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At least 469 records · Page 26Linked to original sources
PubMed1988

Intravenous injections of PAF-acether induce platelet aggregation in rats.

The mechanism of rat thrombocytopenia induced by i.v. injections of platelet-activating factor (PAF-acether) was investigated. Platelet counts performed after diluting the blood samples in 1% formalin in saline showed that PAF-acether (6 micrograms/kg i.v.) induced a significant thrombocytopenia in rats, which peaked within 1 h, followed by a drastic increase of platelet counts at 4 h and a return to basal levels at 24 h. At this time, it was not possible to induce thrombocytopenia with a second challenge with PAF-acether, indicating a clear state of desensitization which disappeared within five days after the first injection of PAF-acether. The pretreatment with the specific PAF-acether receptor antagonist, BN 52021 (2.5-15 mg/kg), 48740 RP (6-25 mg/kg) and WEB 2086 (0.25-1 mg/kg) blocked the thrombocytopenia dose dependently. The lipoxygenase inhibitor nordihydroguaiaretic acid, at 25-100 mg/kg, was also effective against the thrombocytopenia induced by PAF-acether, reinforcing the potential involvement of arachidonic acid derivatives in this process. Adrenal hormones may modulate this process, since adrenalectomized animals responded to PAF-acether with exacerbated thrombocytopenia. No reduction in the platelet counts was noted when the blood was diluted in formalin-free saline, indicating that unstable aggregates were formed in vivo, which tended to resolve in vitro. Our results suggest that the thrombocytopenia induced in rats by PAF results from a reversible process of intravascular platelet aggregation, probably following the secretion of platelet-activating substances released by a first-hit blood cell.

Adrenalectomy↗
PubMed1988

The effect of intravenously injected beta very low density lipoprotein on small and large arterial injuries.

A series of daily injections of beta very low density lipoprotein (beta-VLDL) was administered over 4-5 days to rabbits whose arteries contained either experimental circumferential lesions or areas of intimal thickening. The circumferential lesions were similar to those that occur spontaneously and were produced by the application of longitudinal tension. The intimal thickening was produced by denuding the endothelium with a balloon catheter. Over the period of injection of beta-VLDL the plasma cholesterol levels rose in a pulse-like manner from 60 to 100 mg/dl. Following cessation of injections the cholesterol levels initially rose further and then decreased to normal levels within 4 weeks. Injections of beta-VLDL, commencing 1-2 days after production of the circumferential lesions, resulted in an increase in the number of mononuclear leukocytes (primarily macrophages) and in a moderate accumulation of lipid by these cells and the medial smooth muscle cells. If the injections were started 14 days postinjury there was some accumulation of lipid in the large lesions but none in small lesions. There was no lipid accumulation in any lesions if the beta-VLDL was administered 3 months postinjury or if the animals were injected 2 days after injury and examined 3 months later. A very slight accumulation of lipid occurred in the intimal thickening, or neo-intima, following a series of beta-VLDL injections given to rabbits 2 or 6 weeks after balloon catheter injury. The series of injections produced a significant increase in the number of mononuclear leukocyte profiles per area of the neo-intima, suggesting an increased infiltration of these cells into the injured artery. These results suggest that a small transient increase in the plasma concentration of cholesterol-carrying lipoproteins may lead to increased infiltration of mononuclear leukocytes into areas of intimal thickening or areas of "spontaneously occurring" injury.

Animals↗
PubMed1983

The radiation dose to man following the intravenous injection of radiosulphate (Na2(35)SO4).

An estimation of the radiation dose to mans' testes, the critical organ, for radiosulphate (Na2(35)SO4) has been made by a combination of studies on rats and human volunteers. The radiation dose to rats testes and the rate of disappearance of radiosulphate from the blood and urine of humans have been increased. The calculated radiation dose of 7.7 muGy/MBq to mans' testes is lower than previously reported.

Aged↗
PubMed1986

Hypotensive effect in dogs and rats of intravenous injections of the alpha 1-adrenoreceptor antagonist benoxathian.

The hypotensive effect of the alpha 1-adrenoreceptor antagonist benoxathian has been evaluated in rats and dogs, in comparison to that evoked by WB 4101 and prazosin. In anaesthetized dogs, i.v. injection of benoxathian (25-100 micrograms/kg), WB 4101 (5-25 micrograms/kg) and prazosin (50 micrograms/kg) produced an immediate fall in diastolic blood pressure, which reached a maximum at about 30 sec after drug administration. Whereas the hypotensive effect of prazosin persisted up to 3 hr following injection, the effect of both benoxathian and WB 4101 completely disappeared after 30-60 min. The hypotensive effect of benoxathian was dose-dependent. Pressor responses to i.v. noradrenaline (5 micrograms/kg), adrenaline (5 micrograms/kg) and phenylephrine (20 micrograms/kg) were markedly inhibited (60-75%) by benoxathian (100 micrograms/kg) whilst the pressor response to angiotensin II (0.05 micrograms/kg) was not reduced, but indeed slightly increased. The hypotensive effect of benoxathian (100 micrograms/kg) was abolished following pre-treatment with prazosin (50 micrograms/kg) or hexamethonium (1000 micrograms/kg). In anaesthetized rats similar results were obtained although recovery in blood pressure from the initial drop after i.v. injection of the drugs was slower than in dogs. Benoxathian was slightly more toxic than WB 4101 in rats. In conclusion, present findings show that benoxathian causes a profound hypotensive effect in dogs and in rats through postsynaptic alpha-adrenoreceptor blockade; however its effect, as well as that of WB 4101, is shorter lasting than that of prazosin.

Adrenergic alpha-Antagonists↗