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Biomedical subjects

G Ertl

Publications and source records attributed to G Ertl.

At least 199 records · Page 11Linked to original sources
PubMed1991

[In vivo 31P-cardiac magnetic resonance spectroscopy: methods and the first clinical results].

31P-magnetic resonance (MR) spectra of the heart can be obtained from well-defined myocardial regions by combined MR imaging and variable selected volumes for spectroscopy. 31P-spectra of 33 volunteers and of 43 patients with dilated and hypertrophic cardiomyopathy and with coronary artery disease were quantified using a curve-fitting routine. To optimize our technique, we recorded unsaturated and partially saturated spectra in several volunteers. Relative peak areas and signal-to-noise ratios showed significant changes with varying pulse repetition times. Saturation factors were applied to correct spectra from volunteers and patients for the effects of partial saturation. Under resting conditions, peak areas of volunteers and patients from the various groups were statistically indistinct.

Adult↗
PubMed1991

Effect of mediators on coronary circulation.

A number of vasoactive mediators have been identified in plasma and in the heart. Some of them may be liberated in inflammatory heart disease. The action of mediators on coronary vasculature in various animal models and their potential role in inflammatory heart disease is reviewed. Their role in patients remains to be determined.

Adrenal Glands↗
PubMed1991

[Possibilities of ACE inhibitor therapy in acute myocardial ischemia].

Acute myocardial ischemia results from an increased cardiac workload in presence of a critical coronary stenosis (demand ischemia), coronary occlusion (supply ischemia) or a combination of both. It is complicated by cardiac arrhythmias and deterioration of function of ischemic myocardium and results in an increased load and dilatation of non-ischemic myocardium. Cardiac protection in acute myocardial ischemia can be related to preservation of coronary blood flow, function of ischemic and non-ischemic myocardium or prevention of cardiac arrhythmias. In control animals and humans, ACE-inhibitors have no major effect on coronary blood flow. Myocardial ischemia raises plasma-renin-activity, angiotensin I-conversion by passage through coronary circulation, and plasma-angiotensin-II-concentrations. ACE-inhibitors and angiotensin-II-receptor blockers increase coronary blood flow during myocardial ischemia. Other mechanisms (bradykinin potentiation) may be involved. We found a potentiation of the coronary dilatory effect of the neuropeptide neurotensin (which is probably mediated by prostaglandins) by ACE-inhibitor. ACE-inhibitor may delay infarct development in animal experiments and improve function of ischemic myocardium. The importance of early dilatation of non-ischemic myocardium is unknown and it is unclear whether it may be prevented by an ACE-inhibitor as was shown for late dilatation. Studies on the effect of ACE-inhibitors in exercise-induced angina pectoris are controversial. An antiischemic and coronary dilatory effect has been shown by invasive studies in patients. A preliminary study in unstable angina pectoris was positive. Beneficial hemodynamic and antiarrhythmic effects (as well as excessive hypotension, however) have been shown in patients with acute myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Experimental and clinical possibilities of MR spectroscopy of the heart].

MR-spectroscopy of the heart is a relatively new technique for the study of various aspects of cardiac metabolism. The majority of results has so far been obtained with the isolated perfused heart. Here, 31P-MR spectroscopy can be employed to measure high-energy phosphate metabolism and intracellular pH repeatedly and non-invasively. Using a technique called saturation transfer, velocities of enzymatic reactions, such as the creatine kinase reaction, can be measured. Intra- and extracellular Na+ and K+ concentrations can be registered with 23Na- and 39K-MR in conjunction with shift reagent. 13C-MR can be used to tackle carbohydrate metabolism. In-situ-R-spectroscopy allows determination of high-energy phosphates in intact large mammals. Clinical applications of MR-spectroscopy remain to be defined; preliminary results indicate high diagnostic and prognostic potential for patients with coronary artery disease and congestive heart failure.

Animals↗
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

Coronary arteriolar vasoconstriction in myocardial ischaemia. Vasopressin, renin-angiotensin system and ANF.

