Hirsch G M, Thompson G W, Arora R C, Hirsch K J, Sullivan J A, Armour J A
Department of Surgery, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Ann Thorac Surg. 1999 Aug;68(2):460-8; discussion 468-9. doi: 10.1016/s0003-4975(99)00558-5.
Transmyocardial laser revascularization has been used as an indirect approach to improve myocardial perfusion in patients with refractory angina not amenable to conventional therapy. Three mechanisms have been proposed for its therapeutic effects: direct perfusion of the ischemic myocardium through patent channels; induction of angiogenesis; and regional denervation. We sought to determine whether transmyocardial laser revascularization modifies afferent and efferent axonal function within the affected myocardium.
Studies were performed in 9 dogs that were artificially ventilated and underwent thoracotomy. Changes in ventricular dynamics and intrinsic cardiac neuronal activity were monitored before and after creating 20 transmural channels in the left ventricular ventral free wall with a holmium:yttrium-aluminum-garnet laser in response to three stimuli: application of veratridine or bradykinin to the epicardial sensory neurites of intrinsic cardiac afferent neurons; sympathetic or parasympathetic efferent neuronal activation either electrically (4 V, 10 Hz, 5 ms) or chemically (nicotine, 5 microg/kg intravenously), and direct cardiomyocyte beta-adrenergic receptor stimulation (isoproterenol hydrochloride, 5 microg intravenously).
Sensory neurites of right atrial afferent neurons in the studied epicardial region responded similarly to chemical stimulation before and after transmyocardial laser revascularization. Transmyocardial laser treatment did not reduce local ventricular contractile responses to direct activation of sympathetic or parasympathetic efferent neurons by electrical or chemical means, nor did it affect cardiomyocyte augmentor responses elicited by exogenous beta-adrenergic receptor challenge.
As transmyocardial laser revascularization does not affect afferent or efferent axonal function in the affected ventricle, the efficacy of this form of therapy cannot be ascribed to local denervation.
心肌激光血运重建术已被用作一种间接方法，以改善常规治疗难以奏效的顽固性心绞痛患者的心肌灌注。其治疗效果有三种机制被提出：通过开放通道直接灌注缺血心肌；诱导血管生成；以及局部去神经支配。我们试图确定心肌激光血运重建术是否会改变受影响心肌内传入和传出轴突的功能。
对9只人工通气并接受开胸手术的犬进行研究。在使用钬：钇铝石榴石激光在左心室前壁游离壁制造20个透壁通道前后，监测心室动力学和心脏固有神经元活动的变化，以应对三种刺激：将藜芦碱或缓激肽应用于心脏固有传入神经元的心外膜感觉神经纤维；通过电刺激（4伏，10赫兹，5毫秒）或化学刺激（尼古丁，5微克/千克静脉注射）激活交感或副交感传出神经元，以及直接刺激心肌细胞β-肾上腺素能受体（盐酸异丙肾上腺素，5微克静脉注射）。
在心肌激光血运重建术前后，所研究的心外膜区域右心房传入神经元的感觉神经纤维对化学刺激的反应相似。心肌激光治疗并未降低局部心室对交感或副交感传出神经元通过电或化学方式直接激活的收缩反应，也未影响外源性β-肾上腺素能受体激发引起的心肌细胞增强反应。
由于心肌激光血运重建术不影响受影响心室的传入或传出轴突功能，这种治疗方式的疗效不能归因于局部去神经支配。
