Gilmour K M, Milsom W K, Rantin F T, Reid S G, Perry S F
Department of Physiological Sciences, Federal University of São Carlos, Via Washington Luiz km 235, São Carlos, SP 13565-905, Brazil.
J Exp Biol. 2005 Mar;208(Pt 6):1095-107. doi: 10.1242/jeb.01480.
Experiments were carried out to test the hypothesis that ventilatory and cardiovascular responses to hypercarbia (elevated water P(CO2)) in the tambaqui Colossoma macropomum are stimulated by externally oriented receptors that are sensitive to water CO(2) tension as opposed to water pH. Cardiorespiratory responses to acute hypercarbia were evaluated in both the absence and presence of internal hypercarbia (elevated blood P(CO2)), achieved by treating fish with the carbonic anhydrase inhibitor acetazolamide. Exposure to acute hypercarbia (15 min at each level, final water CO(2) tensions of 7.2, 15.5 and 26.3 mmHg) elicited significant increases in ventilation frequency (at 26.3 mmHg, a 42% increase over the normocarbic value) and amplitude (128%), together with a fall in heart rate (35%) and an increase in cardiac stroke volume (62%). Rapid washout of CO(2) from the water reversed these effects, and the timing of the changes in cardiorespiratory variables corresponded more closely to the fall in water P(CO2) (Pw(CO2)) than to that in blood P(CO2) (Pa(CO2)). Similar responses to acute hypercarbia (15 min, final Pw(CO2) of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg(-1)) tambaqui. Acetazolamide treatment itself, however, increased Pa(CO2) (from 4.81+/-0.58 to 13.83+/-0.91 mmHg, mean +/-S.E.M.; N=8) in the absence of significant change in ventilation, heart rate or cardiac stroke volume. The lack of response to changes in blood P(CO2) and/or pH were confirmed by comparing responses to the bolus injection of hypercarbic saline (5% or 10% CO(2); 2 ml kg(-1)) into the caudal vein with those to the injection of CO(2)-enriched water (1%, 3%, 5% or 10% CO(2); 50 ml kg(-1)) into the buccal cavity. Whereas injections of hypercarbic saline were ineffective in eliciting cardiorespiratory responses, changes in ventilation and cardiovascular parameters accompanied injection of CO(2)-laden water into the mouth. Similar injections of CO(2)-free water acidified to the corresponding pH of the hypercarbic water (pH 6.3, 5.6, 5.3 or 4.9, respectively) generally did not stimulate cardiorespiratory responses. These results are in agreement with the hypothesis that in tambaqui, externally oriented chemoreceptors that are predominantly activated by increases in water P(CO2), rather than by accompanying decreases in water pH, are linked to the initiation of cardiorespiratory responses to hypercarbia.
巨脂鲤对高碳酸血症（水体P(CO₂)升高）的通气和心血管反应是由对水体CO₂张力敏感而非水体pH敏感的外周感受器所刺激。通过用碳酸酐酶抑制剂乙酰唑胺处理鱼类，在有无体内高碳酸血症（血液P(CO₂)升高）的情况下评估了对急性高碳酸血症的心肺反应。暴露于急性高碳酸血症（每个水平持续15分钟，最终水体CO₂张力分别为7.2、15.5和26.3 mmHg）会引起通气频率显著增加（在26.3 mmHg时，比正常碳酸水平值增加42%）和幅度增加（128%），同时心率下降（35%）且心搏量增加（62%）。迅速从水体中洗出CO₂可逆转这些效应，心肺变量变化的时间与水体P(CO₂)（Pw(CO₂)）的下降更为密切相关，而非与血液P(CO₂)（Pa(CO₂)）的下降相关。在经乙酰唑胺处理（30 mg kg⁻¹）的巨脂鲤中观察到对急性高碳酸血症（15分钟，最终Pw(CO₂)为13.6 mmHg）有类似反应。然而，在通气、心率或心搏量无显著变化的情况下，乙酰唑胺处理本身会使Pa(CO₂)升高（从4.81±0.58升高至13.83±0.91 mmHg；平均值±标准误；N = 8）。通过比较尾静脉推注高碳酸盐水（5%或10% CO₂；2 ml kg⁻¹）与口腔注入富含CO₂的水（1%、3%、5%或10% CO₂；50 ml kg⁻¹）的反应，证实了对血液P(CO₂)和/或pH变化缺乏反应。虽然推注高碳酸盐水在引发心肺反应方面无效，但向口腔注入含CO₂的水会伴随通气和心血管参数的变化。类似地，注入酸化至相应高碳酸水pH值（分别为pH 6.3、5.6、5.3或4.9）的无CO₂水通常不会刺激心肺反应。这些结果与以下假设一致：在巨脂鲤中，主要由水体P(CO₂)升高而非伴随的水体pH下降激活的外周化学感受器与对高碳酸血症的心肺反应启动相关。
