Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hype...Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. Fractional flow reserve(FFR, calculated by coronary pressure measurements during adeno sine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis(mean diameter stenosis of 50±1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an α1-, α2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective α1-adrenergic blocker;(c) 20 patients before and after IC bolus of saline. Since minimal luminal diameter remained unchanged before and after phentolamine(1.46±0.06 vs. 1.47±0.06 mm, ns), urapidil 1.46±0.06 vs. 1.39±0.08, ns), and saline(1.56±0.08 vs. 1.55±0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR(phentolamine: 0.79±0.02 vs. 0.77±0.02, p< 0.05; urapidil: 0.78±0.02 vs. 0.75±0.02, p< 0.05). However, only 6 patients showed a change in FFR from ≥0.75 to < 0.75 and no patients showed a change in FFR from ≥0.80 to < 0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. The administration of α-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making.展开更多
目的:观察Β2肾上腺素受体拮抗剂对心肌梗死后心肌细胞胞浆游离CA2+浓度([CA2+]I)的影响。方法:结扎冠状动脉,复制大鼠心肌梗死模型。随机分为心肌梗死后2、4、8周组,正常对照组作假手术。分离大鼠心肌细胞,每组大鼠制备20份样品,再随...目的:观察Β2肾上腺素受体拮抗剂对心肌梗死后心肌细胞胞浆游离CA2+浓度([CA2+]I)的影响。方法:结扎冠状动脉,复制大鼠心肌梗死模型。随机分为心肌梗死后2、4、8周组,正常对照组作假手术。分离大鼠心肌细胞,每组大鼠制备20份样品,再随机分为4小组,分别给予Β2受体拮抗剂ICI118,551、Β1受体拮抗剂阿替洛尔、非选择性Β受体拮抗剂普萘洛尔后,用FURA-2荧光技术测定心肌细胞[C2+]I。结果:心肌梗死后4、8周,ICI118, 551组心肌细胞[CA2+]I增幅显著低于异丙肾上腺素组(24．5％±5．7％ VS 57．8％±13．2％,P<0．01;12．2％±7．9％ VS 44．6％±11．3%, P<0．01);正常对照组和心肌梗死后2周,上述两组心肌细胞[CA2+]I增幅无显著差异(P> 0．05)。正常对照组和心肌梗死后2周,阿替洛尔组心肌细胞[CA2+]I增幅显著低于异丙肾上腺素组(P<0．05);正常对照组及心肌梗死后2、4、8周,普萘洛尔组心肌细胞[CA2+]I增幅均显著低于异丙肾上腺素组(P<0．05)。结论:Β2 受体拮抗剂对于有效抑制心肌梗死后交感神经激动引起的心肌细胞内钙超载可能起重要作用。展开更多
文摘Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. Fractional flow reserve(FFR, calculated by coronary pressure measurements during adeno sine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis(mean diameter stenosis of 50±1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an α1-, α2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective α1-adrenergic blocker;(c) 20 patients before and after IC bolus of saline. Since minimal luminal diameter remained unchanged before and after phentolamine(1.46±0.06 vs. 1.47±0.06 mm, ns), urapidil 1.46±0.06 vs. 1.39±0.08, ns), and saline(1.56±0.08 vs. 1.55±0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR(phentolamine: 0.79±0.02 vs. 0.77±0.02, p< 0.05; urapidil: 0.78±0.02 vs. 0.75±0.02, p< 0.05). However, only 6 patients showed a change in FFR from ≥0.75 to < 0.75 and no patients showed a change in FFR from ≥0.80 to < 0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. The administration of α-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making.
文摘目的:观察Β2肾上腺素受体拮抗剂对心肌梗死后心肌细胞胞浆游离CA2+浓度([CA2+]I)的影响。方法:结扎冠状动脉,复制大鼠心肌梗死模型。随机分为心肌梗死后2、4、8周组,正常对照组作假手术。分离大鼠心肌细胞,每组大鼠制备20份样品,再随机分为4小组,分别给予Β2受体拮抗剂ICI118,551、Β1受体拮抗剂阿替洛尔、非选择性Β受体拮抗剂普萘洛尔后,用FURA-2荧光技术测定心肌细胞[C2+]I。结果:心肌梗死后4、8周,ICI118, 551组心肌细胞[CA2+]I增幅显著低于异丙肾上腺素组(24．5％±5．7％ VS 57．8％±13．2％,P<0．01;12．2％±7．9％ VS 44．6％±11．3%, P<0．01);正常对照组和心肌梗死后2周,上述两组心肌细胞[CA2+]I增幅无显著差异(P> 0．05)。正常对照组和心肌梗死后2周,阿替洛尔组心肌细胞[CA2+]I增幅显著低于异丙肾上腺素组(P<0．05);正常对照组及心肌梗死后2、4、8周,普萘洛尔组心肌细胞[CA2+]I增幅均显著低于异丙肾上腺素组(P<0．05)。结论:Β2 受体拮抗剂对于有效抑制心肌梗死后交感神经激动引起的心肌细胞内钙超载可能起重要作用。
