PubMed Health⌕ Search

Biomedical subjects

M Amrani

Publications and source records attributed to M Amrani.

At least 73 records · Page 4Linked to original sources
PubMed1997

Relative susceptibility of endothelium and myocardial cells to ischaemia-reperfusion injury.

We have investigated the timescale, extent and sequence of endothelial, myocardial and smooth muscle cell dysfunction following ischaemia-reperfusion in the isolated rat heart. Myocardial function in the form of aortic flow was evaluated in the working heart preparation. Vasodilatation induced by endothelium-dependent agent 5-hydroxytryptamine (5-HT) and endothelium-independent substance glyceryl trinitrate (GTN) was used to assess endothelial and smooth muscle function, respectively. The percentage recovery of 5-HT response and aortic flow (endothelial vs. myocardial function) plus 5-HT response and GTN effect (endothelial function vs. smooth muscle response) after a period of ischaemia was statistically analysed by Wilcoxon's signed rank test. A possible correlation between structural and functional changes in coronary vascular endothelium after ischaemia was also explored by comparing endothelial dysfunction with morphological assessment of endothelial damage seen after ischaemia. The experiments were performed at two clinically relevant temperatures of 20 degrees C and 4 degrees C. There was no significant difference in the percentage recovery of aortic flow and 5-HT response or in 5-HT response and GTN effect after 30 min of unprotected ischaemia at 4 degrees C. The same duration of ischaemia at 20 degrees C led to significantly better recovery of GTN effect as compared with 5-HT response, but there was no difference in the recovery of aortic flow and 5-HT response. Sixty minutes of unprotected ischaemia at both temperatures caused significantly better recovery of aortic flow and GTN effect as compared with 5-HT response; 60 min of ischaemia protected by an infusion of a cardioplegic solution (protected ischaemia) at 4 degrees C had no significant effect on the recovery of the three parameters. Periods of 90, 120, 180 and 240 min of protected ischaemia at 4 degrees C, and 60, 90 and 120 min of protected ischaemia at 20 degrees C resulted in significantly better recovery of aortic flow compared with 5-HT response and of GTN effect as compared to 5-HT response. This demonstrates varying susceptibility of different cell types to ischaemic injury and highlights the strong vulnerability of endothelium to ischaemic damage as compared with myocytes and smooth muscle cells. Furthermore, there was lack of correlation between post-ischaemic endothelial dysfunction and microscopically assessed structural damage.

Animals↗
PubMed1996

Reduced glutathione and S-acetylglutathione as selective apoptosis-inducing agents in cancer therapy.

The effect of reduced glutathione (GSH) and S-acetylglutathione (S-acglu) treatment on several tumor cell lines and normal cells in vitro was investigated. GSH and S-acglu applied at concentrations of 1 mM and 2 mM induced apoptosis in malignant cells as shown by DNA-fragmentation and staining of apoptotic cells with 7-amino-actinomycin D while viability and growth of normal cells were not significantly influenced by this treatment. The results demonstrated that GSH and S-acglu may be selective inducers of apoptosis in malignant cells.

Apoptosis↗
PubMed1996

Kinetics of induction and protective effect of heat-shock proteins after cardioplegic arrest.

BACKGROUND: Heat-shock proteins are known to enhance cardiac resistance to ischemia. METHODS: To evaluate the kinetics of heat-shock protein 70 in relation to its effect on postischemic recovery of cardiac mechanical (cardiac output) and endothelial function (as percentage increase of coronary flow in response to 5-hydroxytryptamine), isolated rat hearts were subjected to prolonged hypothermic cardioplegic arrest at different intervals ranging from 12 to 96 hours after heat stress (n = 6 in each interval). RESULTS: Immunoblotting showed the maximal level of heat-shock protein 70, 0.65 +/- 0.10 (arbitrary units +/- standard error of the mean), at 24 hours after heat shock and similar values at 26 and 30 hours (p = not significant). Postischemic recovery of cardiac output and endothelial function (percentage of preischemic value +/- standard error of the mean) observed at 24 hours was 74.0 +/- 2.4 and 58.3 +/- 7.2, respectively. Similar values were observed at 26 and 30 hours (p = not significant). CONCLUSIONS: In a protocol mimicking conditions for cardiac transplantation, postischemic recovery of cardiac output and endothelial function was improved when the interval between heat stress and ischemia ranged from 24 to 30 hours. This correlated with an apparently critical amount of heat-shock protein 70.

Animals↗
PubMed1996

Aging reduces postischemic recovery of coronary endothelial function.

