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Biomedical subjects

P Lechat

Publications and source records attributed to P Lechat.

At least 181 records · Page 10Linked to original sources
PubMed1982

Interactions between the autonomic nervous system and the cardiovascular effects of ouabain in guinea-pigs.

Anaesthetized guinea-pigs were intoxicated with an intravenous infusion of ouabain. This infusion induced a marked pressor response which was reduced in bilaterally adrenalectomized or pithed animals. Ouabain produced initial bradyarrhythmias in 60% of guinea-pigs. Bilateral vagotomy or pretreatment with atropine abolished the bradyarrhythmias and sensitized the animals to the arrhythmic effects of ouabain. Pithing or beta-adrenoceptor blockade reduced the potency of ouabain for producing arrhythmias, but bilateral adrenalectomy did not give protection. Preferential alpha 2-adrenoceptor stimulation with clonidine (10-300 micrograms . kg-1 i.v.) also reduced the arrhythmogenic effects of ouabain, whereas no protection was found with St 91, a clonidine related compound which does not cross the blood-brain barrier. The effect of clonidine was antagonized by piperoxan. Preferential alpha 2-adrenoceptor blockade with piperoxan (6 mg . kg-1 i.v.) did not change the pressor response to ouabain, but sensitized the animals to the arrhythmogenic effects of ouabain. In contrast, the preferential alpha 1-antagonistic agent AR-C 239 (0.3 mg . kg-1 i.v.) abolished the pressor response to ouabain and in addition increased the dose of ouabain required to produced ventricular premature beats and ventricular fibrillation. These experiments indicate: (i) that ouabain produces in guinea-pigs a pressor response which seems to be due to catecholamine release from the adrenal medulla probably by an action on the central nervous system; (ii) that the ventricular arrhythmias induced by ouabain are due in part to stimulation of the central nervous system leading to an increase in beta-adrenoceptor activity; (iii) that central alpha-adrenoceptors appear to be involved in the arrhythmogenic effects of ouabain, as clonidine reduced these effects. On the other hand piperoxan, a preferential alpha 2-adrenoceptor antagonist did not change the pressor response to ouabain and increased the arrhythmogenic effects whereas AR-C 239 had opposite effects.

Adrenalectomy↗
PubMed1982

Effect of sodium cis-beta-4-methoxybenzoyl-beta-bromacrylate (Cytembena) on HeLa cell kinetics.

The treatment of HeLa cells with various concentrations of sodium beta-4-methoxybenzoyl-beta-bromacrylate (Cytembena) results in inhibition of growth and modification of cell cycle distribution. These phenomena were observed at concentrations between 7.5 x 10(-5) and 2.5 x 10(-5) M. The estimation of DNA content by flow cytometry showed an important shift in the distribution of cycling cells with a relative decrease of G0 + G1 cells and a striking accumulation of G2 + M cells. According to our experimental conditions, the blocking up in G2 + M is irreversible at 7.5 and 5 x 10(-5) M.

Acrylates↗
PubMed1982

Reversibility of kanamycin-induced neuromuscular and cardiovascular depressions by 4-aminopyridine, in comparison with neostigmine.

Antagonistic actions of 4-aminopyridine (4-AP) and neostigmine methylsulfate (NSG) on the neuromuscular and cardiovascular depressions by kanamycin (KM) were studied in urethane anesthetized rats, in comparison with D-tubocurarine (D-Tc). Measured parameters were indirectly elicited twitch of tibialis anterior muscle, mean arterial pressure and heart rate. All parameters were progressively depressed by continual infusions (0.2 ml/min) of KM (70 mg/ml) and D-Tc (10 microgram/ml). 4-AP 2.8 mg/kg s.c. significantly antagonized these depressive actions of both of D-Tc and KM, while NSG 0.1 mg/kg s.c. significantly antagonized only those of D-Tc and more strongly than 4-AP did in cardiovascular depression. 4-AP could antagonize the complete neuromuscular blockade and lethality of KM to the equilevel of conscious rats and those of D-Tc to 2.78 and 1.78 time doses of conscious rats in the complete neuromuscular blocking dose and lethal dose respectively. These results suggest that the antagonistic action of 4-AP results from its facilitation activity in the neurotransmitter release and its augmentative activity in the muscle contractility and also indicate a possibility that 4-AP can be used as a relief agent for the neuromuscular and/or cardiovascular depressions induced by some aminoglycoside antibiotics and nondepolarizing neuromuscular blocking drug in the clinical aspect.

4-Aminopyridine↗
PubMed1981

Lymphokine-induced macrophage aggregation: involvement of cyclic-GMP and microtubules.

