Performance of pig heart after 30 or 120 minutes hypothermic arrest.

Performance of pig heart after 30 or 120 minutes hypothermic arrest.
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低温停止 30 或 120 分钟后猪心脏的性能。

DOI:
10.1016/0022-4804(83)90135-x
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发表时间:
1983
期刊:
The Journal of surgical research
影响因子:
--
通讯作者:
Avrunin,JS
Avrunin,JS
中科院分区:
--
文献类型:
--
作者:
Dobbs,WA;Engelman,RM;Rousou,JH;Douglas,DM;Lemeshow,S;Avrunin,JS

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为研究缺血30分钟(n=25)或120分钟(n=27),再灌流60分钟后再灌流60分钟,观察低温(T=15℃)钾停搏和缺血持续时间对心脏的影响,通过测定离体心脏对180分钟灌流(n=12)的反应。部分动物取心肌组织标本测定三磷酸腺苷(ATP)和磷酸肌酸(CP),其中灌注组6只,缺血30min再灌流60min组7只,缺血120min再灌流60min组15只。其余动物分别测定左心功能、心肌氧代谢(MV̇O2)和血浆肌酸激酶(CK),其中长时间灌注组6只,缺血12 0min再灌注组12只,缺血30min再灌注组18只[LVP 13只,MV̇O2 17只,CK 6只]。在长时间的灌流过程中,左心功能(以发展压Δ-P表示)在灌流30min时从初始的175±36下降到128±19 mm Hg,然后更缓慢地下降到180min的终值113±8 mm Hg。这些降幅并未明显低于初值。心肌提取百分比以类似的方式下降,但冠脉血流量在这段时间内保持不变。缺血30或120min的主要作用是使再灌注期的左心室发展压ΔP降至对照组相应值的70%以上(差异有统计学意义),提示延长缺血时间不会导致心功能的进一步恶化。心脏长时间灌流后,对照组血浆CK浓度由35±6升升至59±8 IU/L(P<0.05)。两组再灌流时血浆CK均升高,但与停搏前比较差异无统计学意义。因此,这段时间的低温停搏性心肌缺血似乎不会导致组织坏死,但在30至120分钟的范围内,左心室功能显著下降,这与缺血时间无关。
The effect of the duration of hypothermic (T= 15°C) potassium cardioplegic arrest and ischemia on the heart was determined by measuring the response of the isolatedin situpig heart to 180 min of perfusion (n= 12) to provide appropriate control values for the study of 30 (n= 25) or 120 (n= 27) min of ischemia, followed by 60 min of reperfusion. In some of these animals, myocardial tissue samples were obtained for measurement of adenosine triphosphate (ATP) and creatine phosphate (CP), (6 in the perfusion group, 7 in the 30 min of ischemia and 60 min of reperfusion group and 15 in the 120 min of ischemia and 60 min of reperfusion group). In the remaining animals, measurements of either left ventricular performance (LVP), myocardial oxygen metabolism (MV̇O2) or plasma creatine kinase (CK) were obtained (6 in the prolonged perfusion group, 12 in the 120 min of ischemia and 60 min of reperfusion group, [6 LVP and MV̇O2and 6 CK] and 18 in the 30 min of ischemia and 60 min of reperfusion group [13 LVP, 17 MV̇O2and 6 CK]). During prolonged perfusion, left ventricular performance, expressed as developed pressure,ΔP, fell from an initial value of 175 ± 36 to 128 ± 19 mm Hg at 30 min of perfusion, followed by a more gradual decline to a final value of 113 ± 8 mm Hg at 180 min of perfusion. These decreases were not significantly lower than the initial value. The percentage of myocardial extraction declined in a similar manner, but coronary blood flow was constant over this interval. The primary effect of 30 or 120 min of ischemia was to reduce left ventricular developed pressure,ΔP, during reperfusion to more than 70% of the corresponding value in the control group (these differences were statistically significant) which suggests that prolonging the period of ischemia did not cause further deterioration of cardiac performance. The plasma concentration of CK rose in the control group of hearts subjected to prolonged perfusion from an initial value of 35 ± 6 to a final value of 59 ± 8 IU/liter (P< 0.05). While plasma CK increased during reperfusion in both ischemia/ reperfusion groups, these values were not significantly higher from prearrest values. Thus hypothermic cardioplegic ischemia of this duration did not appear to result in tissue necrosis, but there was a significant reduction in left ventricular performance which was independent of the duration of ischemia between the limits of 30 and 120 min.
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发表时间: 1976-01-01
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