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Biomedical subjects

D A Chamone

Publications and source records attributed to D A Chamone.

At least 37 records · Page 2Linked to original sources
PubMed1992

Papaverine inhibits human platelet aggregation induced by ADP.

1. The in vitro and ex vivo effect of therapeutic levels of papaverine on human platelet aggregation induced by 3-5 microM adenosine-5'-diphosphate (ADP) was evaluated in platelet-rich plasma (PRP) by photometric and impedance aggregometry, and in whole blood by impedance aggregometry. 2. Platelet aggregation induced by 3-5 microM ADP in whole blood was significantly inhibited by 5.32 and 10.64 microM papaverine in vitro. This effect was also observed in PRP enriched with erythrocytes but not in PRP alone or enriched with leukocytes. 3. Papaverine (5.32 microM) significantly enhanced the antiplatelet activity of adenosine (0.75 microM) in human whole blood, an effect that was not observed in PRP. 4. A single oral dose of 100 mg papaverine hydrochloride, given to eight healthy human volunteers 1 h before the platelet aggregation evaluation, significantly inhibited the platelet aggregation induced by 3-5 microM ADP in whole blood. This effect was not observed in PRP. 5. Oral administration of the same dose at 8-h intervals (10 times) to seven additional healthy human volunteers led to a significant negative correlation (r = -0.55, P < 0.01) between the slope of platelet aggregation in whole blood and plasma papaverine levels (0.12-0.75 microM). 6. Papaverine and adenosine, alone or together, had no in vitro effect on whole blood platelet aggregation of male Wistar rats measured by impedance aggregometry. 7. These results suggest that papaverine inhibits human platelet aggregation in whole blood by an interaction with red blood cells.

Adenosine Diphosphate↗
PubMed1992

Increased plasma removal of microemulsions resembling the lipid phase of low-density lipoproteins (LDL) in patients with acute myeloid leukemia: a possible new strategy for the treatment of the disease.

A microemulsion of lipid composition resembling low-density lipoprotein (LDL), but devoid of apolipoproteins and labeled with [14C]-cholesteryl oleate was injected into 16 healthy subjects and into 15 patients with acute myeloid leukemia (AML). Removal from plasma of the lipid label was higher in the leukemic group compared to healthy subjects in terms of fractional clearance rate (0.185 +/- 0.205 and 0.080 +/- 0.030 h-1, respectively, P < 0.03). When the emulsion was again injected into 10 of the AML patients after complete hematological remission, the fractional clearance rate of cholesteryl ester was reduced to one third of the value observed prior to treatment (0.061 +/- 0.038 h-1) and was not different from that obtained for the healthy subjects. Also, in untreated AML patients, serum LDL-cholesterol levels inversely correlated with the values of fractional clearance rate of the microemulsion. This correlation was no longer observed after treatment. These data suggest that the LDL-like microemulsion was selectively taken up by the neoplastic cells presumably by interaction with LDL receptors. Therefore, microemulsions may function as potential carriers for anticancer drugs that are targeted to tumor cells for patients with acute myeloid leukemia. Unlike native LDL, microemulsions are suitable for utilization in routine clinical practice.

Acute Disease↗
PubMed1991

An aqueous extract of guaraná (Paullinia cupana) decreases platelet thromboxane synthesis.

The effects of an aqueous extract of guaraná (Paullinia cupana) on rabbit platelet aggregation and thromboxane synthesis were examined. The guaraná extract (100 mg/ml) and fractions separated by TLC (origin and xanthines) decreased platelet aggregation (37, 27 and 31% of control values, respectively) and platelet thromboxane formation from [14C]-arachidonic acid (78, 70 and 50% of control values, respectively). The decreased thromboxane synthesis could be responsible, at least in part, for the antiaggregatory action of guaraná.

Animals↗
PubMed1990

Aggregation of platelets in whole blood from children with pulmonary hypertension.

The response of aggregation of platelets to adenosine diphosphate (7.5-120 microM) and collagen (1.25 micrograms/ml) was assessed in whole blood (impedance method) in 10 children with pulmonary hypertension (hematocrit range, 42 to 71%). The response to collagen was normal (9.08 +/- 3.47 vs. 10.36 +/- 1.86 ohms in controls, P = NS) while there was a decreased response to adenosine diphosphate (6.98 +/- 3.83 vs. 11.21 +/- 2.02 ohms, P less than 0.01), in spite of high concentrations of the inducer. Lowering the hematocrit in vitro to 40% with autologous platelet-rich plasma resulted in a rise in the platelet count from 171 +/- 63 to 225 +/- 84 x 10(9) platelets/1 (P less than 0.001) and a significant increase in the response to adenosine diphosphate from 6.98 +/- 3.83 to 9.89 +/- 3.66 ohms (P less than 0.02). As in the baseline condition, high concentrations of adenosine diphosphate were required. The response to collagen did not change significantly. The results indicate that aggregatory response of platelets is relatively preserved in these children. The decreased response to adenosine diphosphate may be a result of a low count and interference of red cells on the accretion of platelets on the electrodes. Because high concentrations of adenosine diphosphate were still required after hemodilution to achieve an aggregatory response close to normal, we speculate that leakage of endogenous adenosine diphosphate from red cells may have accounted for partial activation of the platelets, resulting in a relative refractory state to in vitro stimulation.