Vasopressin, the renin-angiotensin system and atrial natriuretic factor (ANF) interact in regulating blood pressure. While the vasoconstrictor effect of vasopressin and the renin-angiotensin system is well documented, the direct vascular effect of ANF is unclear. We studied in anaesthetized dogs the coronary vascular effects of agonists and antagonists of vasopressin and the renin-angiotensin system under control and ischaemic conditions, respectively. In addition, the action of ANF and its relationship to the renin-angiotensin system was analysed. A coronary artery was cannulated and perfused by a bypass system from the femoral arteries of the same animal. Coronary vasoconstriction by vasopressin was potentiated when myocardial ischaemia was induced by lowering coronary perfusion pressure while coronary constriction by angiotension I and II was mitigated. A vasopressin receptor blocker slightly reduced coronary blood flow at high doses (intrinsic activity) while the angiotensin II receptor blocker increased coronary flow in myocardial ischaemia. ANF effects were ambiguous at lower doses (1 ng (kg)-1 i.c.) with coronary constriction in 79% of dogs. At higher doses (1 microgram kg-1) ANF consistently induced coronary dilation. The angiotensin II receptor blocker saralasin significantly reduced this coronary dilator effect of ANF. Thus, in conclusion, a vasoconstrictor effect of endogenous vasopressin could not be shown by this study. In contrast, endogenous angiotensin II might participate in control of coronary blood flow during myocardial ischaemia. The coronary dilator effect of ANF at least in part appears to be due to interference with the renin-angiotensin system.

Angiotensin II↗
PubMed1990

Effects of endothelin-1 in isolated perfused rat heart.

We examined the effects of the vasoconstrictor peptide endothelin-1 in the isolated heart and defined interactions of endothelin-1 with other hormone systems. Isolated isovolumic rat hearts were perfused with Krebs-Henseleit buffer at constant pressure. First, the effect of a single bolus of endothelin-1 (4-400 pmol) was followed for 90 min. The effect of high dosages (40 and 400 pmol) of endothelin-1 on coronary flow was biphasic, with an early vasodilator and a late vasoconstrictor component that was irreversible. Second, cumulative dose-response curves were obtained for endothelin-1 boluses of 0.04-400 pmol. Coronary flow declined with increasing dosages and was almost abolished at 400 pmol. Neither alpha- nor beta-blocking agents (phentolamine and propranolol) nor the Ca2(+)-channel blocker nifedipine altered the effects of endothelin-1, but prostaglandin synthesis inhibition by indomethacin significantly augmented vasoconstriction by endothelin-1. Angiotensin-converting enzyme (ACE) inhibition by captopril antagonized endothelin-1-dependent vasoconstriction to a small extent at 400 pmol. Coronary constriction due to endothelin-1 could not be reversed by nitroglycerin. We conclude that in isolated rat heart endothelin-1 causes marked and long-lasting coronary constriction. The effect is not influenced by sympathetic and Ca2(+)-channel blockade, is enhanced by prostaglandin synthesis inhibition, and is reduced by ACE inhibition.

Adrenergic alpha-Antagonists↗
PubMed1990

Effects of endothelin-1 in the isolated heart under ischemic and cardioplegic conditions.

We examined the effects of the vasoconstrictor peptide endothelin-1 in isolated hearts under ischemic and cardioplegic conditions. Isolated isovolumic rat hearts were perfused with Krebs-Henseleit buffer at constant pressure. Cumulative dose-response curves were obtained for endothelin-1 boluses of 0.04-400 pmol in four groups of hearts. Coronary flow decreased with increasing dosages and was almost abolished at 400 pmol in control hearts perfused at a constant pressure of 100 mm Hg. In hearts made ischemic by reducing coronary perfusion pressure to 35 mm Hg, thus reducing coronary flow by 76%, the constrictor effect of endothelin-1 was well preserved. The endothelin-1 dose-response curve was unaltered when hearts were perfused with buffer containing 30 mM KCl to abolish mechanical activity without reducing extracellular Ca2+ concentration. A fourth group of hearts was perfused with Ca2(+)-free buffer, thus eliminating the source of extracellular Ca2+ as well as mechanical activity. In this group, the constrictor response to endothelin-1 was largely, but not completely, abolished, with a maximal constrictor effect of only 19% as opposed to 87% in control hearts. We conclude that in isolated rat heart endothelin-1 is a potent coronary constrictor under ischemic perfusion conditions and that absence of mechanical activity does not affect the action of endothelin-1, for which the presence of extracellular Ca2+ is essential. The small residual constrictor response with Ca2(+)-free perfusion is probably due to release of Ca2+ from intracellular stores.

Animals↗
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↗