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Biomedical subjects

J Mehta

Publications and source records attributed to J Mehta.

At least 325 records · Page 18Linked to original sources
PubMed1980

Abnormalities of platelet aggregation in sickle cell disease.

In vitro platelet aggregation responses to epinephrine and ADP were significantly lower in patients with sickle cell disease when compared to age- and sex-matched normal subjects. Platelet aggregation responses were reduced in all patients regardless of clinical status. Measurement of circulating platelet aggregates showed normal values in patients with sickle cell disease in steady state or with infection alone, but a significant increase in others with acute vaso-occlusive crises. Recovery from vaso-occlusion was associated with a decline in circulating platelet aggregates. This study suggests that in vivo platelet activation may result in "tired" platelets which are refractory to epinephrine and ADP stimulation in vitro.

Adenosine Diphosphate↗
PubMed1980

Plasma cell granuloma of the lung: endobronchial presentation and absence of response to radiation therapy.

Plasma cell granuloma of the lung is an uncommon, slow-growing, benign "pseudotumor" morphologically and clinically distinct from malignant plasma cell tumor (plasmacytoma). Its histopathology is distinct from sclerosing hemangioma and pseudolymphoma. Most are located in lung parenchyma, but a few present as endobronchial lesions. Patients are usually less than 30 years of age. Surgical excision is the preferred treatment and the prognosis is very good. Experience with radiation therapy is limited to one previously reported case. We report a case of plasma cell granuloma of the lung which is unusual because of the patient's age (71 years), endobronchial location, recurrence after local resection, and absence of response to radiation therapy. Ultrastructural features of the lesion are also described.

Aged↗
PubMed1980

Acute haemodynamic effects of oral prazosin in severe mitral regurgitation.

Acute haemodynamic effects of single dose oral prazosin were studied in eight patients with mitral regurgitation. Heart rate, mean systemic arterial pressure, pulmonary arterial pressure, left ventricular filling pressure, and forward cardiac output were measured in all patients. At peak effect, prazosin reduced mean systemic arterial pressure (95 +/- 4 to 86 +/- 4 mmHg), pulmonary arterial pressure (45 +/- 6 to 23 +/- 4 mmHg), and left ventricular filling pressure (30 +/- 4 to 21 +/- 3 mmHg). Pulmonary and systemic vascular resistance also fell (316 +/- 49 to 208 +/- 43 dynes s cm-5 and 2132 +/- 148 to 1491 +/- 94 dynes s cm-5, respectively). Forward cardiac index increased from 1.89 +/- 0.12 to 2.43 +/- 0.13 l/min per m2 and stroke volume from 43 +/- 5 to 57 +/- 6 ml/beat after prazosin. The onset of these changes occurred between 15 and 30 minutes, peaked between 45 and 60 minutes, and persisted for six hours. These data indicate that in patients with mitral regurgitation oral prazosin promptly improves cardiac performance (judged by increased forward cardiac output and reduced left ventricular filling pressure) as systemic and pulmonary vascular resistance are reduced.

Adult↗
PubMed1980

Use of vasodilators in congestive heart failure.

In order to select the proper vasodilator agent for the treatment of congestive heart failure, the underlying etiology and pathophysiology of heart failure must be understood since they are important determinants of the response to the particular vasodilator being used. Short-term studies are impressive. Most patients respond dramatically to vasodilators. Long-term studies are not available at this time. When they become available, the clinical usefulness of this group of drugs will be put in proper perspective.

Cardiac Output↗
PubMed1980

Psychosexual adjustment and counseling after myocardial infarction.

The current trend in cardiac rehabilitation is toward the empirical and systematic evaluation of the effectiveness of general and specific components. Clearly, resumption of sexual activity is important to the rehabilitation of patients and their partners. In fact, resumption of sexual behavior may be therapeutic in solidfying the marital relationship during stressful readjustment periods. A satisfying sexual relationship can be valuable as a step towards fostering self-confidence and a feeling of returning health. The cardiac rehabilitation program should strive for a multidisciplinary team approach and to initiate intervention and counseling as early as medically possible during the hospitalization. Counseling programs should always include the exploration of the possible concerns of patients and their partners about resumption of sexual activity. Patients should be advised as to the realities of their fears and provided with guidelines for facilitating a satisfying sexual relationship.

Adult↗
PubMed1979

Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart.

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.

Animals↗
PubMed1979

Chemotactic factor-induced generation of superoxide radicals by human neutrophils: effect of metabolic inhibitors and antiinflammatory drugs.

Human peripheral neutrophils generated superoxide radicals as assessed by ferricytochrome C reduction in response to activation by the synthetic chemotactic factor, N-formyl-methionyl-leucyl-phenylalanine. Superoxide generation was inhibited by 2-deoxy-D-glucose (ID50 4 X 10(-5)M), 2-iodoacetate (ID50 5 X 10(-5)M), and N-ethyl-maleimide (ID50 5 X 10(-6)M), suggesting a dependence on anaerobic glycolysis and sulfhydryl groups. Ouabain, microtubule-disrupting agents, inhibitors of respiration, oxidative phosphorylation, and protein and nucleic acid synthesis were without appreciable effects. Indomethacin (ID50 1 X 10(-4)M), ibuprofen (ID50 9 X 10(-4)M, and phenylbutazone (ID50 1 X 10(-5)M) all caused dose-dependent inhibition of superoxide generation at concentrations approximating those plasma and tissue levels obtained in human beings at therapeutic doses. Acetylsalicylic acid (125-500) microgram/ml) and aurothioglucose (10(-3)-10(-6)M) were without appreciable effects. Superoxide generation was inhibited only by relatively high concentrations of hydrocortisone (ID50 greater than 10(-3)M). Because superoxide radicals have been implicated in the pathogenesis of tissue injury in several forms of inflammation and arthritis in vivo, these studies suggest that the production of a potential cytotoxic factor may be subject to pharmacologic manipulation and that at least some of the antiphlogistic effects of the nonsteroidal antiinflammatory agents may be mediated through effects on superoxide production.

