Literature DB >> 8523433

Contractile dysfunction caused by normothermic ischaemia and KCL arrest in the isolated pig heart: a 31P NMR study.

V V Kupriyanov1, M St Jean, B Xiang, K W Butler, R Deslauriers.   

Abstract

The aims of this study were to assess (1) whether contractile dysfunction caused by ischaemia under hyperkalaemic conditions ("cardioplegic ischaemia") is associated with impaired energy production or abnormalities in regulation of contractility and (2) whether hyperkalaemia itself contributes to contractile dysfunction. We used 31P and 23Na NMR spectroscopy in conjunction with measurements of mechanical function and oxygen consumption in Langendorff perfused pig hearts to evaluate the mechanism of contractile failure caused by (1) total global cardioplegic (17 mM [K+]) ischaemia (36 degrees C, 50 min KCl arrest, 45 min ischaemia, 20 min reflow with high KCl) and (2) KCl arrest alone (115 min) without flow cessation. KCl arrest plus ischaemia and subsequent reperfusion (Group I) resulted in decreases in ATP (mean +/- S.D.; 61 +/- 13% of initial, n = 5; P < 0.01) and pressure-rate product (PRP) (31 +/- 9%, n = 17; P = 0.0001) while phosphocreatine (PCr), Pi, total creatine (Cr) and intracellular Na+ levels were unaffected. KCl arrest itself (Group II, n = 6) did not affect PCr, ATP or total Cr levels but decreased the PRP to 59 +/- 12% (P < 0.001). Oxygen consumption rates (Vo2) were reduced in both groups to similar levels (67 +/- 18, P < 0.01 and 77 +/- 13%, P < 0.02, respectively). The efficiency of energy conversion to mechanical work (PRP/delta VO2) decreased to 51 +/- 15 (P < 0.001) and 67 +/- 13% (P < 0.012) of initial levels, respectively. To assess metabolic and contractile reserves of post-ischaemic (n = 7) and KCl-treated (n = 3) hearts, the effects of isoproterenol (Iso) and increased Ca2+ were compared with those in normal beating hearts (Group III, n = 3). In all groups treatment with Iso (0.1 micron) greatly increased PRP (to 526 +/- 116, 203 +/- 16 and 198 +/- 8% of the level prior to stimulation (baseline), P < 0.01, respectively) and Vo2 (162 +/- 9, 153 +/-16 and 128 +/-10% of baseline, P < 0.05, Respectively). Increasing [Ca2+] from 1 to 1.66 mM produced less stimulation than Iso: PRP increased to 195 +/- 23, 156 +/- 13 and 163 +/- 22% (P < 0.05) and Vo2 increased to 138 +/- 22 (P < 0.05), 115 +/- 4 and 120 +/- 10% of baseline in Groups I, II and III, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Entities:  

Mesh:

Substances:

Year:  1995        PMID: 8523433     DOI: 10.1016/s0022-2828(95)90854-4

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  3 in total

1.  Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection.

Authors:  Sergiy M Nadtochiy; Andrew J Tompkins; Paul S Brookes
Journal:  Biochem J       Date:  2006-05-01       Impact factor: 3.857

2.  Myocardial energy metabolism in ischemic preconditioning and cardioplegia: a metabolic control analysis.

Authors:  Achim M Vogt; Albrecht Elsässer; Anja Pott-Beckert; Cordula Ackermann; Sven Y Vetter; Murat Yildiz; Wolfgang Schoels; David A Fell; Hugo A Katus; Wolfgang Kübler
Journal:  Mol Cell Biochem       Date:  2005-10       Impact factor: 3.396

3.  Development of a cardiovascular magnetic resonance-compatible large animal isolated heart model for direct comparison of beating and arrested hearts.

Authors:  Andrew D Scott; Tim Jackson; Zohya Khalique; Margarita Gorodezky; Ben Pardoe; Lale Begum; V Domenico Bruno; Rasheda A Chowdhury; Pedro F Ferreira; Sonia Nielles-Vallespin; Malte Roehl; Karen P McCarthy; Padmini Sarathchandra; Jan N Rose; Denis J Doorly; Dudley J Pennell; Raimondo Ascione; Ranil de Silva; David N Firmin
Journal:  NMR Biomed       Date:  2022-02-12       Impact factor: 4.478

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.