The aging process is known to be associated with profound changes in the heart. To determine whether resistance of coronary endothelial and vascular smooth muscle function to ischemia may be related to age, four groups of rats (n = 6 in each group) of different ages (1, 5, 15, and 26 months) were subjected to cardioplegic arrest for 4 hours at 4 degrees C. The postischemic basal release of nitric oxide by endothelium, as assessed by the percentage loss of coronary flow in response to 0.5 mmol/L L-monomethylarginine, an inhibitor of nitric oxide synthase, was as follows: (mean +/- standard error of the mean): 87.1% +/- 1.7%, 81.2% +/- 2.3%, 79.6% +/- 1.9%, and 74.9% +/- 2.4% in groups 1, 2, 3, and 4, respectively. Stimulated release of nitric oxide, as assessed by percentage increase of coronary flow to 10(-5) mmol/L 5-hydroxytryptamine, an endothelium-dependent vasodilator, was as follows (mean +/- standard error of the mean): 88.3% +/- 1.5%, 83.4% +/- 2.4%, 71.1% +/- 2.7%, and 63.1% +/- 3.3% in groups 1, 2, 3, and 4, respectively. Significant differences were found between each group (p < 0.05) for both basal and stimulated release of nitric oxide. Vascular smooth muscle function, as assessed by the percentage increase in coronary flow in response to glyceryl trinitrate, an endothelium-independent vasodilator, was (mean +/- standard error of the mean): 96.7% +/- 2.1%, 92.3% +/- 5.2%, 92.9% +/- 5.0%, and 98.1% +/- 2.4% in groups 1, 2, 3, and 4 respectively. No significant difference was found between groups (p = not significant). In a protocol mimicking conditions for transplantation, the postischemic recovery of the basal and stimulated release of nitric oxide, but not vascular smooth muscle function, diminished with age.

Aging↗
PubMed1996

Ageing is associated with reduced basal and stimulated release of nitric oxide by the coronary endothelium.

The ageing process is known to be associated with biochemical and functional changes in the heart. In an attempt to determine whether the ability of the coronary endothelium to secrete nitric oxide (NO) both at rest and in response to pharmacological stimulation is age dependent, we studied four groups of rats of different ages (1, 5, 15 and 26 months, respectively). Basal release of NO by endothelium as assessed by response of coronary flow to L-monomethylarginine, an inhibitor of NO synthase, was higher in the younger age groups. Similarly, the response of coronary flow to 5-hydroxytryptamine, a selective probe of endothelial capacity to secrete NO, was diminished in the older animals. This was confirmed by direct measurement of NO by chemiluminescence in the coronary effluent. In contrast, the response to glyceryl trinitrate appeared to be unaltered by age. It is concluded that in rats, basal and stimulated release of nitric oxide by the coronary endothelium deteriorates with age.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Endothelial function in myocardial protection.

Impairment of coronary flow, or low coronary reflow, is an important feature of ischemia-reperfusion injury. It is known to be associated with a significant diminution of basal and stimulated release of nitric oxide. The degree of recovery of low coronary reflow and of basal and stimulated release of nitric oxide diminishes with age and is influenced by the type of cardioplegic solution used. Underlying mechanisms include L-arginine (the physiologic substrate of nitric oxide) deficiency, G protein alteration, and nitric oxide inhibition by free radicals. Under normal conditions, basal release of nitric oxide is known to play a crucial role in the maintenance of basal coronary flow and appears to be essential for sustaining mechanical activity. Methods of preservation targeting reperfusion, ischemia, and preischemia have been evaluated. Pharmacologic modulation, crystalloid solution at 4 degrees C, and induction of heat-shock proteins (an intrinsic protective mechanism) reverse the postischemic dysfunction of nitric oxide release.

Animals↗
PubMed1995

Surgical treatment for acute native aortic valvular infective endocarditis: long-term follow-up.

During the period 1970-1993, 116 patients (63 men, 53 women) with native aortic valvular infective endocarditis were treated surgically. The mean age was 37 years. The main causative organisms were streptococci and staphylococci. Indication for surgery was cardiac failure (70 cases), uncontrolled sepsis (30), peripheral emboli (11) and overwhelming destruction of the aortic valve (five). Hospital and late mortality rates were 8% and 11% respectively. Patients who died in hospital and those who presented a paravalvular leakage had a ring abscess associated with aortic wall destruction. Among 34 patients screened for cerebral septic emboli the condition was confirmed in 15, of whom six were symptom-free. Thus, it is believed that in the presence of root abscess, surgery should be undertaken promptly, regardless of the cardiac status. It is confirmed that cerebral septic emboli should be systematically screened for in the presence of any infective endocarditis.

Acute Disease↗
PubMed1995

Extension of native aortic valve endocarditis: surgical considerations.

