EFFECT OF VASOPRESSIN ON LEFT-VENTRICULAR PERFORMANCE
EFFECT OF VASOPRESSIN ON LEFT-VENTRICULAR PERFORMANCE
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DOI：
10.1152/ajpheart.1993.264.1.h53
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发表时间：
1993-01-01
影响因子：
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通讯作者：
LITTLE, WC
中科院分区：
文献类型：
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作者：
CHENG, CP;IGARASHI, Y;LITTLE, WC
我们评估了精氨酸加压素（AVP）对8只清醒犬左心室（LV）功能的影响。AVP输注后五分钟（6分钟）。kg ~（-1）·min ~（-1）2 min），血浆AVP由3.9 ± 0.9上升到14.7 ± 4.6pg/ml（P < 0.05）。在所有反射完整的情况下，AVP引起LV收缩末期压显著增加（P <0.05）。（112 +/- 8 vs. 122 +/- 7 mmHg，P < 0.05）收缩末期容积（V）（30 +/- 5.8 vs. 38 +/- 7.7 ml，P < 0.05），总全身阻力（6.2 ± 1.8 vs. 10.6 ± 4.0 mmHg.dl-1.min，P < 0.01）和动脉弹性（E（a））（6.8 ± 3.0 vs. 8.6 ± 3.9 mmHg/ml，P < 0.05），而心率（110 +/- 6 vs. 82 +/- 10 beats/min，P < 0.05）和每搏输出量（16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml，P < 0.05）减少。冠状窦血流量无显著变化（82 +/- 19 vs. 78 +/- 22 ml/min，P =不显著）。AVP可降低左室收缩末期P-V关系的斜率（10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml，P < 0.05），LV压力的最大一阶导数（dP/dt（max））-舒张末期容积（V（艾德））关系（135.2 ± 18.7 vs. 63.1 ± 7.7 mmHg·s·1.ml-1，P < 0.05），以及每搏功-V（艾德）关系（81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg，P < 0.05），并将关系向右移动，表明LV性能下降。甲氧胺产生的E（a）的类似增加不会抑制LV性能。阻断自主神经后，AVP也有强心作用。当起搏阻止心率变化时，AVP V1受体阻滞剂可逆转这种效应。我们的结论是，在清醒的动物，生理相关浓度的AVP直接抑制LV收缩性能，这种效果是防止AVP V1受体拮抗剂。
We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 mum. kg-1.min-1 for 2 min) the plasma AVP was elevated from 3.9 +/-0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1.min, P < 0.01) and arterial elastance (E(a)) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dt(max))-end-diastolic volume (V(ED)) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg-s-1.ml-1, P < 0.05), and the stroke work-V(ED) relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in E(a) produced by methoxamine did not depress LV performance. The cardiodepressant effect of AVP was also present after autonomic blockade. When changes in heart rate were prevented by pacing, this effect was reversed by AVP V1-receptor blockade. We conclude that, in conscious animals, physiologically relevant concentrations of AVP directly depress LV contractile performance, and this effect is prevented by an AVP V1-receptor antagonist.