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Biomedical subjects

G Ertl

Publications and source records attributed to G Ertl.

At least 145 records · Page 8Linked to original sources
PubMed1995

Endothelin-1 contributes to ischemia/reperfusion injury in isolated rat heart-attenuation of ischemic injury by the endothelin-1 antagonists BQ123 and BQ610.

A potential detrimental role of endothelin-1 in myocardial ischemia/reperfusion injury was studied by use of the endothelin-1 antagonists BQ123 and BQ610. Isolated isovolumetric rat hearts were perfused at constant pressure. BQ123 (7 micrograms/min) and BQ610 (1.75 micrograms/min) did not alter mechanical function or coronary flow and shifted dose-response curves for endothelin-1 significantly to the right. In rats subjected to 30 min of no-flow ischemia, the increase of left ventricular resting pressure was significantly delayed by BQ123 and BQ610 compared to control (BQ123: 20 +/- 2* mmHg, BQ610: 19 +/- 2* mmHg, control: 44 +/- 4 mmHg at 15 min of ischemia, respectively, *P < 0.05 v control). With reperfusion after 30 min of ischemia, recovery of left ventricular developed pressure was not significantly affected but tended to be better with endothelin-1 antagonist pretreatment (BQ123: 20 +/- 3 mmHg; BQ610: 19 +/- 3 mmHg, control 12 +/- 3 mmHg). However, in hearts subjected to 15 min of ischemia followed by reperfusion, recovery of left ventricular developed pressure was improved by BQ610 pretreatment (BQ610: 52 +/- 8* mmHg, control: 24 +/- 6 mmHg). We conclude: BQ123 and BQ610 effectively antagonize the coronary constrictive effect of endothelin-1. BQ123 and BQ610 delay the development of contracture during ischemia and may improve functional recovery during reperfusion. Our findings suggest that endogenous endothelin-1 may contribute to ischemia/reperfusion injury.

Animals↗
PubMed1995

Contributions of 31P-magnetic resonance spectroscopy to the understanding of dilated heart muscle disease.

In the present work, we studied clinical and haemodynamic correlates of impaired cardiac high-energy phosphate metabolism in patients with heart failure due to dilated cardiomyopathy (DCM). Myocardial 31P-magnetic resonance (MR) spectra were obtained at 1.5 T in 14 volunteers and 23 patients with DCM (mean ejection fraction 34%) in order to quantify the creatine phosphate (CP)/ATP ratio. In addition, patients underwent cardiac catheterization and echocardiography. Compared to volunteers (2.02 +/- 0.11), CP/ATP ratios were significantly reduced in DCM patients (1.54 +/- 0.10; P < 0.05), indicating impaired high-energy phosphate metabolism. CP/ATP ratios correlated with the clinical severity of heart failure estimated from the NYHA class (r = 0.47, P < 0.01); also, CP/ATP correlated with left ventricular ejection fraction (r = 0.54, P < 0.01) and left ventricular end-diastolic wall thickness (r = 0.51, P < 0.01). Thus, 31P-MR spectroscopy can detect abnormal cardiac high-energy phosphate metabolism in patients with heart failure due to DCM. These abnormalities correlate with clinical and haemodynamic parameters. Future studies will have to determine whether 31P-MR spectroscopy can contribute to the routine clinical evaluation of patients with heart failure.

Adenosine Triphosphate↗
PubMed1995

Interference of angiotensin-converting enzyme inhibition with vasoactive peptides in the coronary circulation of dogs.

The coronary effects of angiotensin-converting enzyme (ACE) inhibitors and their mechanisms of action are not well understood. Because these drugs may interfere with hormone systems other than the reninangiotensin system (RAS), we studied modulation of the coronary effects of neurotensin, neuropeptide Y (NPY), and endothelin-1 (ET-1) by pretreatment with captopril in anesthetized, open-chest dogs. The left anterior descending coronary artery (LAD) was cannulated and perfused at a pressure equal to mean aortic blood pressure. Coronary blood flow (CBF) was measured by an electromagnetic flowmeter, subendocardial segment length by ultrasonic crystals. ACE inhibition (captopril 0.25 mg/kg), as an intracoronary (i.c.) injection, followed by an intracoronary infusion (0.25 mg/kg/h) did not affect the relative vasoconstrictor effects of ET-1 (10(-4)-10(-1) micrograms/kg i.c.) or neuropeptide Y (10(-3)-1 microgram/kg i.c.). However preinjection flow of a second dose-response curve of ET-1 was significantly higher in captopril-treated as compared with control animals. The increase in CBF induced by neurotensin (10(-3)-1 microgram/kg i.c.) was potentiated by captopril (40 +/- 14% after vs. 20 +/- 9% before captopril, p < 0.01, at the highest dose used). Changes in hemodynamics or in regional myocardial function could not explain altered effects of neurotensin. We therefore conclude that ACE inhibition does not interfere with the acute vasoconstrictor effects of ET-1 or NPY in this canine model but may reverse the long-term tonic coronary constrictor effect of ET-1. Potentiation of the neurotensin effect on CBF might be due to prevention of hydrolysis of neurotensin or to a cyclooxygenase-dependent mechanism.

Analysis of Variance↗
PubMed1995

Exogenous surfactant application in respiratory failure due to chronic obstructive pulmonary disease.

Recent results of basic research on regulation of surfactant secretion and surfactant physiology not only in the alveolus but also in peripheral small airways allow the conclusion that disorders in surfactant homeostasis may contribute to the pathophysiology of airway obstruction and hyperinflation. We therefore hypothesized that patients with respiratory failure due to obstructive lung disease may benefit from exogenous surfactant. Here we report a case that indicates the clinical situation to be considered for treatment with exogenous surfactant. The benefit for the patient was successful weaning from the ventilator. Improvements in effective compliance, resistance and blood gas parameters were observed following surfactant application.

Aged↗