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常温缺血和氯化钾停搏所致离体猪心脏收缩功能障碍:一项31P核磁共振研究

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

作者信息

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

机构信息

Institute for Biodiagnostics, National Research Council of Canada, Winnipeg.

出版信息

J Mol Cell Cardiol. 1995 Aug;27(8):1715-30. doi: 10.1016/s0022-2828(95)90854-4.

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)

摘要

本研究的目的是评估

(1)高钾血症条件下缺血所致的收缩功能障碍(“心脏停搏缺血”)是否与能量产生受损或收缩调节异常有关;(2)高钾血症本身是否导致收缩功能障碍。我们在Langendorff灌注猪心脏中,联合使用31P和23Na核磁共振波谱技术以及机械功能和氧消耗测量,以评估由以下情况导致的收缩功能衰竭机制:(1)完全性全心停搏(17 mM [K+])缺血(36℃,50分钟氯化钾停搏,45分钟缺血,20分钟高钾氯化钾再灌注);(2)单纯氯化钾停搏(115分钟)且无血流中断。氯化钾停搏加缺血及随后的再灌注(第一组)导致ATP(平均值±标准差;为初始值的61±13%,n = 5;P < 0.01)和压力-速率乘积(PRP)(31±9%,n = 17;P = 0.0001)降低,而磷酸肌酸(PCr)、无机磷(Pi)、总肌酸(Cr)和细胞内钠离子水平未受影响。单纯氯化钾停搏(第二组,n = 6)不影响PCr、ATP或总Cr水平,但使PRP降至59±12%(P < 0.001)。两组的氧消耗率(Vo2)均降低至相似水平(分别为67±18,P < 0.01和77±13%,P < 0.02)。能量转化为机械功的效率(PRP/ΔVO2)分别降至初始水平的51±15(P < 0.001)和67±13%(P < 0.012)。为评估缺血后(n = 7)和氯化钾处理后(n = 3)心脏的代谢和收缩储备,将异丙肾上腺素(Iso)和增加钙离子浓度的作用与正常跳动心脏(第三组,n = 3)进行比较。在所有组中,用Iso(0.1微摩尔)处理均使PRP大幅增加(分别达到刺激前(基线)水平的526±116、203±16和198±8%,P < 0.01)以及Vo2增加(分别为基线的162±9、153±16和128±10%,P < 0.05)。将[Ca2+]从1 mM增加至1.66 mM产生的刺激小于Iso:在第一组、第二组和第三组中,PRP分别增加至195±23、156±13和163±22%(P < 0.05),Vo2分别增加至基线的138±22(P < 0.05)、115±4和120±10%。(摘要截断于400字)

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