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T Pavel

Publications and source records attributed to T Pavel.

15 recordsLinked to original sources
PubMedDate not supplied

Phagocytic response in rats following chemical sympathectomy with 6-hydroxydopamine.

Wistar rats were injected i.p. at 2, 4 and 7 days after birth with 6-OHDA (50 mg/kg). At maturity the phagocytic response of neutrophils was elicited by Escherichia coli (EC) lipopolysaccharide (LPS). Before and at 3 and 24 hours after the injection of LPS (1 mg/kg i.v.) the leucocyte (L) and neutrophil (N) counts and the phagocytic activity of N in blood against EC have been tested. In controls (6 female and 7 male rats) the number of N increases significantly after 3 h. The L and N responses were similar in controls and in treated (SyX) animals. In controls the percentage of phagocytic active N(PA) and the number of bacteria incorporated by 100 n(IB) shows significant rises at 3 h. In the SyX groups (7 females and 7 males) PA does not increase; the IB decreases significantly in females at 3 and 24 h. In conclusion chemical sympathectomy depresses the PR to LPS in rats; this suggests a stimulatory action of the sympathetic system on the phagocytic immune reaction. An immunological sexual dimorphism exists.

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PubMedDate not supplied

A metaanalysis of certain erythropoietin characteristics established before recombinant EPO was obtained.

Beginning with 1975, our group has performed some studies using an erythropoietin (EPO ) extract prepared according to an original technique from sera of anemic rabbits. Our results have contributed to the understanding of the glycoproteinic nature of this extract as well as of some of its biological features. These results were confirmed only after 1985, when recombinant EPO was obtained. The aim of this study is to emphasize some of our priorities, controversial at that time. We have shown the radioprotective effect of an EPO extract, in correlation with red cell proliferation and with an increased rate of nucleic acid metabolism and bone marrow blood flow. Consequently, we proposed the investigation of the bone marrow function using EPO. Our results are correlated with recent data obtained with recombinant EPO. They refer to the ability of EPO to prevent apoptosis, its antioxidant effects, and its ability to modulate the sympathoadrenal response to hypoxia.

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PubMedDate not supplied

Erythropoietin binding to the red cell membranes.

Some characteristics of Epo binding to the red cell membranes were investigated in a system in which the hormone was added to a suspension of cells in a mixture of normal serum phosphate buffered saline (1:7 (V/V)), testing the unbound Epo. Epo binding shows a gradual decrease during the maturation of red cells (0.15 U/ml packed erythrocytes, 0.285 U/ml reticulocytes and 0.375 U/ml erythroblasts from a total of 1.4 U/ml). The binding is also time- and pH-dependent. The amounts of Epo bound within 60 min are independent of temperature, but after 120 min a dissociation of the hormone-receptor complex occurred at 23 and 37 degrees; at 4 degrees C the binding continue, although at a very low rate. RBC membranes bound the hormone at pH 7.8-8 and release it at pH 6.5. The "in vivo" stimulation of beta receptors with isoproterenol increases the erythropoietic response caused by Epo, suggesting a possible relation with the adenylcyclase system.

Anemia↗
PubMedDate not supplied

Influence of some inhibitors and activators of fibrinolysis on transcapillary transport of macromolecules.

The RISA transcapillary transport in the posterior paw was followed up under the influence of some substances inhibiting and activating fibrinolysis (Trasylol, EACA and Streptokinase and Salyrgan, respectively) in 11 dogs under narcosis with chloralose and the cannulation of the lymphatics in the popliteal space. It was found that EACA inhibits the transcapillary RISA transport and streptokinase activates it. Trasylol and Salyrgan produced no changes, the slope of the vanishing curve of the tracer being identical with that of the controls.

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PubMedDate not supplied

The renin-angiotensin system and the effect of propranolol upon the cerebral cortical and hypothalamic circulation in hypoxia.

The regulatory mechanisms of the cerebral blood flow have preoccupied the physiology department of Cluj since the end of the 4th decade. These studies continued over the last years. The researches progressed from the studies of regulation by blood pressure changes to the nervous regulation and to the metabolic one. This paper's subject is the renin-angiotensin and adrenalin system influence on the changes of cerebral blood flow during the general hypoxic hypoxia and cephalic ischemia. Experiments were performed in 10 dogs anaesthetised with a mixture of chloralose, urethan and morphine. Hypoxic hypoxia was obtained by breathing a mixture of 11% oxygen in nitrogen, in a closed system and cerebral ischemic hypoxia by partial compression of the carotid arteries, after the ligation of the vertebral and thyroid arteries. The arterial blood pressure and the cerebral and hypothalamic blood flow, measured with the heated thermoelement, were registered. The plasma renin activity was tested radioimmunologically before, at 1.5 min, 5, 10 and 15 min, after the beginning of hypoxia. In ischemic hypoxia the experiment was repeated after venous perfusion with propranolol (0.6 mg/kg/h). The systemic blood pressure increased in both forms of hypoxia. The cortical and hypothalamic blood flow increased with the systemic arterial blood pressure. The hypothalamic blood flow remained stable or diminished a little. Propranolol increased the cerebral blood flow during ischemic hypoxia up to 300%. The i.v. administration of angiotensin (1-5 mg/kg) increased the cortical flow, while the hypothalamic flow remained self-regulated. Plasma renin activity increased more in general hypoxic hypoxia, than in cephalic ischemic hypoxia. After propranolol the increase was higher in this hypoxia. Propranolol produced a major activation of the renin-angiotensin system and of the cortical blood flow in ischemic cephalic hypoxia, the renin-angiotensin system being located in the cerebral structure. As well high doses of angiotensin produced cerebral vasodilatation in small cerebral vessels. This effect was found in our experiments in the cortical blood flow too. Our results indicate a beneficial propranolol effect on cortical circulation in ischemic hypoxia.

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