生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2001年
1期
7-12
,共6页
缺血-再灌注%远程缺血预处理%肾缺血%肾神经传入放电活动%心脏%8-苯茶碱
缺血-再灌註%遠程缺血預處理%腎缺血%腎神經傳入放電活動%心髒%8-苯茶堿
결혈-재관주%원정결혈예처리%신결혈%신신경전입방전활동%심장%8-분다감
在氨基甲酸乙酯麻醉家兔上, 观察肾脏缺血预处理(RIP)对缺血-再灌注心肌的影响, 旨在证实RIP对心肌有无保护效应, 并明确肾神经在其中的作用。所得结果如下: (1)在心脏45 min缺血和180 min再灌注过程中, 血压、心率和心肌耗氧量呈进行性下降；心外膜电图ST段在缺血期明显抬高, 再灌注过程中逐渐恢复到基础对照值。心肌梗塞范围占缺血心肌的55.80±1.25%。(2) RIP时心肌梗塞范围为36.51±2.8%, 较单纯心肌缺血-再灌注显著减少(P<0.01), 表明RIP对心肌有保护作用。(3)肾神经切断可取消RIP对心肌的保护效应, 但肾神经切断本身对单纯缺血-再灌注所致的心肌梗死范围无明显影响。(4)肾缺血(10 min)时, 肾传入神经放电活动由0.14±0.08增至0.65±0.12 imp/s (P<0.01)。(5) 预先应用腺苷受体拮抗剂8-苯茶碱可明显减弱肾缺血所激活的肾传入神经活动, 提示肾传入活动的增强是由肾缺血产生的腺苷所介导。以上结果表明, 肾短暂缺血-再灌注所诱发的肾神经传入活动在RIP心肌保护效应中起重要作用。
在氨基甲痠乙酯痳醉傢兔上, 觀察腎髒缺血預處理(RIP)對缺血-再灌註心肌的影響, 旨在證實RIP對心肌有無保護效應, 併明確腎神經在其中的作用。所得結果如下: (1)在心髒45 min缺血和180 min再灌註過程中, 血壓、心率和心肌耗氧量呈進行性下降；心外膜電圖ST段在缺血期明顯抬高, 再灌註過程中逐漸恢複到基礎對照值。心肌梗塞範圍佔缺血心肌的55.80±1.25%。(2) RIP時心肌梗塞範圍為36.51±2.8%, 較單純心肌缺血-再灌註顯著減少(P<0.01), 錶明RIP對心肌有保護作用。(3)腎神經切斷可取消RIP對心肌的保護效應, 但腎神經切斷本身對單純缺血-再灌註所緻的心肌梗死範圍無明顯影響。(4)腎缺血(10 min)時, 腎傳入神經放電活動由0.14±0.08增至0.65±0.12 imp/s (P<0.01)。(5) 預先應用腺苷受體拮抗劑8-苯茶堿可明顯減弱腎缺血所激活的腎傳入神經活動, 提示腎傳入活動的增彊是由腎缺血產生的腺苷所介導。以上結果錶明, 腎短暫缺血-再灌註所誘髮的腎神經傳入活動在RIP心肌保護效應中起重要作用。
재안기갑산을지마취가토상, 관찰신장결혈예처리(RIP)대결혈-재관주심기적영향, 지재증실RIP대심기유무보호효응, 병명학신신경재기중적작용。소득결과여하: (1)재심장45 min결혈화180 min재관주과정중, 혈압、심솔화심기모양량정진행성하강；심외막전도ST단재결혈기명현태고, 재관주과정중축점회복도기출대조치。심기경새범위점결혈심기적55.80±1.25%。(2) RIP시심기경새범위위36.51±2.8%, 교단순심기결혈-재관주현저감소(P<0.01), 표명RIP대심기유보호작용。(3)신신경절단가취소RIP대심기적보호효응, 단신신경절단본신대단순결혈-재관주소치적심기경사범위무명현영향。(4)신결혈(10 min)시, 신전입신경방전활동유0.14±0.08증지0.65±0.12 imp/s (P<0.01)。(5) 예선응용선감수체길항제8-분다감가명현감약신결혈소격활적신전입신경활동, 제시신전입활동적증강시유신결혈산생적선감소개도。이상결과표명, 신단잠결혈-재관주소유발적신신경전입활동재RIP심기보호효응중기중요작용。
The effects of renal ischemic preconditioning (RIP) on ischemia-reperfused myocardium were examined in the urethane-anesthetized rabbit to determine whether RIP may provide cardioprotection and to observe the role of the renal nerve in such condition. The results obtained are as follows: (1) During 45 min myocardial ischemia and subsequent 180 min reperfusion, blood pressure, heart rate and myocardial oxygen consumption decreased progressively. Epicardial electrographic ST-segment was elevated significantly in the period of ischemia and returned to the baseline gradually in the course of reperfusion. The myocardial infarct size occupied 55.80±1.25% of the area at risk. (2) RIP significantly reduced the myocardial infarct size to 36.51±2.80% (P<0.01), indicating the cardioprotective effect of such an intervention. (3) Renal nerve section (RNS) completely abolished the cardioprotection afforded by RIP, though RNS per se did not affect the myocardial infarct size produced by ischemia-reperfusion. (4) During 10 min renal ischemia, the averaged multi-unit discharge rate of the renal afferent was increased from 0.14±0.08 to 0.65±0.12 imp/s (P<0.01). (5) Pretreatment with an adenosine receptor antagonist 8-phenyltheophylline (10 mg/kg) markedly attenuated the discharge rate of the renal afferent induced by transient renal ischemia, implying that adenosine released in ischemic kidney activated the renal afferent. It is suggested that activation of renal afferents by transient renal ischemia-reperfusion plays an important role in the cardioprotection afforded by RIP.
