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The Effect of Ischaemic Preconditioning on Cardiac Function After Potassium Channel Opener (Pinacidil) Cardioplegia at Hypothermia and Normothermia
Author(s) -
Jurisevic CA,
Oliver J,
Baker RA
Publication year - 2002
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1046/j.1540-8191.2002.10148.x
Subject(s) - medicine , pinacidil , hypothermia , potassium channel opener , anesthesia , cardiology , potassium , potassium channel , glibenclamide , diabetes mellitus , endocrinology , chemistry , organic chemistry
Objectives: To determine the effect of ischaemic preconditioning on post‐ischemic myocardial recovery in hearts arrested with Pinacidil at both hypothermia and normothermia; and to assess the efficacy of Pinacidil as a cardioplegic agent. Methods: Isolated ejecting Porton rat hearts were perfused at normothermia via a Langendorff apparatus, utilizing retrograde coronary perfusion at a constant pressure (70cm/H 2 O). All animals underwent a 30‐min normothermic stabilization phase, thereafter being divided into the following groups. Hearts arrested with 50ml of hyperkalemic (16mmol/L) Krebs solution at 37°C (A; n = 15 ) or 15°C (B; n = 15 ); hearts arrested with 50ml of Pinacidil (100umol/L) at 37°C (C; n = 15 ) or 15°C (D; n = 15 ); hearts exposed to two 3 min episodes of 37°C zero flow ischaemia (preconditioning) and subsequently arrested with Pinacidil at 37°C (E; n = 15 ) or 15°C (F; n = 15 ). All hearts then underwent 60 min of global ischaemia at their respective cardioplegic temperatures, and 60 min of normothermic perfusion. Results: In non‐preconditioned groups (A‐D) at both hypo‐ and normothermia there were no significant differences between Pinacidil and hyperkalemic arrested hearts in reperfusion coronary flow, percentage recovery of developed pressure, or dP/dT max (systolic and diastolic). At normothermia, time to mechanical and electrical arrest was significantly longer in the Pinacidil group (C; 16.0 min and 21.0 min) than in the hyperkalemic group (A; 5.0 min and 7.6 min; p < 0.01 ). At hypothermia the incidence of reperfusion VF was significantly higher in the Pinacidil group (D; 40%) than the hyperkalemic group (B; 0%; p < 0.001) . In the preconditioned groups (E & F) reperfusion coronary flow was significantly greater than in non‐preconditioned groups (C & D) at both normo‐ and hypothermia. At hypothermia, preconditioned hearts (F), when compared to non‐preconditioned hearts (D), displayed a significantly greater recovery of developed pressure (D; 84.3% c.f. 70.2% at 60 min; p < 0.04 ) and systolic dP/dT max (D; 84.7% c.f. 66.1%; p = 0.01 ) throughout reperfusion. Conclusions: Pinacidil affords myocardial protection similar to that of hyperkalemic cardioplegia despite significantly prolonged mechanical and electrical arrest times. Furthermore, at hypothermia, ischaemic preconditioning confers a myocardial protective benefit in addition to that provided by Pinacidil alone. Thus, Pinacidil cardioplegia in combination with hypothermia and ischaemic preconditioning is an effective and promising cardioprotective strategy.