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Biomedical subjects

P Gaudron

Publications and source records attributed to P Gaudron.

42 records · Page 3Linked to original sources
PubMed1990

Influence of angiotensin-converting enzyme inhibition on cardiac function in myocardial infarction.

Cardiac function in myocardial infarction (MI) depends on the extent of damage in ischemic myocardium and the compensatory response of residual myocardium. Because thrombolytic therapy is performed in many patients, reperfusion of ischemic myocardium may take place at various stages of progression of the ischemic insult. If perfusion is reestablished before necrosis occurs, myocardium may recover immediately or after hours to weeks ("stunned myocardium"). If coronary occlusion persists, necrosis develops in the subendocardium, propagates transmurally and forms a scar after the healing phase. Residual myocardium responds to loss of contractile tissue and material properties of the ischemic zone by hypertrophy and dilatation. This study shows that left ventricular dilatation is accompanied by an increase in stroke volume from 4 days to 4 weeks; however, left ventricular dilatation progresses while stroke volume remains constant from 4 weeks to 6 months, suggestive of noncompensatory left ventricular dilatation. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce lactate production after 60 seconds, and infarct size after 6 hours of coronary occlusion in dogs. Stunned myocardium recovers faster in animal experiments and pacing-induced myocardial ischemia may be prevented by ACE inhibitors. Left ventricular dilatation and mortality is reduced by ACE inhibitors in rats after MI. Several potential mechanisms are discussed to establish a favorable action of ACE inhibitors at various stages of MI. Clinical evidence is still pending; however, large studies are ongoing to clarify potential indications of ACE inhibitors in ischemic heart disease in humans.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Early remodelling of the left ventricle in patients with myocardial infarction.

Sequential alterations of left ventricular volumes and haemodynamics were studied in 29 patients between 4 days and 4 weeks after myocardial infarction. Left ventricular volume was determined by single photon emission computerized tomography (SPECT), infarct size by creatine kinase (CK) analysis, angiography and thallium201 SPECT. Left ventricular volume index (ml m-2) decreased in patients with small infarcts (74.5 +/- 4.9 vs 62.5 +/- 3.0, P less than 0.005), but increased significantly in patients with moderate (74.6 +/- 4.7 vs 83.6 +/- 5.0, P less than 0.0001) and large (71.7 +/- 4.8 vs 90.2 +/- 6.5, P less than 0.0001) infarctions between 4 days and 4 weeks after acute myocardial infarction. The latter groups contained almost two-thirds of our patients. This dilation occurred without significant changes in filling pressures (Swan-Ganz catheter) and resulted in significant augmentation and finally, normalization of stroke volume at 4 weeks (33.2 +/- 3.3 vs 42.6 +/- 2.9), despite persistently depressed ejection fraction (conventional radionuclide ventriculography). It is concluded that left ventricular dilatation post-myocardial infarction is structural (unchanged filling pressure) and compensatory (increased stroke volume) during the interval observed in this study.

Adult↗
PubMed1990

[Modification of hemodynamics by angiotensin converting enzyme inhibitors in heart failure].

Challenge to a new therapeutic principle to treat heart failure is to ameliorate or eliminate symptoms, decelerate progression of the disease and reduce mortality. However, to begin, one would request improvement of objective hemodynamic parameters. Angiotensin converting enzyme (ACE) inhibitors may have acute and chronic, global and regional effects. ACE inhibitors acutely and chronically reduce pre- and afterload without reflex tachycardia. They lower myocardial oxygen consumption and improve the relation of coronary blood flow to myocardial oxygen consumption. Cerebral and renal blood flow generally are beneficially influenced if the blood pressure is not lowered too much. Left ventricular dilatation following extensive myocardial infarction which is prognostically unfavourable, may be retarded or prevented by ACE-inhibitors. It is not yet clear whether mortality may thus be reduced as in patients with severe heart failure. Large multicenter studies currently address this question. It is unclear as well whether the effects of ACE-inhibitors are exclusively due to a reduction of circulating angiotensin II. Most likely, interference is of major importance with local renin-angiotensin systems, other hormone systems and the central and peripheral nervous system.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

An economical hemoperfusion system to determine in vitro clearances of various poisons with different adsorbents.

An economical hemoperfusion system for clearance studies in vitro was developped. It was ascertained, that hemoperfusion using columns which contain 13 g of adsorbent and perfused at a blood flow rate of 1.25 ml/min results in the same relative clearances as when using clinical sized columns containing 300--355 g of the absorbent and run at 100ml/min. The adsorption kinetics of toxicologically important drugs and pesticides are given as examples. To date 27 substances were tested systematically. The investigation has shown, that no adsorbent is without exception the best one, but the efficacy can vary from substance to substance.

Adsorption↗
PubMedDate not supplied

Chronic effects of ACE-inhibition (quinapril) and angiotensin-II-type-1 receptor blockade (losartan) on atrial natriuretic peptide in brain nuclei of rats with experimental myocardial infarction.

Alterations of the central nervous system may be important for imbalance of cardiovascular and fluid regulation in heart failure. The central renin-angiotensin and atrial natriuretic peptide (ANP) systems act as mutual antagonists. The effects of angiotensin converting enzyme (ACE) inhibition (quinapril, 6 mg/kg/day) and angiotensin II type 1 (AT1) receptor blockade (losartan, 10 mg/kg/day) on ANP levels in 18 selected, microdissected brain nuclei were determined in sham-operated rats and rats with left ventricular dysfunction 8 weeks after myocardial infarction (MI). Plasma ANP tended to increase in MI rats and was further increased by quinapril. ANP was decreased in 12 brain areas of MI rats. ANP concentration was also significantly decreased by quinapril in six brain nuclei including subfornical organ and organum vasculosum laminae terminalis (areas lacking blood-brain barrier), and by losartan in 16 brain nuclei outside and within the blood-brain barrier in sham operated rats. However, both quinapril and losartan prevented a further reduction of central ANP as a result of myocardial infarction. These data suggest that there are effects on central ANP that result from chronic left ventricular dysfunction as well as an ACE-inhibitor and AT1-antagonist. Mechanisms and consequences of central ANP depression remain unclear. They could, however, support systemic vasoconstriction and sodium and fluid retention.

Angiotensin Receptor Antagonists↗