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Biomedical subjects

S Lortet

Publications and source records attributed to S Lortet.

25 records · Page 2Linked to original sources
PubMed1990

Changes in heart function and cardiac cell size in rats with chronic myocardial infarction.

Myocardial infarctions were induced in rats by ligation of the left anterior descending (LAD) coronary artery. After 4 weeks, parameters of left (LV) and right ventricular (RV) function and of peripheral circulation were measured in the intact, anesthetized animals. The morphology of the heart chambers was examined at the macroscopic and cell size level. In animals with slight reduction in LV function, LVEDP was elevated from 3.4 +/- 0.8 to 8.8 +/- 1.5 mmHg, LV stroke work was reduced by 14%, and dP/dtmax of both ventricles was depressed by 10% compared with sham-operated controls. Myocytes isolated from the LV and RV were elongated to some extent and had a greater cell volume, but there was no change in heart weight. These rats had infarctions that were small or medium in size. In rats with severe depression in left heart function, cardiac output, LVSP, LV stroke work, mean arterial pressure, and the LV weight/body weight ratio were markedly lower than in sham-operated controls. LVEDP was elevated up to 32 +/- 2 mmHg. These rats had large infarctions. RVSP, RV weight/body weight ratio, and the volume of myocytes isolated from the RV were doubled. RV stroke work was increased by 58%. Myocytes from the LV, RV and from the septum were elongated to about the same extent. The septum had developed a 23% hypertrophy. Histological examination of the lungs revealed marked thickening of the tunica medica of small pulmonary arteries with narrowing of the lumen. These changes are considered to represent the morphological basis for the increased pulmonary vascular resistance that was associated with RV pressure overload and hypertrophy.

Animals↗
PubMed1989

Functional and metabolic effects of ribose in combination with prazosin, verapamil and metoprolol in rats in vivo.

Ribose improves the function of the rat heart in various pathological conditions through its effects on cardiac energy metabolism, while having no direct haemodynamic actions. We therefore studied its functional and metabolic effects in closed chest rats when given in combination with prazosin, verapamil or metoprolol, all of which have direct effects on the circulation. Ribose administration for 24 h at 200 mg.kg-1.h-1 did not affect heart function but increased the available pool of 5-phosphoribosyl-1-pyrophosphate in heart (four fold) and skeletal muscle (1.7-fold), as assessed by the incorporation of 14C-adenine into the adenine nucleotides. The utilisation of adenine for adenine nucleotide synthesis, expressed as the ratio of adenine nucleotide radioactivity to tissue extract radioactivity, was 70% in heart and 20% in skeletal muscle under control conditions, and 97% and 88% after 24 h of ribose administration. Ribose decreased the 14C-adenine incorporation into the adenine nucleotides in kidney, lungs and liver. After 24 h infusion of prazosin (100 micrograms.kg-1.h-1), heart rate and LVdP/dtmax were not changed, but LVSP (-20%), mean aortic pressure (-16%) and peripheral resistance (-40%) were decreased. Cardiac output was enhanced (+40%). Verapamil (2mg.kg-1.h-1) and metoprolol (2mg.kg-1.h-1) infused for 24 h decreased the pressure-rate and pressure-volume product of the left ventricle to the same extent (-40%). Verapamil had no influence on cardiac output, while metoprolol depressed it (-30%). Simultaneous administration of prazosin, verapamil or metoprolol with ribose did not affect the ribose induced increase in the myocardial 5-phosphoribosyl-1-pyrophosphate pool.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1989

Inotropic response of the rat heart during development and regression of triiodothyronine-induced hypertrophy.

