of several cardiac functions in vivo.

Animals↗
PubMed1986

Human basophil releasability. I. Age-related changes in basophil releasability.

Releasability of human basophils (i.e., the response to a standard stimulus) is an important parameter in several pathophysiologic conditions. We studied the IgE (anti-IgE)- and non-IgE-mediated (f-met peptide and Ca2+ ionophore A23187) releasability of human basophils obtained from 63 normal donors whose ages ranged from 1 to 86 years. The maximum percent of histamine release induced by anti-IgE was significantly correlated (rs = 0.57; p less than 0.001) with the age of donors. The sensitivity to a standard concentration of anti-IgE (3 X 10(-2) mcg/ml) was also correlated with the age of cell donors (rs = 0.68; p less than 0.001). In the population of 63 donors tested, the maximum percent of histamine release and the cell sensitivity to anti-IgE appeared to be independent of the serum concentration of IgE. However, we found a positive correlation (rs = 0.55; p less than 0.05) between serum IgE level and anti-IgE-induced histamine release in the group less than 20 years of age. In contrast, a negative correlation (rs = -0.32; p less than 0.05) between serum IgE level and anti-IgE-induced histamine secretion was found in the group greater than 21 years of age. The maximum percent of histamine release induced by f-met peptide and Ca2+ ionophore A23187 appeared to be independent to both the age of the donors and the serum IgE level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

The Wiskott-Aldrich syndrome: studies of platelets, basophils and polymorphonuclear leucocytes.

Platelets, basophils and neutrophils from a patient with the Wiskott-Aldrich syndrome (WAS) were exposed to stimuli that activate specific membrane receptor or directly initiate biochemical events (e.g. the Ca2+ ionophore A23187 and ionomycin or arachidonic acid). Platelets from this patient did not aggregate in response to ADP, collagen, thrombin or adrenaline, which activate specific membrane receptors. Platelet aggregation, however, was normal in response to compound A23187, ionomycin or exogenous arachidonic acid. Histamine release from basophils of the WAS patient was normal in response to anti-IgE, a formylated peptide (f-met peptide), and to A23187. Similarly, the release of the lysosomal enzymes, beta-glucuronidase and lysozyme, from neutrophils of the WAS patient in response to serum treated zymosan (Zx), f-met peptide, and A23187 was not significantly different from that of his parents and 13 normal donors. These results suggest that the primary defect in WAS is selectively present in platelets and is located in a biochemical step between receptor activation and Ca2+ influx and/or initiation of arachidonate metabolism.

Arachidonic Acid↗