Human lymphokine (LK) is known to induce guinea pig macrophage aggregation. This effect can be quantitatively measured with a Born modified platelet aggregometer. This method has been well correlated with the state of delayed hypersensitivity. Previous findings about the mechanism of action of the aggregation indicated that this aggregation is not due to an increase in the cellular level of c-AMP. It is doubtful whether c-AMP is a messenger of the LK action. Using a radio-immunoassay, small but significant increases were found in c-GMP levels of LK-aggregated macrophages. In addition, exogenous dibutyryl c-GMP and carbamylcholine induced a macrophage aggregation, as did the divalent cation ionophore A-23187. These data, together with the fact that LK-induced macrophage aggregation is inhibited by colchicine and at 0 degree C, suggest that microtubule polymerization is involved in this process.

Calcium↗
PubMed1981

Effects of calcitonin-induced hypocalcemia on the neuromuscular and cardiovascular depressive actions of kanamycin in anesthetized and conscious rats.

It was examined whether calcitonin (CT)-induced hypocalcemia could modify the pharmacological actions of kanamycin sulfate (KM). CT produced a dose dependent and long-lasting hypocalcemia in urethane anesthetized and conscious rats. In anesthetized rats, KM infusion depressed the indirectly elicited contractions of the tibialis anterior muscle (MC), mean arterial pressure (AP), heart rate (HR) and respiratory rate. CT did not influence the stability of the above parameters and slightly modified the neuromuscular depression of KM. In conscious rats, KM infusion produced spontaneous and complete head drop, loss of corneal reflex, respiratory arrest and also depressed AP and HR. Much higher doses of KM were required to induce the same pharmacological actions in conscious than in anesthetized rats. CT dose-dependently potentiated the pharmacological actions of KM. A highly significant linear correlation between the serum total calcium levels and the KM dose inducing spontaneous head drop was observed. These data indicate that, in conscious rats, the actions of KM are dependent on the serum calcium levels. In the same experimental conditions, neither CT-induced hypocalcemia nor anesthesia did modify significantly the pharmacological actions of d-tubocurarine.

Anesthesia↗
PubMed1980

[Inhibitory effect of cytembena (sodium-cis-beta-methoxybenzoyl-beta-bromoacrylate) on the cell kinetics of HeLa cells in culture].

The inhibiting effect of Cytembena on HeLa cell kinetics has been demonstrated and analyzed. The percentage of cycling cells decreases, according to the concentration, between 7.5 and 2.5 x 10(-5) M. Estimation of DNA by cell flow cytophotometry shows an important shift in the distribution of cycling cells with a relative decrease of G1 cells and a very important accumulation of G2 cells. According to our experimental conditions, the blocking up in G2 is irreversible only at 7.5 x 10(-5) M.

Acrylates↗
PubMed1980

[Optimal trypsin concentration for rat heart cell cultures].

Three concentrations (0.5, 1 and 2 per 1000, w/v) of a single batch of trypsin were compared regarding their influence on cultured cardiac cell of newborn rats. All three allowed to obtain cardiac cells in good conditions, as evidence by beating frequencies and [16-14C]-palmitate beta-oxidation. However the 0.5 per 1000 concentration appeared to be the optimal one, inducing a smaller loss of cells during the first two days in culture.

Animals↗
PubMed1980

Studies on in vitro colony formation by mouse bone marrow cells using different inflammatory pleural exudates. Relation to colony stimulating factor (CSF).

An inflammatory exudate obtained in Swiss mice 3 hours after intrapleural injection of dextran was able to increase the number of cultivated peritoneal macrophages in S phase. This exudate was also able to stimulate the formation of colonies from mice bone marrow progenitors of macrophages and granulocytes in methylcellulose culture. The stimulating activity of this acute inflammatory exudate was compared with that of colony stimulating factor (GM.CSF). The qualitative and quantitative results showed that the biological activity of the mitogenic factor of this inflammatory exudate, inflammatory mitogenic factor (IMF) was very close to GM.CSF at optimal concentration, but when used at the same concentration, the exudate was less active than GM.CSF. A stimulating activity was also found with another inflammatory pleural exudate induced by calcium pyrophosphate. The comparative kinetics of the action of the two exudates on CFUc appeared alike but the rise was earlier with calcium pyrophosphate. These results suggest the release of a growth factor for monocyte-macrophage in different acute inflammatory exudates.

Animals↗
PubMed1980

Effect of in vitro treatment with indomethacin on mouse granulocyte-macrophage colony-forming cells in culture (CFUC). Possible role of prostaglandins.

The effect of indomethacin (6 mg/kg daily orally for 2, 3 or 4 days) on myelopoiesis was studied in mice by estimating 1) differential cell counts of bone marrow, 2) proliferation of the CFUC in presence of GM-CSF, 3) proliferative state of CFUC after tritiated thymidine suicide. After 4 days of treatment, a rise in the recognizable myeloid precursors, an increase of both the colony forming capacity and the number of CFUC in S-phase were observed. These data suggest that indomethacin produced an hyperplasia of the committed stem cell compartment. The decrease of PGE2 amounts in bone marrow cells following treatment with indomethacin could explain the hyperplasia observed. These in vivo results are in accordance with the in vitro data which show that PG could control the proliferation and differentiation of myeloid progenitor cells.

Animals↗