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Biomedical subjects

B Lasserre

Publications and source records attributed to B Lasserre.

At least 37 records · Page 2Linked to original sources
PubMed1988

A selective inhibitor of thromboxane synthetase activity of rabbit heart tissue: a pyridazinic derivative.

The effects of 2-(2 dimethylaminoethyl) 5-benzylidene 6-methyl (2H,4H)-3-pyridazinone (III) were studied on the biosynthesis of TXA2 and PGI2 in vitro the TXA2 and PGI2 synthetase activity of heart tissue. Biosyntheses of TXA2 and PGI2 were carried out using arachidonic acid as a substrate and horse platelet and aorta microsomes as sources of TXA2 and PGI2 synthetases respectively. TXB2 and 6-keto PGF1 alpha were determined by RIA. III--did not significantly modify either the biosynthesis of PGI2 in vitro or the PGI2 synthetase activity of heart tissue. did not significantly inhibit TXA2 biosynthesis in vitro but markedly reduced the TXA2 synthetase activity of heart tissue: for a microsomal fraction concentration of 100 micrograms protein, the ID50 was 6.37 X 10(-5) M +/- 1.29 X 10(-8) M. Thus III behaves as a specific inhibitor of the TXA2 synthetase activity of heart tissue and could have a beneficial use in therapeutics.

Animals↗
PubMed1988

Creation of a strain of genetically obese-hypertensive rats.

A strain of genetically obese-hypertensive rats (SHR-fa/fa) was created by transferring the fatty/fa gene of hyperlipaemic obese non-inbred rats into the genome of an SHR inbred strain by five successive crossings of SHR-fa+ brother-sister matings. SHR-fa/fa rats were heavier than their SHR littermates. They showed a severe hypertension, their systolic arterial blood pressure being higher than that previously found in genetically hypertensive rats. Their blood glucose content was not significantly different from that of their SHR littermates but their plasma triglycerides were increased by more than 500 per cent. While obesity and hypertension occurred from the 5th week following the rat's birth, the increase in blood triglycerides was manifest earlier.

Animals↗
PubMed1987

An inhibitor of prostacyclin biosynthesis derived from aminopyridazine.

The effects of 3-dimethylamino 5-(3' trifluoromethylbenzylidene) 6-methyl (4H)-pyridazine (PC88) on the biosynthesis of PGI2, using horse aorta microsomes as a source of enzyme and arachidonic acid as a substrate, were investigated. Under the experimental conditions adopted, PC88 was shown to dose-dependently inhibit PGI2 biosynthesis (ID50 = 6.9 x 10(-4) M +/- 1.87 x 10(-7) M). This inhibitory effect of PC88 was complex: it was of neither competitive nor non-competitive type. 3-dimethylamino 5-(2',6'-dichlorobenzylidene 6-methyl-(4H)-pyridazine (PC89) enhanced the biosynthesis of PGI2. It is worth noticing the replacement of the 2 Cl at carbon atoms 1 and 4 by a CF3 at carbon atom 2 of the phenol ring. This appears to reverse the activity of the molecule on the synthesis of PGI2. PC88 and PC89 were both inhibitors of TXA2 synthetase.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

[Eating to live].

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Adolescent↗
PubMed1986

Study of the PG E2 synthetase activity of different regions of dog and rabbit hearts.

Prostaglandin E2 synthetase activity of the microsomal fraction from different parts of dog and rabbit heart was tested with 3H-arachidonic acid as substrate. PG E2 synthesized was separated and purified by TLC and determined by the radiometric method or by bioassay. In the experimental conditions adopted, it was shown that the heart tissue is endowed with an enzyme system capable of synthesizing PG E2 but this PG E2 synthetase activity is not uniformly distributed in the different parts of the heart. It is highest in the right atrium and the activity of the atria is higher than that of the ventricles. It is species-dependent. The closely similar repartition of PG E2 synthetase activity and sympathetic nerve endings strongly suggests that PG E2 modulates adrenergic neurotransmission in the heart.

Animals↗
PubMed1985

Enhanced prostacyclin biosynthesis and decreased thromboxane formation by 3-dimethylamino 5-(2',6'-dichlorobenzylidene) 6-methyl (4H)-pyridazine (PC 89).

The effects of 3-dimethylamino 5-(2',6'-dichlorobenzylidene) 6-methyl (4H)-pyridazine (PC 89) on the biosynthesis of PG I2 and TX A2 using horse aorta and horse platelet microsomes as sources of enzymes and arachidonic acid as substrate, were investigated. PC 89 (1.10(-6) M- 1.10(-3) M) dose-dependently - enhanced the biosynthesis of PG I2: the AD50 was 6.8 X 10(-6) M +/- 1.2 X 10(-9) M, the Vmax did not vary significantly with concentrations: PC 89 increased the affinity of enzyme for substrate - but inhibited TX A2 biosynthesis (ID50 = 3.31 X 10(-3) M +/- 4.8 X 10(-7) M): this inhibiting action was not of competitive type. Owing to this dual activity of preventing TX A2 formation and stimulating PG I2 biosynthesis, PC 89 could be a valuable drug for myocardial ischemia and atherosclerosis therapeutics.

Animals↗
PubMed1983

[Treatment of zona].

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Combined Modality Therapy↗
PubMed1982

[Physical and psychological future of patients with coronary disease. To whom should ambulatory rehabilitation be proposed? (author's transl)].

To ambulatory rehabilitation programme was proposed to 91 patients during their stay in hospital for myocardial infarction or aortocoronary bypass surgery. A retrospective study showed that 51 patients did follow the programme, whereas 40 patients preferred their own method of self-rehabilitation. Serial exercise tests demonstrated progressive and considerable improvement in physical aptitude among those who followed the programme, but the psychological, socio-familial and professional outcome was globally the same in both groups. The present study therefore confirms the numerous advantages of the rehabilitation programme but also shows that many of the potential candidates to such programmes are capable of returning by themselves to a normal and active life.

Ambulatory Care↗
PubMed1981

Assessment of myocardial sympathetic activity in coronary heart disease.

We measured adrenaline, noradrenaline and dopamine beta-hydroxylase in arterial and in coronary sinus blood in 14 patients with coronary artery disease, at rest and under pacing-induced ischemia. Pacing increased the concentrations of adrenaline and noradrenaline in both arterial and coronary sinus blood. The origin of the adrenaline increase appears to be extramyocardial. The arteriovenous differences indicated that the heart extracts adrenaline and releases noradrenaline. These differences were not significantly changed by pacing, nor by the administration of propranolol. No marked changes in the concentrations of dopamine beta-hydroxylase were observed, except under pacing after propranolol, in which case a release from the heart occurred.

Adult↗