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Biomedical subjects

M A Barradas

Publications and source records attributed to M A Barradas.

At least 55 records · Page 3Linked to original sources
PubMed1988

Platelet aggregation and thromboxane A2 release in primary biliary cirrhosis and effect of D-penicillamine treatment.

Platelet function was assessed in 28 patients with primary biliary cirrhosis (PBC), of whom 10 were receiving D-penicillamine. Patients not on D-penicillamine treatment had platelet aggregation similar to that in the healthy control group; the group treated with D-penicillamine showed significantly enhanced platelet aggregation in response to threshold doses of adrenaline and collagen but not ADP. Median thromboxane B2 production was also higher in D-penicillamine treated patients than in controls or untreated patients; this difference did not reach statistical significance. The addition of D-penicillamine in vitro to platelet rich plasma from normal subjects was shown to enhance adrenaline- and collagen-induced platelet aggregation. Abnormalities of platelet function in PBC patients did not correlate with serum cholesterol concentration or with liver function tests but were related to the stage of disease. The present study emphasises the need to consider the aetiology, disease stage and type of treatment when assessing platelet function and prostanoid release in liver disease.

Aged↗
PubMed1988

Increased histamine content in leukocytes and platelets of patients with peripheral vascular disease.

Since histamine has recently been shown to play an important role in the pathogenesis of atherosclerosis in experimental nonketotic diabetes, and since leukocytes and platelets contain most of the histamine in blood, we have determined the levels of histamine in these cells from patients with peripheral vascular disease (PVD), insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The leukocyte and platelet histamine concentration in PVDs was significantly greater than that in controls, IDDMs and NIDDMs. Histamine content of leukocytes and platelets from IDDMs and NIDDMs did not differ from that in control subjects. The higher histamine content of leukocytes and platelets in PVD may lead to a greater release of this amine at sites of vascular endothelial damage. Increased histamine release may increase endothelial permeability and contribute to further vascular injury as observed in experimental models of diabetes and hypercholesterolemia.

Adult↗
PubMed1988

Intraplatelet serotonin in patients with diabetes mellitus and peripheral vascular disease.

Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. Intraplatelet 5-HT content in normal subjects showed an age-related decline (r = -0.45; P less than 0.008), as has been previously demonstrated. The median 5-HT content in platelets of the young normal subjects was 4.36 (range: 3.62-6.79) nmol 10(-9) platelets, while that in the elderly normal subjects was 3.87 (range: 2.8-6.0) nmol 10(-9) platelets and that in young + elderly subjects was 4.05 (range: 2.8-6.8) nmol 10(-9) platelets. The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. The presence of hypertension in DM patients caused a small but significant (P less than 0.05) decrease in intraplatelet 5-HT content, whilst its presence had no effect in PVD patients. In a smaller study, it was established that NIDDM and PVD patients have significantly (P less than 0.002) greater plasma 5-HT concentrations than controls. Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Treatment of hypertension with captopril: preservation of regional blood flow and reduced platelet aggregation.

The BP of 12 patients with essential hypertension was controlled with captopril over a period of three months. Cerebral blood flow, muscle blood flow (anterior tibialis muscle), platelet aggregation and platelet thromboxane A2 release were measured during a baseline drug-free period, and measurements repeated during the treatment phase on achieving BP control, after one and three months. Cerebral blood flow rose during the early phase of treatment and then dropped to baseline levels during chronic therapy. Muscle blood flow, both at rest and following maximal exercise, was unaffected by captopril therapy. Platelet aggregation was diminished during therapy, and this finding was paralleled by a reduction in platelet thromboxane A2 generation. Control of hypertension with maintenance of regional blood flow and beneficial changes in platelet function during treatment with captopril may improve the overall risk profile of hypertensive patients. Inhibition of platelet aggregation and thromboxane A2 release may contribute to the antihypertensive action of captopril and the maintenance of regional blood flow.

Aged↗
PubMed1988

Double-blind placebo-controlled trial of buflomedil in intermittent claudication.

In a double-blind placebo-controlled trial, buflomedil was shown to cause a significant increase both in median claudication provoking time from 63 sec (range: 24-136 sec) to 124 sec (range: 53-261 sec) (p less than 0.01), and in maximum walking distance (MWD) from 169m (range: 157-308 m) to 293 m (range: 107-429 m) (p less than 0.01). The MWD after three months' buflomedil treatment was also significantly (p = 0.05) prolonged when compared with the MWD in the appropriate placebo group. In contrast, treatment with the placebo caused no significant change in these indices. Subjective improvement was observed in 12 out of 14 patients on buflomedil, whilst it occurred in only 6 out of 14 patients on the placebo (p less than 0.05). The clinical improvement was not associated with an increase in the ankle pressure index or a reduction in platelet aggregation and thromboxane A2 release.

Aged↗
PubMed1988

Platelet thromboxane A2 synthesizing capacity is enhanced by fasting but diminished by diabetes mellitus in the rat.

In order to investigate whether the hyperaggregability of platelets in diabetic and starved rats was due to an increase in the inherent capability of these platelets to synthesize thromboxane A2, we assessed the total thromboxane A2 synthesizing capacity of platelets in rats with streptozotocin-induced diabetes and rats which have been semistarved (nine days) or fasted for various periods (24-72 h). Fasting for 48 h or more and semistarvation resulted in highly significant increases in thromboxane A2 synthesizing capacity. Experimental diabetes, however, resulted in a marked diminution in thromboxane A2 synthesizing capacity. This decrease in thromboxane A2 synthesizing capacity was prevented in diabetic rats treated with insulin. We conclude that while the hyperaggregability of starvation is associated with an increase in thromboxane A2 synthesizing capacity, that of diabetes is associated with a fall in this capacity. The decrease of this capacity in diabetic animals can be prevented by insulin treatment. Total thromboxane A2 synthesizing capacity is therefore not a major determinant of either platelet hyperaggregability or of agonist induced platelet thromboxane A2 release.

