Biomedical subjects

L Rochette

Publications and source records attributed to L Rochette.

At least 145 records · Page 8Linked to original sources

PubMed1987

Comparison of the effect of antidepressant drugs on arrhythmias in the isolated rat heart subjected to myocardial ischaemia and reperfusion.

Rat isolated hearts were perfused according to the Langendorff's method. The hearts were prelabelled with 3H-noradrenaline (3H-NA) and the left coronary artery was occluded during 10 min. The liberation of 3H-NA and the development of ventricular arrhythmias were investigated during ischaemia and the following reperfusion period. In control preparations, reperfusion was followed by ventricular fibrillation and a sudden release of radioactivity in the coronary effluent. Antidepressants such as imipramine, metapramine, mianserin and nomifensine prevented reperfusion arrhythmias in a concentration-dependent manner and caused bradycardia. Amineptine, however, was ineffective in preventing reperfusion arrhythmias even in a high concentration, this agent did not decrease heart rate. Nevertheless none of the antidepressants changed the rate of liberation of 3H-NA during the ligation and reperfusion periods. A quinidine like action seems the most appropriate explanation for the cardiac effects of these antidepressant drugs.

Animals↗

PubMed1987

Protective effect of angiotensin converting enzyme inhibitors (CEI): captopril and perindopril on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion in rat.

The purpose of the present study was to evaluate the effects of two CEI: captopril and perindopril on reperfusion arrhythmias and noradrenaline 3H (NA3H) release in the isolated rat heart on arrhythmias in pentobarbitone anaesthetized rats subject to left coronary artery ligation. In vitro, in control preparations, reperfusion after 10 min of local ischemia produced by coronary ligation was accompanied by a sudden release of NA3H in coronary flow and long lasting ventricular arrhythmias. Reperfusion arrhythmias were prevented by perfusion medium containing a high dose of CEI and CEI did not change the patterns of NA3H release. In vivo, mortality due to ventricular fibrillation was significantly reduced in rats pretreated with captopril or perindopril 15 min prior to coronary ligation. CEI reduced the severity of ventricular tachycardia (VT) and fibrillation (VF).

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1987

[Arterial hypertension, myocardial hypertrophy and disorders of cardiac rhythm induced by ligation of the left coronary artery in the rat].

Cardiac hypertrophy and hypertension are major elements in sudden cardiac death in patients with coronary artery disease. To investigate in animals the hypothesis that left ventricular hypertrophy (LVH) and/or hypertension increase the incidence of severe ventricular arrhythmias, we have undertaken a 30 min period of coronary artery ligation in anaesthetized spontaneously hypertensive rats (SHR), normotensive (NT) Wistar Kyoto (WKY) and Wistar (W) rats. Mean systolic blood pressure (SBP) was 190 +/- 4 mmHg in SHR vs 123 +/- 5 mmHg in WKY and 116 +/- 4 mmHg in W (p less than 0.001). LVH index was 2.81 +/- 0.04 in SHR vs 196 +/- 0.03 in WKY and 1.65 +/- 0.05 in W (p less than 0.01). Incidence (IVF) and duration (DVF) of ventricular fibrillation were significantly more elevated in SHR than in NT rats. IVF was 100 p. 100 in SHR vs 36 p. 100 in WKY and 27 p. 100 in W (p less than 0.001); DVF was 61 +/- 17 s in SHR vs 6 +/- 6 s in WKY and W (p less than 0.001). In addition the calcium channel blocker nicardipine (N) has been administered orally to SHR either chronically during eight weeks (20 mg/kg-1 per os twice daily) or acutely as a single dose of 20 mg/kg. After long term treatment (LT) with N the LVH index and SBP were significantly reduced when compared to vehicle treated (VT) SHR; whereas a single administration of N (AT) only decreased SBP without affecting LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

[Effects of Ginkgo biloba extract on 2 models of experimental myocardial ischemia].

Ginkgo biloba extract, a free radical scavenger containing kaempferol and quercetin esters, which are potent radical scavengers, was studied on various models of cardiac ischaemia, both in vitro and in vivo. On the two in vitro models of ischaemia-reperfusion described (rat and guinea-pig hearts) Ginkgo biloba extract was without effect on cardiac functional parameters. However, it induced a significant decrease in the intensity of ventricular fibrillation during the reperfusion stage. On normal or hypertrophied heart in vivo, Ginkgo biloba extract provided effective protection against the electrocardiographic disorders induced by ischaemia. On the different models of global or localized ischaemia (followed or not by reperfusion), a decrease of arrhythmia without change in cardiovascular parameters was regularly noted.

