Fasting limits norepinephrine release with myocardial ischemia and reperfusion

• Published in: Cardiovascular drugs and therapy 1999-09, Vol.13 (5), p.399-405
• Main Authors: SCHAEFER, S, LI FENG WANG, VAN DER VLIET, A, HRISTOVA, M, VULLIET, P. R, SHU DUO FAN
• Format: Article
• Language: English
• Subjects: Adrenergic Uptake Inhibitors - therapeutic use; Animals; Biological and medical sciences; Blood Glucose; Creatine Kinase - metabolism; Desipramine - therapeutic use; Diseases of the cardiovascular system; Fasting - metabolism; Food; Hemodynamics; Insulin - blood; Male; Medical sciences; Myocardial Ischemia - drug therapy; Myocardial Ischemia - metabolism; Myocardial Ischemia - therapy; Myocardial Reperfusion; Norepinephrine - metabolism; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); Rats; Rats, Sprague-Dawley
• ISSN: 0920-3206; 1573-7241
• DOI: 10.1023/A:1007847805298

Fasting for 24 hours improves functional recovery and reduces injury due to global ischemia and reperfusion. Since fasting affects catecholamine kinetics, and norepinephrine (NE) release has been implicated as a mediator of dysrhythmias and injury with myocardial ischemia, we hypothesized that fasting would limit NE release following ischemia and reperfusion as a mechanism of its beneficial effects. Hearts were isolated and perfused from rats either fed normally or fasted for 24 hours. Following baseline perfusion, hearts were subjected to 20 minutes of ischemia followed by reperfusion. Hemodynamics (developed and end-diastolic pressure) and dysrhythmias were monitored, and creatine kinase release on reperfusion was measured as a marker of cellular injury. NE tissue content was assessed prior to ischemia and NE release was measured upon reperfusion with and without blockade of the uptake1 carrier using desipramine. The release of NE was reduced by fasting (0.52+/-0.14 vs. 1.47+/-0.15 nmol/gdw, p