Effect of Ibopamine on Ventricular Remodeling After Experimental Myocardial Infarction

Comparison of zofenopril and lisinopril to study the role of the sulfhydryl‐group in improvement of endothelial dysfunction with ACE‐inhibitors in experimental heart failure

“…The dose of NAC was comparable to that used by Galen & Siebeneich (1998) and who reported its favourable effects on diabetes‐induced endothelial dysfunction in rats. To avoid a potential effect of early pharmacological intervention on infarct‐size and wound healing ( van Gilst et al ., 1994 ; Buikema et al ., 1997 ), treatment was started at 2 weeks after induction of MI (i.e. established MI).…”

“…A transversal slice through the midst of the LV containing the infarcted area was fixed in Bouin's fluid, embedded in paraffin and 5 μm sections were cut for histological analysis. Infarct size was determined by planimetry and was expressed as the percentage of scare to total LV circumference, as described in detail elsewhere ( van Gilst et al ., 1994 ). Rats that were assigned to MI‐groups but which appeared to have an infarct‐size <20% (2/12 for ZOF, 4/12 for LIS and 4/12 for NAC) were excluded from analysis.…”

Acetylcholine stimulated dilatation and stretch induced myogenic constriction in mesenteric artery of rats with chronic heart failure

“…Male Sprague‐Dawley rats (275–300 g, Harlan, Zeist, The Netherlands) were housed in groups of four to five rats at the animal facility of the University of Groningen with free access to food and drinking water. After a 10‐day acclimatization period, rats underwent surgery for induction of experimental MI, as described previously [18,19]. In short, rats were placed on a homeothermic blanket, anaesthetized with 2% isoflurane in 2.5 L oxygen/min, intubated and mechanically ventilated (Amsterdam Infant Ventilator, Hoek/Loos, Schiedam, The Netherlands).…”

Myogenic constriction is increased in mesenteric resistance arteries from rats with chronic heart failure: instantaneous counteraction by acute AT1 receptor blockade

“…Total epicardial and endocardial circumferences of the left ventricle and the epicardial and endocardial scar length of the infarcted areas were determined by means of a computerized planimeter (Quantimet 520, Cambridge Instruments). Infarct size was then calculated by dividing the sum of the scar lengths by the sum of the total circumferences and was expressed as percentage of scare to total LV circumference, as described in detail elsewhere (van Gilst et al ., 1994).…”