Banka V S, Scherlag B J, Helfant R H
Cardiovasc Res. 1975 Jan;9(1):65-72. doi: 10.1093/cvr/9.1.65.
Contractile force and intraventricular conduction during progressive ouabain infusion were examined in 15 dogs using a Walton-Brodie strain gauge arch and sequential atrial and bundle of His pacing. This permitted: (1) contractile force determination; (2) overdrive of arrhythmias; (3) maintenance of normal contraction sequences; (4) 'normal' ventricular depolarization; (5) rate control; (6) conduction measurements of the H-V interval (His-Purkinje conduction), QRS (intramyocardial conduction), and H-S interval (total intraventricular conduction). Contractile force increased 21.2 plus or minus 4.3% at the onset of toxicity. After toxicity, there was a significant further increase (P smaller than 0.01) to 50.1 plus or minus 12.4%. However, immediately before ventricular fibrillation, a 43.8 plus or minus 8.2% decrease occurred (P smaller than 0.01). H-V time showed no change (from 30 plus or minus 2.7 to 31.5 plus or minus 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5 plus or minus 3.1 ms (P smaller than 0.05). QRS did show significant prolongation (69.5% plus or minus 5.3 to 79.5 plus or minus 6.9 ms; P smaller than 0.05) at the onset of toxicity, but this was more marked (79.5 plus or minus 6.9 to 130.5 plus or minus 8.1 ms; Pplus or minus 0.01) after toxicity. H-S time was significantly prolonged (99.5 plus or minus 6.2 to 111.0 plus or minus 8.9 ms) before (P smaller than 0.02) and after (P smaller than 0.01) toxicity (111.0 plus or minus 8.9 to 171.1 plus or minus 10.6 ms). During toxicity there is progressive increase in contractile force with continued ouabain infusion Progressive prolongation of intramyocardial conduction occurs in nontoxic and toxic doses, but His-Purkinje conduction is prolonged only in supratoxic doses.
在15只犬中，使用沃尔顿-布罗迪应变片弓形装置以及心房和希氏束顺序起搏，检测了在逐步输注哇巴因期间的收缩力和心室内传导。这使得能够：(1) 测定收缩力；(2) 超速驱动心律失常；(3) 维持正常收缩序列；(4) 实现“正常”的心室去极化；(5) 控制心率；(6) 测量H-V间期（希氏-浦肯野传导）、QRS波（心肌内传导）和H-S间期（全心室内传导）。在毒性发作时，收缩力增加了21.2±4.3%。毒性发作后，收缩力进一步显著增加（P<0.01），达到50.1±12.4%。然而，在心室颤动即将发生前，收缩力下降了43.8±8.2%（P<0.01）。H-V间期在毒性发作时无变化（从30±2.7毫秒变为31.5±2.4毫秒），但在毒性发作后延长至40.5±3.1毫秒（P<0.05）。QRS波在毒性发作时确实出现了显著延长（从69.5%±5.3毫秒延长至79.5±6.9毫秒；P<0.05），但在毒性发作后更为明显（从79.5±6.9毫秒延长至130.5±8.1毫秒；P<0.01）。H-S间期在毒性发作前（P<0.02）和发作后（P<0.01）均显著延长（从99.5±6.2毫秒延长至111.0±8.9毫秒，再从111.0±8.9毫秒延长至171.1±10.6毫秒）。在毒性发作期间，随着哇巴因持续输注，收缩力逐渐增加。在无毒和有毒剂量下，心肌内传导都会逐渐延长，但希氏-浦肯野传导仅在超毒性剂量下延长。