Animals↗

PubMed1985

Effect of alpha-adrenoceptor antagonists (phentolamine, nicergoline and prazosin) on reperfusion arrhythmias and noradrenaline release in perfused rat heart.

Rat isolated hearts were perfused through the left atrium with a modified Krebs-Henseleit solution or mounted on a Langendorff perfusion system. The hearts were prelabelled with [3H]-noradrenaline [( 3H]-NA) and the left main coronary artery was ligated for 10 min after which reperfusion followed. The liberation of [3H]-NA and the development of ventricular tachycardia and fibrillation were monitored throughout. During the occlusion period, ventricular arrhythmias did not occur and heart rate was not significantly altered in the control series. In contrast, reperfusion was followed by ventricular fibrillation and ventricular tachycardia in all the hearts in the control series (Langendorff or 'working' models). The alpha-adrenoceptor antagonists phentolamine (7.1 X 10(-6) M and 7.1 X 10(-5) M) and nicergoline (3.1 X 10(-6) M) diminished or prevented reperfusion arrhythmias. However, prazosin (5.2 X 10(-6) M) was not effective. The lower concentration of phentolamine did not alter the pattern of [3H]-NA release, whereas, high doses of phentolamine and nicergoline increased the release of [3H]-NA. Prazosin (5.2 X 10(-6) M) caused a very marked increase in release of [3H]-NA but was not antiarrhythmic. A 'membrane-stabilizing' effect seems the most appropriate explanation for these antiarrhythmic effects of alpha-antagonist agents.

Adrenergic alpha-Antagonists↗

PubMed1984

Role of beta-adrenoreceptor antagonism in the prevention of reperfusion ventricular arrhythmias: effects of acebutolol, atenolol, and d-propranolol on isolated working rat hearts subject to myocardial ischemia and reperfusion.

The role of catecholamines in the genesis of ventricular arrhythmias during the reperfusion period following coronary occlusion remains incompletely understood. An isolated rat heart preparation, free from the influence of autonomic innervation or of circulating catecholamines, was used to assess the effects of beta-adrenoceptor blockade. The hearts were prelabeled with tritiated norepinephrine ( NE3H ), and the total radioactivity and that in NE3H were measured in the effluent coronary flow. The left main coronary artery was ligated for 10 minutes after which reperfusion followed. The liberation of NE3H and the development of ventricular tachycardia and fibrillation were monitored throughout. The cardioselective beta-antagonist agent, acebutolol, in a high concentration (1.1 X 10(-4)M), had good beta-antagonist effect in response to the added isoproterenol (10(-6)M); this concentration of acebutolol also suppressed sustained reperfusion ventricular arrhythmias but unexpectedly increased the release of NE3H . Atenolol, another cardioselective agent, did not prevent reperfusion ventricular arrhythmias even in a high concentration of 40 mg/L (1.5 X 10(-4)M). The d-isomer of propranolol, with poorer beta-antagonist properties than the l-isomer, prevented such ventricular arrhythmias in a concentration of 1.3 X 10(-5)M, which was low when compared to that of atenolol. It is proposed that the beta-antagonist activity of the compounds tested could not explain the inhibition of reperfusion ventricular arrhythmias and that another quality such as membrane-stabilizing activity may be involved.

Acebutolol↗

PubMed1982

Effect of chronic clonidine treatment on the turnover of noradrenaline and dopamine in various regions of the rat brain.

The turnover of noradrenaline (NA) and dopamine (DA) was estimated in various rat brain regions by measuring the depletion of the amines after inhibition of their biosynthesis by alpha-methyltyrosine. Acute treatment with clonidine (0.1 mg/kg) reduced NA turnover in the brain stem, hypothalamus and rest of the brain but had no effect on DA turnover in the corpus striatum and rest of the brain. After chronic clonidine treatment (0.1 mg/kg, twice daily for 156 days), NA turnover was not affected by an additional injection of clonidine in the brain stem or in the hypothalamus but was still markedly reduced in the rest of the brain. In addition, DA turnover was reduced in the corpus striatum and rest of the brain, an effect which was also observed after a single injection of a high dose of clonidine (1 mg/kg). These findings suggest that a chronic administration of clonidine may cause regionally differential changes in the sensitivity of central NA receptors.