Adenosine Diphosphate↗
PubMed1990

Plasma anticoagulant system in patients with pulmonary hypertension.

Adults with pulmonary hypertension and polycythemia (N = 22) have low levels of plasma antithrombin III (84 +/- 18 vs 98 +/- 13% for controls, N = 35, P less than 0.005) and protein C (66 +/- 21 vs 125 +/- 30%, N = 8, P less than 0.0002) but normal levels of total protein S. Data are reported as means +/- SD and percent normal values obtained for pooled plasma from normal healthy adults. Children with the same disorder (N = 6) also had low protein C levels (66 +/- 16 vs 85 +/- 5%, P less than 0.025). Total protein S was normal for children, but free protein S was decreased (66 +/- 13 vs 91 +/- 23%, P less than 0.025). Since the levels observed in these patients are above those reported for congenital deficiencies, the reduction in plasma levels of anticoagulant proteins may be the result of chronic intravascular coagulation. Furthermore, normal levels of plasminogen and fibrin degradation products suggest a localized disorder or an acquired decrease in fibrinolytic activity.

Adolescent↗
PubMed1989

PAF-acether, superoxide anion and beta-glucuronidase as parameters of polymorphonuclear cell activation associated with cardiac surgery and cardiopulmonary bypass.

1. Seven patients submitted to myocardial revascularization surgery with cardiopulmonary bypass were studied. Blood samples were obtained immediately before and 24 h after surgery. The parameters studied were the production of platelet activating factor (PAF-acether) and superoxide anion, cellular beta-glucuronidase activity as well as polymorphonuclear cell (PMN) and platelet counts. 2. Twenty-four h after surgery, there was a 54% decrease in platelet number (P less than 0.005), a 121% increase in PMN number (P less than 0.005), a 353% increase in PAF-acether (P less than 0.01), a 211% increase in superoxide anion (O2-) and a 104% increase in beta-glucuronidase (P less than 0.05) levels when compared with the pre-surgery levels. 3. The present results indicate that PMN are more reactive after surgery with cardiopulmonary bypass.

Blood Cell Count↗
PubMed1988

Deficient release of prostacyclin-like activity by rat stomach under stress.

It is known that a confinement procedure will promote histological alterations in the gastric mucosa of rats. It is our hypothesis that, under these conditions, there should be an alteration in prostacyclin metabolism. Our findings corroborate this idea, which makes us suppose that the deficient release of prostacyclin-like activity by the rat's stomach may play an important role in gastric mucosa vitality and in its consequent damage.

Animals↗
PubMed1988

Platelet regeneration time: a statistical approach.

The determination of platelet regeneration half-time (PRT t1/2) by measuring malondialdehyde after intake of acetylsalicylic acid is a simple nonisotopic method for the estimation of platelet survival. There is no available information concerning the populational distribution of PRT t1/2. Consequently, there is controversy about the utilization of parametric or nonparametric statistical tests in studies of PRT. In the present study, we demonstrate the closeness of the fit of log PRT t1/2 to the normal (Gaussian) distribution.

Aspirin↗
PubMed1987

Unexpected low prevalence of delta antibodies in the east Amazon region and São Paulo: evidence for regional differences in the epidemiology of delta hepatitis virus within Brazil.

Antibodies (anti-HD) to hepatitis delta virus (HDV) were tested by radioimmunoassay in 207 human serum samples from the eastern Amazon (states of Pará and Amapá) and São Paulo, Brazil. 42 Amazon HBsAg asymptomatic carriers were negative for anti-HD. 84 São Paulo HBsAg asymptomatic carriers were also negative. Among the 81 HBsAg patients from São Paulo with different liver diseases, only one had anti-HD. Liver biopsy of this chronic active hepatitis case was positive for HBsAg, HBcAg and HDAg in liver, by an immunoperoxidase technique. The low prevalence of HDV infections in São Paulo and eastern Amazon was unexpected and contrasts with the recent reports of high prevalence in the western Amazon region. Such regional differences emphasize the need for extensive and precise worldwide epidemiological studies of HDV.

