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在缺血或再灌注期间,内源性A(1) 腺苷受体激活可改善小鼠心脏的恢复情况。

Intrinsic A(1) adenosine receptor activation during ischemia or reperfusion improves recovery in mouse hearts.

作者信息

Peart J, Headrick J P

机构信息

Centre for Cardiovascular Research, Griffith University Gold Coast Campus, Southport QLD 4217, Australia.

出版信息

Am J Physiol Heart Circ Physiol. 2000 Nov;279(5):H2166-75. doi: 10.1152/ajpheart.2000.279.5.H2166.

Abstract

We assessed the role of A(1) adenosine receptor (A(1)AR) activation by endogenous adenosine in the modulation of ischemic contracture and postischemic recovery in Langendorff-perfused mouse hearts subjected to 20 min of total ischemia and 30 min of reperfusion. In control hearts, the rate-pressure product (RPP) and first derivative of pressure development over time (+dP/dt) recovered to 57 +/- 3 and 58 +/- 3% of preischemia, respectively. Diastolic pressure remained elevated at 20 +/- 2 mmHg (compared with 3 +/- 1 mmHg preischemia). Interstitial adenosine, assessed by microdialysis, rose from approximately 0.3 to 1.9 microM during ischemia compared with approximately 15 microM in rat heart. Nonetheless, these levels will near maximally activate A(1)ARs on the basis of effects of exogenous adenosine and 2-chloroadenosine. Neither A(1)AR blockade with 200 nM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) during the ischemic period alone nor A(1)AR activation with 50 nM N(6)-cyclopentyladenosine altered rapidity or extent of ischemic contracture. However, ischemic DPCPX treatment significantly depressed postischemic recovery of RPP and +dP/dt (44 +/- 3 and 40 +/- 4% of preischemia, respectively). DPCPX treatment during the reperfusion period alone also reduced recovery of RPP and +dP/dt (to 44 +/- 2 and 47 +/- 2% of preischemia, respectively). These data indicate that 1) interstitial adenosine is lower in mouse versus rat myocardium during ischemia, 2) A(1)AR activation by endogenous adenosine or exogenous agonists does not modify ischemic contracture in murine myocardium, 3) A(1)AR activation by endogenous adenosine during ischemia attenuates postischemic stunning, and 4) A(1)AR activation by endogenous adenosine during the reperfusion period also improves postischemic contractile recovery.

摘要

我们评估了内源性腺苷激活A(1) 型腺苷受体(A(1)AR)在Langendorff灌注的小鼠心脏缺血性挛缩和缺血后恢复调节中的作用。该小鼠心脏经历了20分钟的完全缺血和30分钟的再灌注。在对照心脏中,心率-血压乘积(RPP)和压力随时间变化的一阶导数(+dP/dt)分别恢复到缺血前的57±3%和58±3%。舒张压仍维持在20±2 mmHg的较高水平(缺血前为3±1 mmHg)。通过微透析评估,缺血期间心肌间质腺苷从约0.3 μM升至1.9 μM,而大鼠心脏中的该水平约为15 μM。尽管如此,基于外源性腺苷和2-氯腺苷的作用,这些水平将使A(1)ARs接近最大程度激活。单独在缺血期用200 nM 8-环戊基-1,3-二丙基黄嘌呤(DPCPX)阻断A(1)AR或用50 nM N(6)-环戊基腺苷激活A(1)AR均未改变缺血性挛缩的速度或程度。然而,缺血期给予DPCPX显著降低了缺血后RPP和 +dP/dt的恢复(分别为缺血前的44±3%和40±4%)。单独在再灌注期给予DPCPX也降低了RPP和 +dP/dt的恢复(分别降至缺血前的44±2%和47±2%)。这些数据表明:1)缺血期间小鼠心肌中的间质腺苷低于大鼠心肌;2)内源性腺苷或外源性激动剂激活A(1)AR不会改变小鼠心肌的缺血性挛缩;3)缺血期间内源性腺苷激活A(1)AR可减轻缺血后心肌顿抑;4)再灌注期内源性腺苷激活A(1)AR也可改善缺血后收缩功能的恢复。

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