Animals↗

PubMed1982

Dopamine and norepinephrine turnover in various regions of the rat brain after chronic manganese chloride administration.

Rats were treated with MnCl2 X 4H2O (1 mg/100 g/day, i.p.) for a period of 4 months. The turnover of dopamine (DA) and norepinephrine (NE) was measured in several brain regions (brain stem, hypothalamus, corpus striatum and "rest of the brain") by the decay in endogenous DA and NE after inhibition of tyrosine hydroxylase by alpha-methylparatyrosine. Monoamine oxidase (MAO) activity and manganese levels were also estimated. Manganese treatment produced a decrease in DA level and turnover in the corpus striatum but not in the rest of the brain. An increase in contents of NE was observed both in the brain stem and hypothalamus. NE turnover was found to be increased in the brain stem, decreased in the hypothalamus and unaltered in the rest of the brain. MAO activity was not significantly altered in all the brain regions studied. These results which show that chronic administration of manganese may cause regionally different changes in catecholamine turnover were discussed in relation to the accumulation of manganese in the brain regions and to other metabolic changes associated with manganese toxicity.

Animals↗

PubMed1980

Effect of substrate on release of myocardial norepinephrine and ventricular arrhythmias following reperfusion of the ischemic isolated working rat heart.

Isolated rat hearts were prelabeled with 3H-norepinephrine (NE), submitted to coronary artery ligation, and perfused through the left atrium with a modified Krebs-Henseleit solution containing 3 mM potassium and four different substrates: 5.5 mM glucose, 5.5 mM glucose plus 0.15 or 0.5 mM palmitate bound to albumin in a molar ratio of 6:1, and 11 mM glucose. The coronary artery ligature was removed after 30 min of perfusion of the ischemic working heart. With all substrates the release of radioactivity in the coronary effluent remained relatively constant during the ischemic period. Reperfusion was associated with a sudden release of radioactivity and of 3H-NE, but the intensity of the efflux was influenced by the nature of the perfusion substrate. The highest release was observed with 5.5 mM glucose and the lowest release in the presence of 0.15 mM palmitate. Intermediate and similar releases were seen with the two other substrates. On reperfusion of the ischemic heart, ventricular arrhythmias (tachycardia and fibrillation) were very marked with 5.5 mM glucose and in the presence of 0.5 mM palmitate. They were significantly delayed in the presence of 0.15 mM palmitate and almost absent with 11 mM glucose. These results do not show a relationship between the amount of NE liberated during the post-ischemic period and the extent of ventricular reperfusion arrhythmias. We conclude that either myocardial NE is not implicated in the genesis of reperfusion arrhythmias or that cardiac vulnerability to the arrhythmogenic effect of NE is influenced by the metabolic state of the myocardium, which is dependent on the nature of the perfusion substrate.

Animals↗

PubMed1980

[Release of noradrenaline and ventricular arrhythmias in the isolated perfused working rat heart in the presence of fatty acids. Effect of coronary artery occlusion and re-perfusion (author's transl)].

After an initial perfusion using the Langendorff technique, rat hearts were perfused through the left atrium according to the working heart technique. Hearts were preloaded with l noradrenaline 3H (3H-NA) and the release of radioactivity and 3H-NA in the coronary effluent was evaluated. Coronary flow, cardiac output, myocardial oxygen consumption and the electrocardiogram were simultaneously recorded. The perfusion medium consisted of a modified Krebs Henseleit solution containing 3 mM potassium and 0.5 mM sodium palmitate complexed with serum albumin in a molar ratio of 6/1. 1. The addition of palmitate to the perfusion fluid during the Langendorff perfusion produced increases in coronary flow and oxygen consumption, but the release of 3H-NA was not significantly modified, and no irregularities in ventricular concentration were observed. Likewise, the working of the heart did not alter the rate of 3H-NA release. 2. Ischemia was induced on the working heart by left coronary artery ligation for 15 min. It resulted in a reduction in coronary flow and in a similar decrease in the rate of release of 3H-NA. During the first minutes of the occlusion period, there was a slight increase in the incidence of ventricular extrasystoles, but ventricular tachycardia or fibrillation were never encountered. 3. Re-perfusion was accompanied by the occurrence of ventricular tachycardia and fibrillation in all the hearts. These arrhythmias were almost uninterrupted during the first 3 min of re-perfusion, and lasted to a lesser extent up to the 9th minute. Re-perfusion resulted in a sudden release of 3H-NA which was multiplied by a factor 4 during the first 2 min, and then decreased progressively. 4. These results suggest that a release of NA from the myocardial ischemic zones plays a role in the genesis of cardiac arrhythmias following reperfusion.