Among 101 consecutive patients operated on for native infective aortic valve endocarditis (53 males, 48 females, mean age 39 years), 69 presented various forms of infectious extension to the surrounding areas. Twenty-six lesions were noted in the aortic roots: 18 annular abscesses, one abscess of the Valsalva sinus and seven aortic wall destructions. Among the subaortic valve pathology, 27 cases of septal lesions were noted and in one case the mitral fibrous trigone was involved. The mitral apparatus was infected in 26 cases, the tricuspid valvule in one case. Both tricuspid and mitral valvular replacements had to be performed in five cases. Among the 16 postoperative atrioventricular blocks, 14 needed a pacemaker. The most frequent causative microorganisms were Staphylococcus aureus and Streptococcus. Surgical management of the lesions consisted of extensive debridement followed by either simple repair of defects or complex reconstructions involving pericardial or synthetic patches or other more complex operations. Early and late mortality rates were 8.5% and 16%; early and late reoperation rates were 6% and 9.5%, respectively. The mean follow-up time was 148 months (12-265 months) with a survival rate of 74% (SE: +/- 0.08) at 10 years. We conclude that, although surgical correction of infective endocarditis may need a complex approach, it provides good results with an acceptable surgical risk.

Adult↗
PubMed1995

L-arginine reverses low coronary reflow and enhances postischaemic recovery of cardiac mechanical function.

OBJECTIVE: To evaluate the effect of L-arginine, the physiological substrate of nitric oxide (NO), upon coronary flow (CF) and mechanical function during reperfusion following cardioplegic arrest. METHODS: Two groups of isolated rat hearts were subjected to cardioplegic arrest for 4 h at 4 degrees C. In group 1 (n = 10) cardioplegic arrest was followed by 4 consecutive periods of reperfusion with Krebs buffer (control), Krebs plus L-lysine (1 mmol/1), Krebs plus L-arginine (1 mmol/1) and Krebs plus L-NGmonomethylarginine (L-NMMA), a specific inhibitor of NO synthesis, (0.5 mmol/1). In group 2, hearts (n = 8) were perfused by Krebs, then L-NMMA, during both pre- and postischaemic periods. In group 3, hearts (n = 8) were perfused by Krebs, then L-arginine (1, 2 and 4 mmol/1). In group 4 (n = 5), NO released into the perfusate was measured before ischaemia and during reperfusion. RESULTS: In group 1, L-arginine enhanced the postischaemic CF (ml/min +/- s.e.m.) from 15.0 +/- 0.4 to 17.2 +/-0.4. This was reduced by L-NMMA to 11.3 +/- 0.3. Postischaemic cardiac output (% of preischaemic value +/- s.e.m.) was increased from 55.8 +/- 2.4 to 80.1 +/- 2.5 by L-arginine and dropped to 54.3 +/- 2.3 with L-NMMA. In group 2, the pre- and postischaemic loss of coronary flow (CF) by L-NMMA was 51% and 31% respectively. In group 3, L-arginine did not modify CF. In group 4 the preischaemic level of NO (in nmol/ml/min) in the coronary effluent, measured by chemiluminescence, was 14.84 +/- 0.83 and dropped significantly (P < 0.05) to levels ranging from 3.80 +/- 0.56 to 4.75 +/- 0.51 during the postischaemic period. CONCLUSION: Exogenous administration of L-arginine improves low coronary reflow and postischaemic mechanical function.

Animals↗
PubMed1994

Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest.

The aim of this study was to investigate the role of heat-shock proteins after heat-shock stress on the post-ischemic recovery of cardiac mechanical and endothelial function following a prolonged cardiac arrest. Isolated working rat hearts were subjected to a cardioplegic arrest for 4 hours at 4 degrees C. Three groups (n = 8 in each) were studied: (1) control, (2) sham-treated, and (3) heat-shocked rats. Postischemic recovery of cardiac output and endothelial function (as percent of preischemic control values) was 57.8% +/- 2.8% and 20.8% +/- 3.9% in group 1, 50.9% +/- 4.0% and 26.3% +/- 5.9% in group 2, and 74.0% +/- 2.4% and 51.2% +/- 8.0% in group 3, respectively. Both postischemic myocardial and endothelial function were improved by heat stress.

Animals↗
PubMed1994

Complete myocardial revascularization with arterial grafts without using the mammary artery.

We report on the case of a 60-year-old male patient who developed a crescendo angina 9 years after a coronary artery bypass procedure. Coronary angiography revealed triple vessel disease. None of the internal mammary arteries were available and the saphenous veins had previously been stripped. A complete myocardial revascularization by means of arterial grafts was still achieved by using both the epigastric arteries, and an in situ right gastroepiploic artery.

Abdominal Muscles↗
PubMed1994

Isolation of the left coronary artery ostium by an aortic cusp attachment: a rare cause of myocardial ischemia.