Adult↗
PubMed1982

Reversible deficient prostacyclin release in childhood hemolytic uremic syndrome.

Plasma was taken from infants and children with acute hemolytic uremic syndrome (HUS) or following remission from this disease. The capacity of these plasma to stimulate release of prostacyclin-like activity from "exhausted" rat aorta rings was studied. Plasma from 10 out 12 children in the acute phase of HUS, but from only 3 out of 15 children following remission failed to stimulate prostacyclin release (p less than 0.005). These findings suggest that, for the majority of children, the plasma abnormality in the acute phase of the disease is acquired rather than congenital.

Acute Disease↗
PubMed1981

The effect of clinical prostacyclin infusions in advanced arterial disease on platelet function and plasma 6-keto PGF1 alpha levels.

We have infused synthetic prostacyclin (PGI2) continuously for approximately 72 h at the maximum tolerated dose (ranging from 5 to 60 ng/kg/min) into nine patients with advanced arterial disease. Prior to the infusion seven out of nine patients had spontaneous platelet aggregation and five out of six patients tested had an abnormal circulating platelet aggregate ratio. During the infusion only one patient still had spontaneous aggregation and all the abnormal circulating platelet aggregate ratios returned to the normal range. However, none of the patients showed any suppression of ADP induced aggregation. The level of exogenous PGI2 required in vitro prior to the infusion to completely inhibit ADP induced aggregation was 5-10 ng/ml in three of the four patients tested. Ten healthy adults showed complete inhibition with 1 ng/ml of PGI2. It appears that the platelets of some patients with arterial disease are more resistant to the anti-aggregating properties of PGI2. Plasma 6-keto PGF1 alpha levels, measured by radioimmunoassay, were within the normal range (100-381 pg/ml) in all but one of the patients prior to the infusion. During the infusion plasma 6-keto PGF1 alpha levels rose proportionally to the infusion dose. After stopping the infusion 6-keto PGF1 alpha levels declined according to an exponential process with a half life of 18-29 min, prolonged to 47 min in one patient who was anuric. The linear increase in 6-keto PGF1 alpha levels suggests this as a useful indicator of increased circulating PGI2.

Adult↗
PubMed1981

Familial bleeding tendency with partial platelet thromboxane synthetase deficiency: reorientation of cyclic endoperoxide metabolism.

Three family members from three successive generations presented with a moderate bleeding tendency and a functional platelet defect. They had absent aggregation with arachidonic acid (0.6--3 microM), reversible aggregation with ADP (4 microgram) and cyclic endoperoxide analogues, single wave aggregation only with adrenaline (5.4 microgram) and a prolonged template bleeding time (> min). Malondialdehyde formation was reduced after N-ethylmaleimide stimulation (2--6 nmol/10(9) platelets; control values 8--12 nmol) and serum thromboxane B2 values were reduced (33--101 ng/ml; control values 200--700 ng/ml). When the platelets were incubated with [3H]arachidonic acid the final metabolite of the lipoxygenase pathway (HETE) was produced in normal amounts but the production of thromboxane B2 and HHT was decreased whereas prostaglandin F2a, and E2 and probably D2 were increased. Evidence for enhanced production of prostaglandin D2 was also provided by the rise in the patient's platelet cyclic AMP levels following stimulation with arachidonic acid. The patient's washed platelets stimulated the production of 6-keto PGF 1a by aspirin-pretreated cultured bovine endothelial cells. The plasma levels of 6-keto PGF1a (439--703 pg/ml; normal 181 +/- 46 pg/ml) were raised. The decreased production of thromboxane B2, HHT and malondialdehyde and increased formation of prostaglandin F2a, E2, D2 and of 6-keto PGF1a are compatible with a partial platelet thromboxane synthetase deficiency and reorientation of cyclic endoperoxide metabolism. The markedly prolonged bleeding time would result not only from reduced formation of thromboxane A2 but also from increased production of the aggregation inhibiting prostaglandins PGI2 and PGD2.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1981

Increased release of vascular prostacyclin-like activity after long-term treatment of diabetic rats with Bay g 6575.

10 male Wistar rats were made diabetic by an intravenous injection of streptozotocin. 10 sex and age-matched rats served as control animals. 5 of the diabetic and 5 of the control rats received Bay g 6575 (20 mg/kg orally) for 6 days each week throughout the whole study period (9-11 months). From these animals aorta was removed for prostacyclin bioassay based upon its platelet aggregation inhibitory effect. The diabetic rats treated with Bay g 6575 released significantly more prostacyclin than the controls (p less than 0.005). Our study suggests further experiments in other animal models more susceptible to diabetic vascular lesions than the rat model to evaluate the possible beneficial role of the treatment with Bay g 6575.

Adenoma↗