Gargaglioni Luciane H, Bicego Kenia C, Steiner Alexandre A, Branco Luiz G S
Faculdade de Odontologia de Ribeirão Preto, Avenida do Café s/no, Departamento de Morfologia, Estomatologia e Fisiologia, Universidade de São Paulo, 14040-904 Ribeirão Preto, SP, Brazil.
Respir Physiol Neurobiol. 2003 Oct 16;138(1):37-44. doi: 10.1016/s1569-9048(03)00172-1.
In the present study, we tested the hypothesis that lactate, which is a classic companion of hypoxic stress in mammals, is a modulator of hypoxia-induced hyperventilation. To this end, pulmonary ventilation (V(E)) of male Wistar rats was measured by whole body plethysmograph, and dichloroacetate (DCA, 100 mg/kg) was used to inhibit lactate production. Plasma lactate levels, arterial pH (pHa), arterial carbon dioxide partial pressure (PaCO(2)), arterial oxygen partial pressure (PaO(2)), plasma bicarbonate (HCO3(-)) and oxygen consumption (VO(2)) were determined as well. In normoxia, intraperitoneal DCA elicited a decrease only in plasma lactate levels. Hypoxia caused an increase in V(E), pHa and plasma lactate levels and parallel to decreases in PaCO(2), PaO(2) and VO(2) in the control group. DCA administration markedly reduced the ventilatory response to hypoxia by acting on tidal volume (V(T)). This reduced ventilatory response caused by DCA was independent of VO(2). In conclusion, the present study indicates that lactate contributes to the initiation and maintenance of hypoxia-induced hyperventilation in rats, modulating the adjustments in V(T).
在本研究中，我们验证了以下假设：乳酸作为哺乳动物低氧应激的典型伴随物，是低氧诱导的过度通气的调节因子。为此，使用全身体积描记法测量雄性Wistar大鼠的肺通气量（V(E)），并使用二氯乙酸（DCA，100 mg/kg）抑制乳酸生成。同时还测定了血浆乳酸水平、动脉pH值（pHa）、动脉二氧化碳分压（PaCO(2)）、动脉氧分压（PaO(2)）、血浆碳酸氢盐（HCO3(-)）和耗氧量（VO(2)）。在常氧条件下，腹腔注射DCA仅引起血浆乳酸水平下降。低氧导致对照组V(E)、pHa和血浆乳酸水平升高，同时PaCO(2)、PaO(2)和VO(2)下降。给予DCA通过作用于潮气量（V(T)）显著降低了对低氧的通气反应。DCA引起的这种通气反应降低与VO(2)无关。总之，本研究表明乳酸有助于大鼠低氧诱导的过度通气的起始和维持，调节V(T)的调整。