6-Aminonicotinamide↗
PubMed1979

Platelet function studies in coronary artery disease. V. Evidence for enhanced platelet microthrombus formation activity in acute myocardial infarction.

Circulating platelet microthrombi were evaluated during the acute and convalescent phases of illness in 44 patients admitted to the hospital for chest pain. Similar studies were performed in 10 healthy volunteers and 6 patients with infection. Circulating platelet microthrombi were significantly increased during the acute phase in 22 patients with transmural myocardial infarction compared with values in the other 22 patients without myocardial infarction, the healthy volunteers and the patients with infection alone. This increase in circulating platelet microthrombi declined to normal levels by the 7th hospital day in all but two patients who had evidence of extension of myocardial infarction and died. In contrast, circulating platelet microthrombi were similar in acute and convalescent phases of patients with chest pain but without myocardial infarction and were comparable with values in healthy volunteers. This study suggests that increased circulating platelet microthrombi may be related to tissue necrosis associated with transmural myocardial infarction.

Acute Disease↗
PubMed1979

Comparison of haemodynamic effects of oral prazosin, oral hydralazine, and intravenous nitroprusside in same patients with chronic heart failure.

The haemodynamic effects of oral prazosin and hydralazine were evaluated in patients with refractory heart failure and compared with those of intravenous nitroprusside in the same patients. Both oral agents were well tolerated and appeared to have beneficial haemodynamic effects. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin resulted in a more significant decline in left ventricular filling pressure and pulmonary vascular resistance than did hydralazine. Haemodynamic alterations induced by prazosin were similar to those induced by nitroprusside, which suggests a relatively balanced reduction of preload and afterload. With hydralazine, the increase in cardiac output without change in left ventricular filling pressure or pulmonary vascular resistance suggests minimal effect on preload but significant reduction in afterload.

Adult↗
PubMed1979

Platelet function studies in heart disease. VI. Enhanced platelet aggregate formation activity in congestive heart failure: inhibition by sodium nitroprusside.

We studied 11 patients with congestive heart failure and 10 normal volunteers for in vivo platelet aggregate formation activity. The patients with heart failure had significantly (p less than 0.01) more circulating platelet aggregates than the normal volunteers. During sodium nitroprusside infusion, the number of circulating platelet aggregates declined to normal levels and in vitro platelet aggregation responses to epinephrine and adenosine diphosphate were also suppressed significantly (p less than 0.01). This was associated with a 30% decline in systemic vascular resistance and a 28% increase in cardiac output. In other in vitro experiments, sodium nitroprusside was found to have direct, dose-related platelet aggregation inhibitory actions. This study suggests that an increase in vascular resistance in certain heart failure patients may in part be related to an increase in circulating platelet aggregates. Direct inhibition of platelet aggregation by sodium nitroprusside may be a mechanism of its beneficial effects in heart failure.

Adult↗
PubMed1979

Demonstration of a specific neutrophil receptor for a cell-derived chemotactic factor.

The crystal-induced chemotactic factor, a cell-derived chemoattractant for neutrophils, binds specifically to a site on human neutrophils but not to erythrocytes or lymphocytes, suggesting a relationship between the presence of specific binding sites on the neutrophils and the ability to be chemotactically activated. The Scatchard analysis revealed an equilibrium dissociation constant at 37 degrees C of 0.446 micrometer and the presence of approximately equal to 6.44 x 10(5) binding sites for 125I-crystal-induced chemotactic factor per cell. Binding was not displaced by the synthetic chemotactic factors F-Met-Leu-Phe and Gly-His-Gly or by complement-activated plasma providing evidence of the specificity of the receptor.

Binding Sites↗
PubMed1979

Mechanism of action of colchicine in acute urate crystal-induced arthritis.

Phagocytosis of urate crystals by human or rabbit neutrophils induces the synthesis and release of a glycoprotein, the crystal-induced chemotactic factor (CCF), which is chemotactically active both in vitro and in vivo. It has been proposed that CCF is a prime mediator of the acute gouty attack. Colchicine has been shown to decrease the production and release of this factor in vitro. In these studies, colchicine, at nonleukopenic doses, is shown to abrogate the acute arthritis induced by monosodium urate crystals in rabbits, but to have no effect upon the arthritis induced by the injection of the purified cell-derived chemotactic factor. Serum colchicine levels were 0.48-0.58 muM at 30 min and 0.12-0.3 muM at 90 min after intravenous injection of 0.2 mg/kg colchicine. Peripheral blood polymorphonuclear leukocytes obtained from colchicine-treated animals migrated normally towards a chemotactic stimulus but failed to produce CCF after phagocytosis of monosodium urate crystals. The dialyzed synovial fluid from rabbits injected with microcrystalline sodium urate contained chemotactic activity that was not present when animals were also given intravenous colchicine or injected intra-articularly with the chemotactic factor formyl-methionyl-leucyl-phenylalanine. Furthermore, the synovial fluid from rabbits injected with microcrystalline sodium urate significantly decreased (125)I-CCF binding to neutrophils. The binding of (125)I-CCF to its neutrophil receptor was not significantly reduced by the synovial fluid of colchicine-treated rabbits nor by the synovial fluid of control rabbits injected with the chemotactic factor formyl-methionyl-leucyl-phenylalanine. Colchicine (10 and 0.1 muM) was shown to have no effect upon the binding of (125)I-CCF to its cell receptor.

Animals↗