Search PubMed⌕ Search

Biomedical subjects

J Mehta

Publications and source records attributed to J Mehta.

At least 307 records · Page 17Linked to original sources
PubMed1982

Induction of a chemotactic factor from human neutrophils by diverse crystals.

The purpose of this study was to isolate and compare the chemotactic factor generated by human neutrophils after phagocytosis of three structurally different crystals. An apparently identical chemotactic factor for neutrophils was isolated from the granular fraction of human neutrophils allowed to phagocytose MSU, CPPD, or amorphous DC. The isolated chemotactic factors migrated identically on SDS polyacrylamide gel electrophoresis, with a relative motility of 8.05, and competed with MSU-induced chemotactic factor for binding sites on the human neutrophils in an identical fashion. The data support the concept that the generation of the chemotactic factor represents a general response of the neutrophil to the phagocytosis of foreign particles.

Binding, Competitive↗
PubMed1982

Severe intracoronary thromboxane release preceding acute coronary artery occlusion.

Abnormalities of thromboxane (TXA2)-prostacyclin (PGI2) balance have been described in patients with coronary artery disease. Whether these abnormalities precede or follow an acute coronary event is debated. We report a patient in whom spontaneous acute right coronary artery occlusion was observed during coronary angiography. Measurements of arachidonic acid metabolites demonstrated imbalance in TXA2-PGI2 equilibrium preceding coronary occlusion. Marked increase in TXA2 in coronary sinus but not in the aortic blood suggested intracoronary release. Absence of PGI2 in the coronary venous blood at baseline and during tachycardia stress was evidence for failure of atherosclerotic coronary vessels to generate PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Long-term maintenance therapy with prazosin in congestive heart failure.

We evaluated the effects of long-term maintenance therapy with oral prazosin (6-20 mg, mean 14 +/- 2 mg/d) in 14 patients with congestive heart failure. The patients were followed for 6 +/- 1 months. Eleven of the fourteen patients reported subjective improvement. Two patients required increased diuretics because of gain in body weight. Systolic blood pressure showed a slight but sustained decrease suggesting persistent vasodilator effect. Reductions in echocardiographic left ventricular end-diastolic (6.35 +/- 0.25-5.88 +/- 0.25 cm, p less than 0.05) and end-systolic (5.16 +/- 0.35-4.73 +/- 0.28 cm, p less than 0.05) diameters were observed at 2 months. However, the cardiothoracic ratio on chest x ray was unaltered. Maximum exercise tolerance time increased in eight patients (57%) during prazosin therapy. Improvement in exercise tolerance time was observed in patients with most marked clinical improvement, suggesting presence of cardiac reserve. Two patients died suddenly after reporting subjective improvement. This study shows sustained clinical improvement in most patients with heart failure treated with oral prazosin.

Adult↗
PubMed1981

Demonstration of calcium-dependent chemotactic factor activatable esterase activity in human neutrophils: relationship with chemotaxis and chemotactic deactivation.

An increase in esterolytic activity, as measured by [3H] BAEE hydrolysis, was demonstrated in human neutrophil suspensions following incubation with three distinct chemotactic factors. The increased activity was demonstrated in intact cells as well as in cell lysates. The FMLP-enhanced enzymatic hydrolysis of BAEE was found to be calcium dependent. Esterase activation by FMLP was maximal at 1.0 mM of added calcium. Similar dose-response curves for esterase activation, chemotaxis, and chemotactic deactivation were obtained with the chemotactic factor FMLP, suggesting that in human neutrophils all three functions utilize some of the same early molecular events following chemotactic factor binding to th neutrophil surface.

Arginine↗
PubMed1981

Effects of prostacyclin on systemic and coronary hemodynamics in the dog.

The hemodynamic effects of intravenous and intracoronary prostacyclin (PGI2) were evaluated in anesthetized, open-chest instrumented dogs. Coronary artery and aortic blood flows, aortic and left ventricular (LV) diastolic pressure, and heart rate were measured continuously. With intravenous PGI2 both left anterior descending (LAD) and circumflex (LCX) coronary artery blood flows remained unchanged; both arterial and LV diastolic pressures declined; coronary resistance declined progressively with increasing PGI2; peak reactive hyperemic flow following 10-second coronary artery occlusion declined progressively with increased PGI2; heart rate responses were variable at low doses but increased at high dose; and aortic blood flow increased consistently. With intracoronary PGI2 both LAD and LCX coronary blood flows increased promptly in dose-related manner. In dogs with critical coronary artery narrowing (loss of reactive hyperemia) created by an external plastic occluder, intravenous prostacyclin (0.5 microgram/kg/min) did not alter flow in narrowed coronary artery, but increased flow in the non-narrowed coronary artery (p less than 0.02) as both systemic arterial and LV diastolic pressure declined. These results show that PGI2 has potent direct coronary and systemic vasodilator actions.

