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Nω-硝基-L-精氨酸甲酯、硝普钠和去甲肾上腺素对麻醉猫静脉回流的影响。

The effects of N omega-nitro-L-arginine methyl ester, sodium nitroprusside and noradrenaline on venous return in the anaesthetized cat.

作者信息

Bower E A, Law A C

机构信息

Physiological Laboratory, University of Cambridge.

出版信息

Br J Pharmacol. 1993 Apr;108(4):933-40. doi: 10.1111/j.1476-5381.1993.tb13489.x.

Abstract
  1. The vascular actions of N omega-nitro-L-arginine methyl ester (L-NAME), sodium nitroprusside and noradrenaline were investigated in cats under chloralose anaesthesia with controlled vascular tone and ventilation. Cardiac output, heart rate, vascular pressures and mean circulatory filling pressure (MCFP) were measured. Total peripheral resistance (TPR) and resistance to venous return (Rvr) were calculated from steady-state readings. 2. L-NAME (37 mumol kg-1, i.v.) administered to ten cats receiving noradrenaline (6 nmol kg-1 min-1, i.v.) increased aortic pressure by 47.5 +/- 7.1 mmHg from 106 mmHg, and MCFP by 1.56 +/- 0.36 mmHg from 10.0 mmHg (means +/- s.e. means). Mean changes in portal venous pressure, RAP and heart rate were not significant. Cardiac output fell by 29.7 +/- 3.3% from 130 ml min-1 kg-1. TPR rose by 108 +/- 7.2% from 796 mmHg l-1 min kg and Rvr by 58.4 +/- 4.5% from 64 mmHg l-1 min kg. 3. Infusion of sodium nitroprusside into cats receiving noradrenaline evoked dose-related falls in aortic pressure, MCFP, TPR and Rvr. Changes in portal venous pressure, RAP and heart rate were not significant and cardiac output fell slightly. After L-NAME, sensitivity to nitroprusside was increased by 139 +/- 34% for MCFP, 176 +/- 19% for TPR and 351 +/- 39% for Rvr, and cardiac output rose slightly. The nitroprusside infusion required to restore TPR after L-NAME was estimated to be 5.8 x 10(+/- 0.41) nmol kg-1 min-1, which was approximately three times more than that required to restore MCFP. 4. Infusion of noradrenaline evoked dose-related increases in aortic and portal venous pressures, heart rate, cardiac output, MCFP, TPR and Rvr. After L-NAME and nitroprusside (4.4 nmol kg-1 min-1, i.v.),TPR and Rvr were not significantly different, but MCFP was reduced by 1.76 +/- 0.24 mmHg, and cardiac output by 22 +/- 1.9%. After subsequent expansion of the circulating blood volume (5-7.5 ml kg-1 dextran-saline), mean values for all parameters were restored to their previous levels. Sensitivity to noradrenaline was not significantly altered for heart rate, TPR and Rvr but was reduced by 31.8 +/- 12%for MCFP and by 66.5 +/- 18% for cardiac output.5. The depression of cardiac output by L-NAME is attributed to the increase in Rvr, partly compensated by the rise in MCFP. For a given rise in MCFP, the increase in R, was seven times greater after L-NAME than after noradrenaline, and the difference in the relative actions of the two drugs on resistance and capacitance vessels largely accounts for their contrasting effects on venous return. A procedure is suggested for replacement of vascular nitric oxide by nitroprusside infusion and blood volume expansion.
摘要
  1. 在氯醛糖麻醉下,对猫进行血管张力和通气控制,研究了Nω-硝基-L-精氨酸甲酯(L-NAME)、硝普钠和去甲肾上腺素的血管作用。测量了心输出量、心率、血管压力和平均循环充盈压(MCFP)。根据稳态读数计算总外周阻力(TPR)和静脉回流阻力(Rvr)。2. 给10只接受去甲肾上腺素(6 nmol kg-1 min-1,静脉注射)的猫静脉注射L-NAME(37 μmol kg-1)后,主动脉压从106 mmHg升高47.5±7.1 mmHg,MCFP从10.0 mmHg升高1.56±0.36 mmHg(均值±标准误均值)。门静脉压、RAP和心率的平均变化不显著。心输出量从130 ml min-1 kg-1下降29.7±3.3%。TPR从796 mmHg l-1 min kg升高108±7.2%,Rvr从64 mmHg l-1 min kg升高58.4±4.5%。3. 给接受去甲肾上腺素的猫输注硝普钠会引起主动脉压、MCFP、TPR和Rvr的剂量相关下降。门静脉压、RAP和心率的变化不显著,心输出量略有下降。注射L-NAME后,对硝普钠的敏感性,MCFP提高139±34%,TPR提高176±19%,Rvr提高351±39%,心输出量略有上升。估计注射L-NAME后恢复TPR所需的硝普钠输注量为5.8×10(±0.41)nmol kg-1 min-1,约为恢复MCFP所需量的三倍。4. 输注去甲肾上腺素会引起主动脉和门静脉压、心率、心输出量、MCFP、TPR和Rvr的剂量相关增加。注射L-NAME和硝普钠(4.4 nmol kg-1 min-1,静脉注射)后,TPR和Rvr无显著差异,但MCFP降低1.76±0.24 mmHg,心输出量降低22±1.9%。随后循环血容量扩充(5 - 7.5 ml kg-1右旋糖酐生理盐水)后,所有参数的平均值恢复到先前水平。心率、TPR和Rvr对去甲肾上腺素的敏感性无显著改变,但MCFP降低31.8±12%,心输出量降低66.5±18%。5. L-NAME对心输出量的抑制归因于Rvr的增加,部分由MCFP的升高得到补偿。对于给定的MCFP升高,L-NAME后Rvr的增加是去甲肾上腺素后增加的7倍,两种药物对阻力血管和容量血管的相对作用差异在很大程度上解释了它们对静脉回流的相反影响。建议了一种通过输注硝普钠和扩充血容量来替代血管一氧化氮的方法。

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本文引用的文献

1
Homeometric autoregulation in the heart.
Circ Res. 1960 Sep;8:1077-91. doi: 10.1161/01.res.8.5.1077.
2
Relative importance of venous and arterial resistances in controlling venous return and cardiac output.
Am J Physiol. 1959 May;196(5):1008-14. doi: 10.1152/ajplegacy.1959.196.5.1008.
3
Mechanism of the increased venous return and cardiac output caused by epinephrine.
Am J Physiol. 1958 Jan;192(1):126-30. doi: 10.1152/ajplegacy.1957.192.1.126.
6
Heterogeneous behavior of the canine arterial and venous wall. Importance of the endothelium.
Circ Res. 1982 Oct;51(4):439-47. doi: 10.1161/01.res.51.4.439.
8
Endothelium removal augments vasodilation by sodium nitroprusside and sodium nitrite.
Eur J Pharmacol. 1985 Aug 7;114(1):93-6. doi: 10.1016/0014-2999(85)90527-8.

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