Animals↗

PubMed1977

Time-dependent changes in the rate of noradrenaline synthesis in various rat brain areas during cold exposure.

The synthesis of noradrenaline (NA) was studied in vivo in the hypothalamus, the brain stem and the "rest of brain" of rats which were exposed to 4 degrees C for 0.5, 2.5 or 24 h. The rate of NA synthesis was estimated 30 min after an i.v. injection of 3H tyrosine (TY) by evaluation of the ratio: 3H-NA specific activity/3H-TY specific activity. Cold exposure did not have the same effect on NA synthesis in the three brain areas. In the hypothalamus, the rate of NA synthesis was increased by a factor of 1.7 and 2 after 0.5 and 2.5 h of cold exposure, respectively and returned to control values after 24 h of cold exposure. In the brain stem, NA synthesis was enhanced by a factor of 1.5 at 2.5 h and returned also to control values at 24 h. In the "rest of brain", cold exposure did not alter NA synthesis at the three intervals studied. These results indicate that the activation of central noradrenergic neurones by cold is only a transient response which is restricted to specific brain areas and which can be interpreted as the consequence of an initial general stress associated with cold exposure.

Acclimatization↗

PubMed1977

[Evaluation of the carotid blood distribution in the rat using radioactive microspheres (author's transl)].

The carotid blood distribution has been evaluated using radioactive microspheres in 13 regions of the head and in 10 cerebral structures of rats, and the intracerebral distribution of blood has been studied comparatively after injection of microspheres into the left cardiac ventricle or into the internal carotid artery. The principal results indicate that the cerebral tissue is not supplied by the external carotid blood, whereas about 30% of the internal carotid blood goes to the brain, and that pontomedullary region receives its blood mainly from the vertebral artery.

Animals↗

PubMed1977

[Estimation of regional circulation in rats: results obtained by using 15 and 50 micron diameter microspheres and rubidium].

Radioactive microspheres, 15 or 50 micron in diameter, were used to estimate the distrubtion of cardiac output and the degree of shunting of microspheres through the systemic and pulmonary circulations in anaesthetized rats. Extraction of 15 micron spheres by the pulmonary capillaries was nearly 100% and the amounts of microspheres per gram of lung tissue were not significantly different in the various lobes of lung. After injection into the left ventricle, the proportion of microspheres shunted to the lungs was almost identical using 15 or 50 micron spheres. Similar results were observed after injection into the internal of external carotid artery. The distribution of cardiac output showed a significant difference between 15 and 50 micron spheres, the proportion of 50 micron spheres found in the stomach being higher, which suggests the existence in this organ of arteriovenous shunts larger than 15 micron. The rubidium method yielded higher fractions of cardiac output in the liver (hepatic artery), lung and skin whereas the microspheres distribution to the heart, spleen and digestive tract exceeded that of rubidium. The origins of these differences are discussed.

Animals↗

PubMed1976

Evolution in vivo of the synthesis rate of catecholamines in various peripheral organs of the rat during cold exposure.

The synthesis of catecholamines (CA) has been studied in the heart, spleen, submaxillary glands and adrenals of rats exposed to 4 degrees C for 2.5, 24 or 48 h. The synthesis rate has been estimated 30 min after an i.v. injection of 3H tyrosine (TY) by the evaluation of the ratio: 3H-CA specific activity/3H-TY specific activity. In the sub-maxillary glands, cold exposure reduced the noradrenaline (NA) synthesis by 40% at times 24 and 48 h. In the spleen, NA synthesis was multiplied by a factor 1.6 at times 2.5 and 24 h and 2.8 at time 48 h. In the heart, it was increased by a factor 1.3 after 2.5 h, 2.8 after 24 h and 5.5 after 48 h: an important fall in cardiac NA level was observed during the first 24 h of cold exposure indicating that the synthesis capability was unsufficient to compensate the cold-induced NA release. In the adrenals, adrenaline + NA synthesis was not significantly enhanced during the first 24 h of cold exposure and increased by a factor 2.4 at time 48 h. The important increases in CA synthesis which are observed during the 24-48 h interval are likely consecutive to the induction of tyrosine hydroxylase which has been reported in the rat exposed to cold.