A 34-year-old woman experienced a 3-month history of recurrent chest pain on exertion. Extensive investigation, including coronary angiography, revealed severe aortic incompetence with suspicion of single-vessel coronary disease. At operation the aortic valve was tricuspid but the left coronary cusp was adherent to the aortic wall, resulting in isolation of the left coronary artery with only a tiny communication with the aortic lumen. The three cusps were excised. An aortic valve replacement was performed with an aortic homograft. The postoperative course was uneventful and myocardial ischemia was totally relieved.

Adult↗
PubMed1993

Right gastroepiploic artery used as a pedicled graft in a retrograde fashion.

The right gastroepiploic artery is currently regarded as a most valuable arterial conduit for myocardial revascularization. We have documented a particular case wherein the proximal (pyloric) part of the right gastroepiploic artery could not be freed and was damaged because of previous cholecystectomy. The pedicle was divided at the pyloric side and raised up to be anastomosed to the posterior descending artery in a retrograde fashion. The purpose of this report is to emphasize the fact that a previous abdominal operation does not necessarily hamper the use of the gastroepiploic artery as a pedicled graft. It is also pointed out that retrograde flow in the pedicle was sufficient in this case to provide good revascularization.

Arteries↗
PubMed1993

Role of catalase and heat shock protein on recovery of cardiac endothelial and mechanical function after ischemia.

The aim of this study was to investigate the roles of heat shock proteins and catalase after heat shock stress in the recovery of cardiac mechanical and endothelial function following a prolonged ischemic, cardioplegic arrest. Isolated working rat hearts were subjected to an ischemic cardioplegic arrest for 4 hours at 4 degrees C. Six groups, each of 6 hearts, were studied: control; control treated with 3-aminotriazole, an inhibitor of catalase; sham; sham + 3-aminotriazole; heat-shocked rats; heat shocked rats + 3-aminotriazole. Postischemic recovery of cardiac output and endothelial function (as % of preischemic control values) were respectively 54.6 +/- 1.9 and 21.2 +/- 3.0 in the control group; 52.3 +/- 2.9 and 19.1 +/- 3.9 in the control + 3-aminotriazole group; 72.2 +/- 2.7 and 54.2 +/- 7.6 in the heat shocked group; and 68.0 +/- 4.0 and 21.0 +/- 5.8 in the heat shocked + 3-aminotriazole group. SDS PAGE and western blotting showed induction of heat shock proteins in the heat stressed animals. Measurement of catalase activity showed significant inhibition in the 3-aminotriazole treated groups. It is concluded that, following heat shock stress, the enhanced endothelial recovery after prolonged ischemic cardioplegic arrest is dependent on catalase activity but that this does not apply to the recovery of mechanical functional.

Amitrole↗
PubMed1992

Improved preservation of endothelial function at 4 degrees C.

Hypothermia combined with chemical cardioplegia is routinely used clinically for perioperative myocardial protection and for donor heart preservation. Profound hypothermia can have an adverse influence on post-preservation endothelial and myocardial functions. In this study, we investigated the effect of temperature on endothelial and myocardial functions following global cardiac ischaemia in the isolated rat heart. A 5-hydroxytryptamine (5-HT)-induced increase in coronary flow was used as a selective probe to assess endothelial function, while myocardial function was measured by a working rat heart model. After recording control observations for endothelial and myocardial functions, hearts were kept ischaemic for 30 or 60 min without cardioplegia (groups 1 and 2, respectively) and for 60, 90 or 120 min following a single infusion of St. Thomas' Hospital solution (groups 3, 4 and 5, respectively). In each group, hearts were kept ischaemic at 20 degrees C or at 4 degrees C (n = 12 in each group). Endothelial and myocardial functions were reevaluated and compared with control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Role of basal release of nitric oxide on coronary flow and mechanical performance of the isolated rat heart.

1. The role of nitric oxide (NO) in the regulation of coronary flow and mechanical function was studied in isolated working rat hearts. 2. The inhibition of basal release of NO by L-Ng-monomethylarginine (L-NMMA; 500 microM), a specific inhibitor of its synthesis, induced a reduction of coronary flow to 39.1% (+/- 3.4) of its basal level. 3. Associated with this was a drop of cardiac output to 58.10% (+/- 5.42) of control values. 4. This mechanical dysfunction, which was more pronounced in hypertrophied hearts, appears to be related to ischaemia, as it was prevented by simultaneously administered glyceryl trinitrate. Furthermore, L-NMMA did not alter the contractile activity of isolated cardiac myocytes, thereby excluding a direct toxic effect. 5. These findings provide evidence that NO plays a crucial role in the maintenance of basal coronary flow and appears to be essential for sustaining mechanical activity.

Animals↗