Animals↗
PubMed1981

Platelet function studies in coronary artery disease. X. Effect of dipyridamole.

To evaluate the effects of dipyridamole on blood platelet function in patients with coronary artery disease, platelet counts and aggregation were examined in aortic and coronary venous blood. Before administration of dipyridamole, platelet counts and aggregation in response to adenosine diphosphate were less (p less than 0.02) in coronary venous than in aortic blood. Dipyridamole administration (100 mg) resulted in an increase in platelet counts and platelet aggregation in coronary venous blood so that the differences in aortic and coronary venous blood values were eliminated. These phenomena were probably related to inhibitory actions of dipyridamole on platelet adhesion to atherosclerotic vessels. To further study the mechanism of action, the direct effects of dipyridamole on in vitro platelet aggregation were evaluated. Although dipyridamole, in the concentrations used, had no effect on in vitro platelet aggregation, it greatly potentiated the aggregation inhibitory actions of exogenous prostacyclin. In vivo potentiation of endogenous prostacyclin and inhibitory actions on platelet adhesion are the most likely mechanisms of the potentially beneficial actions of dipyridamole.

Adenosine Diphosphate↗
PubMed1981

Platelet function in hypertension and effect of therapy.

Platelet function was evaluated in 10 hypertensive and 11 normal subjects. In the placebo phase, the plasma beta thromboglobulin level (an index of platelet activation in vivo) was significantly (p less than 0.01) higher in the hypertensive than in the normal subjects; other tests of platelet function gave similar results in the two groups. After control of blood pressure with lofexidine (a centrally acting imidazoline derivative), plasma beta thromboglobulin levels decreased in 9 of the 10 hypertensive patients, but increased in one who showed no change in blood pressure. These studies suggest that enhanced platelet activation in primary hypertension may be associated with increased vascular resistance.

Adult↗
PubMed1981

Role of blood platelets and prostaglandins in coronary artery disease.

In the last decade, several studies evaluating blood platelet function in patients with coronary heart disease have been reported. Although several platelet function abnormalities such as enhanced platelet aggregation, decreased platelet survival and increase in platelet release reaction in the stable condition and during stress in patients with myocardial ischemia have been recognized, the mechanism of these abnormalities is just beginning to be understood. Discovery of certain platelet and endothelium-generated prostaglandins has provided some information as to the possible mechanism of platelet dysfunction. Abnormalities of prostaglandin production and platelet sensitivity to various prostaglandins may have an important bearing on the enhanced platelet aggregation in vivo, genesis of atherosclerosis and probably precipitation of acute ischemic events. Since the discovery of these prostaglandins, the precise mode of action of several commonly used platelet-active drugs has been clarified. Development of new drugs acting at selective steps in the prostaglandin pathways may provide some exciting novel therapeutic procedures in patients with coronary heart disease.

Acute Disease↗
PubMed1981

Short-term efficacy of oral verapamil in rest angina. A double-blind placebo controlled trial in CCU patients.

To determine the efficacy and safety of oral verapamil in patients with rest angina admitted to the Coronary Care Unit (CCU), a double-blind placebo-controlled trial was undertaken. Of the 65 patients with rest angina screened for the study, 15 met the inclusion criteria (at least two episodes of chest pain associated with ST-T segment changes per 24 hours) during single-blind placebo phase (Day 1). Patients were then randomized to receive either placebo or verapamil (80 mg every 6 hours) on Day 2. Protocol was designed such that those who did not respond to the placebo (nonresponders) received verapamil, 80 mg every 6 hours, whereas verapamil nonresponders received increased doses (120 mg every 6 hours) on Day 3. Those who did respond (responders) continued to receive their medication. Similar action was taken on Day 4, depending on chest pain frequency and clinical evaluation. The study drug was unblinded on Day 4. At the end of the four-day period, 13 patients were receiving verapamil (nine patients, 80 mg every 6 hours, and four patients, 120 mg every 6 hours) and all but one were responders. One patient received placebo all through the period of the study and was also considered to be a responder. In the remaining one patient evidence of myocardial necrosis developed after he received a single dose of verapamil (80 mg on Day 2). Except for the prolongation of PR interval in two patients while taking verapamil, no side effects from verapamil therapy were observed. These data demonstrate the efficacy of oral verapamil in reducing episodes of myocardial ischemia in the majority of all patients with rest angina.