Adrenal Medulla↗

PubMed1976

Effect of the activation of alpha-adrenoreceptors on the synthesis and release of noradrenaline by peripheral adrenergic nerves in vivo.

The synthesis and release of noradrenaline (NA) in the heart and submaxillary glands were studied in the rat following s.c. injections of oxymetazoline (50 mug/kg) or noradrenaline (500 mug/kg). NA release was evaluated from the decline in tissular specific radioactivity after administration of 3H-NA and NA synthesis by the estimation of the amounts of 3H-NA synthesized from 3H-tyrosine (TY) or 3H-Dopa, 30 min after the injection. Oxymetazoline treatment delayed the release of NA, the NA biological half-lives rising from 12 up to 36 hours in the heart and from 5.9 up to 21 hours in sub-maxillary glands. This inhibitory effect on NA release was interpreted as the consequence of the stimulation of alpha-adrenoreceptors. Thirty minutes after its injection, oxymetazoline increased both NA endogenous levels and 3H-NA amounts formed from 3H-TY: 3H-NA specific activities were not significantly altered. NA treatment led to an acceleration of NA release in the heart (NA biological half-life decreasing from 12 to 2.2 hours) but not in sub-maxillary glands. After injection of 3H-TY, the amounts of 3H-NA found in the heart and sub-maxillary glands were strongly reduced. Similar results were observed in the heart using 3H-Dopa as a precursor. These data are interpreted as the consequence of the removal of the newly synthesized 3H-NA by exogenous NA. The results obtained with oxymetazoline point out a dissociation between the NA release which is reduced and the NA synthesis which is unaltered. This indicates that NA synthesis rate by sympathetic nerve terminals is not immediately regulated by its release intensity. These data do not support the end-product feedback inhibition hypothesis according to which tyrosine hydroxylase is regulated by the intraneuronal NA concentration.

Adrenergic Fibers↗

PubMed1976

[Effect of cold exposure on synthesis of cerebral dopamine (author's transl)].

The synthesis of dopamine (DA) has been studied in the striatum and cortex of rats exposed to a temperature of 40C for 2.5 or 24 h. The synthesis rate has been estimated 30 mn after an i.v. injection of 3H tyrosine (TY), by the evaluation of the ratio: 3H-DA specific activity 3H-TY specific activity. Cold exposure modified DA synthesis differently in the two brain areas. In the striatum, DA synthesis was multiplied by a factor of 1.5 after 2.5 h of cold exposure and returned to normal value after 24 h. In the cortex, cold exposure did not significantly change DA synthesis (at any of the two times studied).

Animals↗

PubMed1975

Effect of the norepinephrine receptor stimulating agent "clonidine" on the turnover of 5-hydroxytryptamine in some areas of the rat brain.

The effect of clonidine (0.05 mg/kg i.p.) on 5-hydroxytryptamine (5-HT) turnover has been studied in the whole brain and in various cerebral areas of the rat (brain stem, hypothalamus, striatum and "rest" of the brain). In the whole brain, clonidine produced a significant decrease (-23%) in 5-hydroxyindole acetic acid level and a slight increase (+7%) in 5-HT level. These variations were not observed in all the cerebral structures. The 5-hydroxyindole acetic acid levels were reduced in the hypothalamus and in the rest of the brain; they were not significantly altered in the brain stem and increased in the striatum. The effect of clonidine on the 5-HT synthesis has been studied by evaluation of the rises in 5-HT levels induced by pargyline: these rises were found significantly increased in the brain stem and the hypothalamus and not significantly altered in the other cerebral structures. These findings give support to the hypothesis according to which the norepinephrine receptor stimulation inhibits the activtity in the 5-HT neurons: clonidine reduces primarily the relase of 5-HT without an immediate effect on its synthesis. The differences observed among the various cerebral areas might be explained by the fact that relations between nor-epinephrine and 5-HT neurons do not exist identically in all cerebral structures.

Animals↗

PubMed1975

[Rates of endogenous noradrenaline release in rat brain, heart and intestines: comparison of results obtained after biosynthesis inhibition and 3H-tyrosine labeling].

After labelling of noradrenaline stores with tyrosine 3H, the rate constant of NA efflux was calculated from the change of the NA-3H and TY-3H specific activities. The biological half-life of NA was 2,2 h in the brain, 24 h in the heart and 3,3 h in the intestine. These values were similar to those obtained after inhibition of NA synthesis by alpha-methylparatyrosine.

Animals↗