The inotropic response of rat hearts in vivo was tested by infusion of 2 mmol/kg/h calcium chloride after 14 days of daily 3,3',5-triiodo-L-thyronine (T3) treatment and 14 days following discontinuation of T3 treatment. The hyperthyroid state was characterized by marked cardiac hypertrophy (57% increase in the heart weight/body weight ratio) which was more pronounced in the right ventricle (63% increase). Heart rate and cardiac output index were elevated by 56 and 63%, respectively, and total peripheral resistance was reduced by 40%. Left ventricular systolic pressure (LVSP) was elevated by 15%, the maximal rate of rise in left ventricular pressure (LV dp/dtmax) by 106%, and LV pressure-volume performance by 192%. Right ventricular systolic pressure (RVSP) was elevated by 71%, RV dp/dtmax by 126%, and RV pressure-volume performance by 371%. Intravenous infusion of calcium induced an elevation in heart rate and LV dp/dtmax, the increase of the latter was less pronounced than in the control heart. After 14 days subsequent to discontinuation of T3 treatment, there was a regression of cardiac hypertrophy. However, the LV was still hypertrophied by 12% and the RV by 24%. Heart rate and contractility were normal. The pressure-volume performance of both LV and RV was still enhanced by 24 and 18%, respectively. The inotropic response of the LV to calcium infusion was similar to that of the normal heart. Thus, 14 days after discontinuation of T3 treatment, the regression of cardiac hypertrophy was not complete, although heart rate and contractility as well as the inotropic response to calcium, were normal. The remaining cardiac hypertrophy correlated with the still existing elevation in the pressure-volume performance.

Adrenergic beta-Agonists↗
PubMed1988

[Pyrimidine nucleotide triphosphate control of the phosphorylation of cytidine in the rat heart].

The phosphorylation of 5 microM cytidine by the isolated perfused rat heart was increased by 50 and 120% respectively, when the myocardial UTP content was increased by 30%, 1 hr. after the treatment of animals with isoprenaline (5 mg/kg; s.c.) and by 50%, 6 hrs. after the treatment of animals with galactosamine (430 mg/kg; i.p.). On the other hand, this rate of synthesis of cytidylic nucleotides from cytidine was not decreased when the intracellular UTP and cytidylic nucleotide levels were increased through 130 and 90% respectively (12 hrs. after isoprenaline treatment).

Animals↗
PubMed1987

Synthesis of pyrimidine nucleotides in the heart: uridine and cytidine kinase activity.

These experiments were designed to determine through the study of uridine and cytidine kinase activity, the precise mechanisms of plasma nucleoside salvage leading to pyrimidine nucleotide synthesis in the rat heart. The kinetic parameters were: Km = 10 microM, V = 4 nmol g-1 min-1 for cytidine kinase activity and Km = 43 microM and V = 18 nmol g-1 min-1 for uridine kinase activity. Competing activity as concerns the two nucleosides was shown to occur, suggesting that in the rat myocardium as in other cells, one and the same enzyme phosphorylates both uridine and cytidine. UTP and CTP were shown to exert a potent inhibitory action on nucleoside phosphorylation; two factors thus exert a joint influence on the control of pyrimidine nucleotide synthesis in the rat heart: the extracellular concentration of precursor and the intracellular level of UTP and CTP. The kinetic parameters for kinase activities are discussed, taking into account the actual concentration of plasmatic nucleosides. Comparison of these data with respectively those for incorporation of nucleosides into the pyrimidine nucleotides of isolated rat heart and with nucleotide turnover rates in vivo suggests that, under physiological conditions, the utilization of plasma cytidine is crucial to the synthesis of myocardial pyrimidine synthesis.

Animals↗
PubMedDate not supplied

Pyrimidine nucleotide synthesis from exogenous cytidine in the isolated rat heart.

The rate of incorporation of exogenous cytidine into the pyrimidine nucleotides of isolated perfused rat hearts bears a Michaelis-Menten kinetic relationship to the extracellular concentration of the precursor, with an apparent Km of 10 microM and a maximal rate of incorporation of about 60 nmol per gram (ww) per 30 minutes. The myocardial cytosine nucleotide content was significantly increased by a 30 minute supply of 15 microM cytidine and more than doubled after a 2 hour administration period of 50 microM cytidine. In the latter case, the rate of cytidine incorporation fell by 30% (with respect to the initial uptake) during the last 30 minutes of administration. These results suggest that the uptake of cytidine can play an important part in the myocardial cytosine nucleotide metabolism under physiological conditions.

Animals↗