Biomedical subjects
Publications and source records attributed to L Caprino.
The effects of cadmium and mercury on ADP breakdown by vessel walls were investigated. These metals reduce the ADP clearance promoted by arterial tissue. This effect could be attributed to the inhibition of vessel wall ADP-ase enzyme, which plays an important role in the genesis of thrombotic phenomena.
The method developed to evaluate the hemocompatibility of artificial materials involves the determination of thromboxane production during the clotting of rabbit blood, in test tubes of different materials. The concentration of serum TXB2 obtained after incubation of whole blood in glass test tubes, for 40 min at 37 degrees C, averaged 416.8 +/- 23.3 ng/ml (mean +/- SE). Polymethylpentene, recognised as having a relatively poor blood compatibility, elicited 309.5 +/- 17.2 ng/ml of serum TXB2, while silicone and Avcothane, considered of better hemocompatibility, showed thromboxane levels of 276.2 +/- 28.2 and 222.9 +/- 31.5 ng/ml, respectively. These values validate the usefulness of the proposed method as a preliminary in vitro screening test of artificial materials intended for biomedical application.
Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) is a weak anti-inflammatory drug and has been shown to inhibit thrombus formation following electrically stimulated vascular damage in the microcirculation of the hamster cheek pouch. The drug was found to inhibit thromboxane A2 (TXA2) production ex vivo as determined by radioimmunoassay (RIA) and to reversibly antagonise the effect of TXA2 on smooth vascular tissue. However, in contrast to acetylsalicylic acid (ASA), it does not inhibit vessel cyclooxygenase. The apparent vascular protective effect of ditazole could not be ascribed to an enhanced production of vascular prostacyclin (PGI2) since the latter, when estimated ex vivo by RIA, was not enhanced following oral treatment with the drug. It is suggested that the mode-of-action of ditazole may be different from the cyclo-oxygenase/PG synthetase blocking action of most other non-steroidal anti-inflammatory drugs.
Mercuric chloride [25-50 micrograms/ml platelet-rich plasma (PRP)] lowers the threshold concentration of arachidonic acid (AA) required for triggering rabbit platelet aggregation and causes a marked increase of thromboxane production. The metal, added as HgCl2, does not modify (50 micrograms/ml PRP) or block (100 micrograms/ml PRP) the platelet aggregation wave induced by a normal aggregating dose of AA. Whether or not AA-induced platelet aggregation takes place, a large increase in thromboxane production is observed. Methyl mercury, assayed as reference drug, induces platelet aggregation and a significant increase of thromboxane levels. Finally, HgCl2 and methyl mercury, in a concentration range of 0.125-0.5 micrograms/microliters in the incubation liquid, induce an increased prostacyclin release from rat aortic tissue.
The intravenous LD50 of the hypothalamic tetradecapeptide somatostatin was determined in mice and rats of both sexes. It was found that somatostatin has a sex-related toxicity both in mice and rats. The interaction of low and high doses of peptide with the LD50s of two central nervous system (CNS) drugs, namely pentobarbital and strychnine, was also studied in male and female mice. Differential effects were observed as follows: a very low dose (0.1 mg/kg) of somatostatin does not affect the toxicity of these compounds, whereas the injection of 1 mg/kg of peptide increased pentobarbital toxicity and decreased the toxicity of strychnine. However, an increase in the toxicity of both substances was obtained with very high non-lethal doses of peptide (20 and 30 mg/kg, in female and male mice, respectively).
The effects of urokinase on ADP breakdown by vessel-wall, platelet aggregation and the related prostaglandin system "in vitro" were investigated. It is confirmed that urokinase does not induce platelet aggregation both in humans and rabbits "in vitro". Conversely, in high concentrations, urokinase inhibits ADP-induced platelet aggregation in human and rabbit platelet-rich plasma. No effects were observed on rabbit platelet thromboxane A2 release and on rat vascular prostacyclin production, both measured by radioimmunoassay of thromboxane B2 and 6-keto-F1 alpha prostaglandin, respectively. Moreover, the incubation of urokinase with vascular endothelium resulted in an increased disappearance rate.
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The age-related changes of different T-cell activities in guinea pigs and the effect of Thymostimulin (TS), a thymus extract, on the immunocompetence of these cells was studied. Mitogen-induced proliferation of peripheral blood lymphocytes was increased by TS in vitro. The intraperitoneal administration of TS (5 mg/kg) to aged animals restored the helper function of T lymphocytes and enhanced the reactivity to mitogens of both peripheral blood lymphocytes and spleen lymphocytes. The data obtained suggest that as in other species, there is an age-associated decline of immunological response, in guinea pigs too, probably due to a deficiency of thymic hormone(s) and that TS could correct this deficiency.
The immunocompetence of newborn guinea pigs was evaluated in comparison with that of adults. The capacity of spleen cells from neonatal guinea pigs to produce antibodies to SRBC was found to be reduced, while no differences were observed in the capacity of those cells to respond to mitogenic stimulation or to form E rosettes with rabbit red blood cells. The in vivo treatment of newborn animals with a thymic factor (TS) induced an increase in the number of antibody-producing cells and an increase in the response to mitogenic stimulation but no variation in the number of rosette-forming cells. The effect of TS on both responses to SRBC and to mitogenic stimulation, was dose dependent.
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The effects of acetylsalicylic acid (ASA) indometacin and ditazole on prostacyclin production from rabbit aortic rings were studied in comparison to their inhibiting activity on platelet aggregation. The result were expressed as the ratio between the drug dose inhibiting by 50% prostacycline production and the minimum oral antiaggregating dose. The following ratios were found: 2.4 for ASA, 7.3 for indometacin and 20.4 for ditazole.
The atherosclerotic condition is associated with a reduction of PGI2 synthesis; moreover, in the presence of elevated serum cholesterol levels, pressor responses to norepinephrine are potentiated. In order to verify if a complete inhibition of PGI2 production affects the vascular reactivity, it was assayed two cycloxygenase inhibitors (lysine acetylsalicylate and indomethacin) in rats. The two drugs significantly potentiated the blood pressure responses to norepinephrine, and completely inhibited PGI2-like substances production by arterial rings. The prostacyclin infusion (15 ng/kg/min, i.v.) completely reversed such potentiation, without any major modification in the basal blood pressure values. These results show that PGI2 production is responsible for vascular tone modulation and may partially explain the altered vascular reactivity in the atherosclerotic condition.
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The process of thrombus formation, as a consequence of the interaction of artificial surfaces with blood, is related to the activation of blood platelets. A simple ex vivo method, which is suitable for the evaluation of the platelet-surface interaction is described. This method has been used to compare the haemocompatibility of several artificial materials, including nylon-6, Silastic and pyrolytic carbon.
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