Elam M, Sverrisdottir Y B, Rundqvist B, McKenzie D, Wallin B Gunnar, Macefield V G
Department of Clinical Neurophysiology, Inst for Clinical Neuroscience, Sahlgrenska University Hospital, Götenburg, Sweden.
Acta Physiol Scand. 2003 Mar;177(3):405-11. doi: 10.1046/j.1365-201X.2003.01080.x.
Congestive heart failure (CHF) and obstructive sleep apnoea syndrome (OSAS) are both associated with an intense sympathoexcitation, including an increased muscle sympathetic nerve activity (MSNA). We have studied the firing characteristics of single vasoconstrictor fibres to the muscle vascular bed in CHF and OSAS patients, at rest and during transient sympathoexcitatory stimuli, to elucidate the mechanisms by which vasoconstrictor output is augmented in these conditions.
The main alternatives for augmenting sympathetic output are an increased firing frequency of individual nerve fibres and an increased recruitment of nerve fibres. Starting with the frequency alternative, the inherent bursting character of MSNA provides two possibilities to increase the firing of individual fibres: (1) by increasing the proportion of neural bursts in which the fibre is active (increased firing probability) and (2) by increasing the number of spikes a fibre generates per burst (increased multiple within-burst firing). At rest and in cardiac sinus rhythm, an increased firing probability is seen in both CHF and OSAS patients, whereas increased multiple within-burst firing is found in OSAS but not in CHF. In response to transient sympathoexcitatory stimuli (such as pre-mature heart beats), both patient groups show marked shifts towards multiple within-burst firing. Thus, both mechanisms for augmenting discharge frequency are operating in these two pathological conditions, but the firing characteristics at rest differ significantly. During recording sessions in sympathoexcited patients, we have encountered vasoconstrictor fibres that are active almost exclusively during periods of transient sympathoexcitation, while being virtually silent at rest. This suggests that recruitment of previously inactive vasoconstrictor fibres, the second main alternative for increasing vasoconstrictor output, contributes to transient sympathoexcitatory responses in these patients. Although it seems reasonable to assume that recruitment may also contribute to the resting level of MSNA in CHF and OSAS, this issue is difficult to resolve in microneurographic studies.
In conclusion, pathological sympathoexcitation appears to depend on both recruitment and increased firing frequency. A shift towards multiple within-burst firing, at rest or in response to transient stimuli, may constitute a risk factor per se as it entails neural volleys with high instantaneous firing frequencies and consequently higher release of neurotransmitters.
充血性心力衰竭（CHF）和阻塞性睡眠呼吸暂停综合征（OSAS）均与强烈的交感神经兴奋有关，包括肌肉交感神经活动（MSNA）增加。我们研究了CHF和OSAS患者在静息状态以及短暂交感神经兴奋刺激期间，单根血管收缩纤维向肌肉血管床的放电特征，以阐明在这些情况下血管收缩输出增加的机制。
增强交感神经输出的主要方式有增加单根神经纤维的放电频率以及增加神经纤维的募集。从频率方面来看，MSNA固有的爆发特性提供了两种增加单根纤维放电的可能性：（1）通过增加纤维活跃的神经冲动比例（增加放电概率），以及（2）通过增加纤维每次爆发产生的尖峰数量（增加爆发内多重放电）。在静息状态和心脏窦性心律时，CHF和OSAS患者均出现放电概率增加，而OSAS患者出现爆发内多重放电增加，CHF患者则未出现。对短暂交感神经兴奋刺激（如早搏）的反应中，两组患者均显著转向爆发内多重放电。因此，在这两种病理状态下，增加放电频率的两种机制均起作用，但静息时的放电特征有显著差异。在交感神经兴奋的患者记录过程中，我们遇到了几乎仅在短暂交感神经兴奋期活跃而在静息时几乎沉默的血管收缩纤维。这表明募集先前不活跃的血管收缩纤维，即增加血管收缩输出的第二个主要方式，对这些患者的短暂交感神经兴奋反应有贡献。尽管可以合理推测募集也可能对CHF和OSAS患者的MSNA静息水平有贡献，但在微神经图研究中这个问题难以解决。
总之，病理性交感神经兴奋似乎既依赖于募集又依赖于放电频率增加。在静息时或对短暂刺激的反应中转向爆发内多重放电本身可能构成一个危险因素，因为这会导致具有高瞬时放电频率的神经冲动，从而导致更高的神经递质释放。