Animals↗
PubMed1987

Histamine uptake by human platelets.

We have investigated the uptake of histamine by human platelets. Incubations were carried out in platelet rich plasma prepared by using sodium citrate as an anticoagulant at histamine concentrations of 2.5 nmol X 1(-1), with and without stirring, in a platelet aggregometer cuvette at 37 degrees C. Stirring increased platelet histamine uptake significantly. Conventional platelet aggregating agents (e.g. adrenaline) significantly increased platelet histamine uptake at sub-aggregatory concentrations. Histamine uptake by platelets may be a useful index of platelet behaviour when studying the effect of subaggregatory concentrations of platelet agonists in conditions where platelet aggregation is altered, e.g. peripheral vascular disease and diabetes mellitus.

Adult↗
PubMed1987

Platelet hyperaggregability in cystic fibrosis.

Platelet function was investigated in 15 patients with cystic fibrosis (CF) and in ten age-matched controls. Marked hyperaggregability of platelets to adrenaline, collagen and arachidonic acid was observed in platelet rich plasma (PRP) prepared from patients with cystic fibrosis. Thromboxane A2 (TXA2) release from these platelets was also markedly enhanced. Hyperaggregability and increased TXA2 release observed in patients with CF was not due to the higher platelet counts in these patients since hyperaggregability was observed even in those patients whose platelet counts were similar to those in controls. Platelet hyperaggregability and increased thromboxane release in these patients were also independent of their body weight and occurred despite supplementation with vitamin E. Hyperaggregability of platelets in CF may be clinically relevant since it may contribute to the pathogenesis of bronchoconstriction through the release of TXA2 and other bronchoconstrictor platelet products such as serotonin.

Adolescent↗
PubMed1987

Cyclosporine A enhances platelet aggregation.

In view of the reported increase in thromboembolic episodes following cyclosporine A (CyA) therapy, the effect of this drug on platelet aggregation and thromboxane A2 release was investigated. The addition of CyA, at therapeutic concentrations to platelet rich plasma from normal subjects in vitro was found to increase aggregation in response to adrenaline, collagen and ADP. Ingestion of CyA by healthy volunteers was also associated with enhanced platelet aggregation. The CyA-mediated enhancement of aggregation was further enhanced by the addition in vitro of therapeutic concentrations of heparin. Platelets from renal allograft recipients treated with CyA also showed hyperaggregability and increased thromboxane A2 release, which were most marked at "peak" plasma CyA concentration and less so at "trough" concentrations. Platelet hyperaggregability in renal allograft patients on long-term CyA therapy tended to revert towards normal following the replacement of CyA with azathioprine. Hypertensive patients with renal allografts on nifedipine therapy had normal platelet function and thromboxane release in spite of CyA therapy. These observations suggest that CyA-mediated platelet activation may contribute to the pathogenesis of the thromboembolic phenomena associated with the use of this drug. The increased release of thromboxane A2 (a vasoconstrictor) may also play a role in mediating CyA-related nephrotoxicity.

Adult↗
PubMed1987

Ethanol ingestion inhibits human whole blood platelet impedance aggregation.

The authors investigated the effect of ethanol on platelet impedance aggregation in whole blood (WB-PIA). Healthy moderate drinkers were given ethanol, 1 mL/kg body weight, to drink. Thirty minutes after ingestion of ethanol, WB-PIA was significantly inhibited when compared with baseline values. There was no significant inhibition when the same volunteers ingested water instead of ethanol. These observations suggest that WB-PIA is a sensitive technic for the detection of the effect of ethanol on platelets. These findings also support the view that blood ethanol levels achievable during social drinking impair platelet function, thus possibly accounting, at least in part, for the reported "protection" from ischemic heart disease in moderate drinkers. The sensitivity of human platelets to the inhibitory effect of ethanol suggests that continued drinking will adversely influence the incidence of initial bleeds and of rebleeding in gastrointestinal hemorrhage associated with alcoholism.

Adult↗
PubMed1987

Effect of heparin and contrast medium on platelet function during routine cardiac catheterisation.

Platelet function was studied during coronary angiography of patients complaining of chest pain. The following changes occurred 5 min after injecting 100 IU.kg-1 body weight of a conventional high molecular weight heparin: (a) a significant fall in platelet count; (b) a significant enhancement of platelet aggregation in platelet rich plasma (turbidometric technique) and in whole blood (platelet aggregation technique); and (c) significantly enhanced release of platelet thromboxane A2, a vasoconstrictor. These changes tended to reverse towards baseline values 5 min after injecting a contrast medium (Conray 420), which was found to inhibit platelet aggregation. Thus heparinisation with a high molecular weight heparin seems to cause pronounced activation of platelets in patients undergoing coronary angiography, and this may contribute to the pathogenesis of cardiac ischaemia that may occur during this procedure. Since coronary artery bypass surgery in similar patients involves the use of heparin at much higher doses without the concomitant use of an antiaggregatory contrast medium, it is possible that platelet hyperaggregability may contribute to the well documented ischaemic brain injury associated with this form of surgery. Furthermore, the use of high molecular weight heparin after successful coronary angioplasty or thrombosis may influence the incidence of reocclusion. These findings therefore suggest that low molecular weight heparinoids should be evaluated in these situations since these anticoagulants are only weak activators of platelet aggregation.

Adult↗