Sabino João Paulo J, Traslaviña Guillermo A Ariza, Branco Luiz G S
Department of Morphology, Physiology and Basic Pathology, Dental School of Ribeirao Preto, University of São Paulo, 14040-904 Ribeirao Preto, SP, Brazil.
Department of Physiology, College of Medicine of Ribeirao Preto, Sao Paulo University, Brazil.
Respir Physiol Neurobiol. 2016 Sep;231:21-7. doi: 10.1016/j.resp.2016.05.016. Epub 2016 May 27.
Central hydrogen sulfide (H2S) has been reported to act as a gaseous neuromodulator involved in the ventilatory and cardiovascular control of normotensive rats, whereas no information is available in spontaneously hypertensive rats (SHR). We recorded minute ventilation (VE), mean arterial pressure (MAP) and heart rate (HR) before and after blocking of enzyme Cystathionine β-synthase (CBS) producing H2S in neural tissue by microinjection of aminooxyacetate (inhibitor of CBS) into the fourth ventricle of Wistar normotensive rats (WNR) and SHR followed by 30min of normoxia (21% inspired O2) or hypoxia (10% inspired O2) exposure. Microinjection of AOA or saline (1μL) did not change VE, MAP and HR during normoxia in both WNR and SHR. In WNR, hypoxia caused an increase in VE, HR and a decrease in MAP and these responses were unaltered by AOA. In SHR, hypoxia produced a higher increase of VE, and decrease in MAP and HR when compared to WNR, and these responses were all blunted by AOA. In conclusion, endogenous H2S plays important modulatory roles on hypoxia-induced ventilatory and cardiovascular responses, inhibiting the cardiovascular and stimulating the respiratory systems in SHR.
据报道，中枢硫化氢（H₂S）作为一种气体神经调节剂，参与正常血压大鼠的通气和心血管控制，而自发性高血压大鼠（SHR）中尚无相关信息。我们记录了通过向Wistar正常血压大鼠（WNR）和SHR的第四脑室微量注射氨基氧乙酸（CBS抑制剂）来阻断神经组织中产生H₂S的胱硫醚β-合酶（CBS）前后的分钟通气量（VE）、平均动脉压（MAP）和心率（HR），随后进行30分钟的常氧（吸入21% O₂）或低氧（吸入10% O₂）暴露。在WNR和SHR的常氧期间，微量注射AOA或生理盐水（1μL）均未改变VE、MAP和HR。在WNR中，低氧导致VE和HR增加，MAP降低，且这些反应不受AOA影响。在SHR中，与WNR相比，低氧使VE升高幅度更大，MAP和HR降低幅度更大，且这些反应均被AOA减弱。总之，内源性H₂S对低氧诱导的通气和心血管反应起重要调节作用，在SHR中抑制心血管系统并刺激呼吸系统。
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