Administration, Oral↗
PubMed1981

Chemotactic factor receptor modulation and cytoskeletal structures.

The microfilament-disrupting agents cytochalasins A, B, and D were shown to impair the binding of the chemotactic factors [3H]formylmethionylleucylphenylalanine and 125 I-labeled crystal-induced chemotactic factor to their neutrophil receptor. Scatchard plot analysis revealed a decrease of the available binding sites in the cytochalasin B-treated cells. Cytochalasin B showed the same inhibitory profile on intact cells and on a membrane-rich preparation, suggesting that the effect was not dependent on an intact microfilament apparatus. The microtubule modifiers colchicine and vinblastine had no effect on the binding of the chemotactic factor to its cell receptors

Binding Sites↗
PubMed1981

Determination of a specific receptor for formyl-methionyl-leucyl-phenylalanine on th pulmonary alveolar macrophage and its relationship to chemotaxis and superoxide production.

3H-FMLP, a chemotactic peptide that resembles Escherichia coli chemotactic factor, is chemotactic for PAM, binds specifically to a site on the cell, and induces the generation of superoxide radicals by the cell. Scatchard analysis revealed an equilibrium dissociation constant at 26 degrees C of 1.45 x 10(-8)M and the presence of 1.7 , 10(5) receptors per cell. Binding was not inhibited by a partially purified C5a preparation or by the neutrophil-derived CCF but was inhibited by various N-formylated peptides. The order of potency of each peptide to inhibit 3H-FMLP binding was identical to the order of potency of each peptide to induce generation of superoxide by the PAM. Only small amounts of beta-glucuronidase activity and no lysozyme were detected in the supernatant after incubation of the cells for 30 min with varying concentrations of FMLP.

Animals↗
PubMed1980

Platelet function studies in coronary heart disease. IX. Increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in angina pectoris.

Platelet prostaglandin generation (malondialdehyde production) and platelet sensitivity to prostacyclin (a vasodilator and platelet aggregation inhibitor) and to epoxymethanodienoic acid (EMA) (a vasoconstrictor and platelet aggregation stimulant endoperoxide analog) were studied in patients with angina pectoris and in control subjects. Platelet malondialdehyde production was higher in patients than in control subjects (mean +/- standard error of the mean 2.50 +/- 0.30 versus 1.70 +/- 0.13 nmol/10(9) platelets, p < 0.02). Platelets from patients were significantly less sensitive to prostacyclin's antiaggregatory effects than were those from control subjects (amount of prostacyclin required for 50 percent platelet aggregation inhibition 1.90 +/- 0.35 versus 0.68 +/- 0.05 ng, p < 0.02). Furthermore, less EMA was required to induce 50 percent platelet aggregation in patients with angina pectoris than in the normal subjects (133 +/- 8 versus 194 +/- 16 ng, p < 0.001). These observations suggest that increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in certain patients with coronary artery disease are important potential mechanisms in the pathogenesis of myocardial ischemia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1980

Platelet function studies in coronary artery disease. VII. Effect of aspirin and tachycardia stress on aortic and coronary venous blood.

The effects of orally administered aspirin (650 mg) on platelet aggregation patterns and counts in aortic and coronary venous blood were evaluated in patients with coronary artery disease. Studies were conducted at rest and during the stress of tachycardia. Before administration of aspirin, platelet aggregation and counts were lower (p less than 0.01) in coronary venous blood than in aortic blood. The stress of tachycardia resulted in increased (p less than 0.01) platelet aggregation only in coronary venous blood. After administration of aspirin, differences in platelet aggregation and counts between coronary venous and aortic blood at rest were eliminated, and the tachycardia-associated increase in coronary venous blood platelet aggregation was significantly reduced. These observations suggest that aspirin influences and abolishes the changes that occur in blood platelet function as platelets traverse the atherosclerotic myocardial vascular bed. The absence of an increase in platelet aggregation during the stress of tachycardia after administration of aspirin may have important pathophysiologic and therapeutic implications.

Adult↗