Fu Liang-Wu, Longhurst John C
Department of Medicine, College of Medicine, University of California at Irvine, Irvine, CA 92697, USA.
J Physiol. 2005 Jun 15;565(Pt 3):1007-17. doi: 10.1113/jphysiol.2005.084004. Epub 2005 Mar 17.
Cardiac spinal afferents are activated during myocardial ischaemia. Our previous studies have shown that during ischaemia, histamine and bradykinin (BK) stimulate cardiac spinal afferents. Because the two mediators are released together during ischaemia, the present study examined the interactions between these two mediators with respect to their influence on ischaemically sensitive cardiac afferents. Single-unit cardiac afferent activity was recorded from the left sympathetic chain or rami communicantes (T(2)-T(5)) in anaesthetized cats. Fifty-five ischaemically sensitive cardiac afferents (conduction velocity (CV) = 0.2-5.6 m s(-1), 8 Adelta- and 47 C-fibres) were identified. Administration of histamine (10 microg kg(-1)) and BK (1 microg) in combination into the left atrium (LA) caused an additive response in 16 afferents compared with administration of either BK or histamine alone (2.62 +/- 0.39 versus 1.67 +/- 0.20 versus 1.24 +/- 0.23 impulses s(-1) (imp s(-1)), BK + histamine versus BK versus histamine). To further evaluate interactions between these mediators, we observed that injection of histamine (10 microg kg(-1), LA) 4 min after the administration of BK (1 microg, LA) induced a significantly larger cardiac afferent response than the response to histamine before BK (1.24 +/- 0.23 versus 1.96 +/- 0.39 imp s(-1), before versus after, n = 10). In contrast, six other afferents responded reproducibly to repeated injections of histamine (10 microg kg(-1), LA) in the absence of BK. BK sensitization of the afferent response to histamine lasted for less than 10 min. Cyclooxygenase blockade with indomethacin (5 mg kg(-1), i.v.) abolished BK sensitization of the response to histamine (1.09 +/- 0.11 versus 1.11 +/- 0.10 imp s(-1), n = 10). Conversely, the response of most (7/9) cardiac afferents to repeat application of BK (1 microg, LA) 4 min after histamine (10 microg kg(-1), LA) was attenuated compared with the BK response before histamine (1.84 +/- 0.25 versus 1.31 +/- 0.18 imp s(-1), before versus after, P < 0.05). Repeat BK (1 microg, LA) induced a consistent response in five other afferents in the absence of histamine. Thus, BK interacts with histamine, and together they cause a larger response than either one alone. BK sensitizes cardiac afferents responding to histamine in a time-dependent fashion, and the BK sensitization effect is dependent on an intact cyclooxygenase pathway. Conversely, histamine reduces the response of most afferents to BK.
心肌缺血期间心脏的脊髓传入神经会被激活。我们之前的研究表明,在缺血期间,组胺和缓激肽(BK)会刺激心脏的脊髓传入神经。由于这两种介质在缺血期间会一起释放,因此本研究考察了这两种介质之间关于它们对缺血敏感的心脏传入神经影响的相互作用。在麻醉猫的左交感神经链或交通支(T₂ - T₅)记录单单位心脏传入神经活动。确定了55条缺血敏感的心脏传入神经(传导速度(CV)= 0.2 - 5.6 m s⁻¹,8条Aδ纤维和47条C纤维)。与单独给予BK或组胺相比,联合给予组胺(10 μg kg⁻¹)和BK(1 μg)注入左心房(LA)在16条传入神经中引起相加反应(分别为2.62 ± 0.39、1.67 ± 0.20和1.24 ± 0.23冲动·秒⁻¹(imp s⁻¹),BK + 组胺组对比BK组对比组胺组)。为了进一步评估这些介质之间的相互作用,我们观察到在给予BK(1 μg,LA)4分钟后注射组胺(10 μg kg⁻¹,LA)诱导的心脏传入神经反应比给予BK前组胺诱导的反应显著更大(分别为1.24 ± 0.23和1.96 ± 0.39 imp s⁻¹,给予BK前对比给予BK后,n = 10)。相反,另外6条传入神经在无BK时对重复注射组胺(10 μg kg⁻¹,LA)有可重复的反应。BK对组胺传入神经反应的致敏作用持续不到10分钟。用吲哚美辛(5 mg kg⁻¹,静脉注射)阻断环氧化酶消除了BK对组胺反应的致敏作用(分别为1.09 ± 0.11和1.11 ± 0.10 imp s⁻¹,n = 10)。相反,与给予组胺前BK的反应相比,在给予组胺(10 μg kg⁻¹,LA)4分钟后,大多数(7/9)心脏传入神经对重复给予BK(1 μg,LA)的反应减弱(分别为1.84 ± 0.25和1.31 ± 0.18 imp s⁻¹,给予组胺前对比给予组胺后,P < 0.05)。在无组胺时,重复给予BK(1 μg,LA)在另外5条传入神经中诱导出一致的反应。因此,BK与组胺相互作用,并且它们一起引起的反应比单独任何一种引起的反应都更大。BK以时间依赖性方式使对组胺有反应的心脏传入神经致敏,并且BK致敏作用依赖于完整的环氧化酶途径。相反,组胺降低了大多数传入神经对BK的反应。