McKendry J E, Milsom W K, Perry S F
Department of Biology, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5.
J Exp Biol. 2001 Apr;204(Pt 8):1519-27. doi: 10.1242/jeb.204.8.1519.
Adult Pacific spiny dogfish (Squalus acanthias) were exposed to acute (approximately 20 min) hypercarbia while we monitored arterial blood pressure, systemic vascular resistance (R(S)), cardiac output (V(b)) and frequency (fh) as well as ventilatory amplitude (V(AMP)) and frequency (f(V)). Separate series of experiments were conducted on control, atropinized (100 nmol kg(-1)) and branchially denervated fish to investigate putative CO(2)-chemoreceptive sites on the gills and their link to the autonomic nervous system and cardiorespiratory reflexes.In untreated fish, moderate hypercarbia (water CO(2 )partial pressure; Pw(CO2)=6.4+/-0.1 mmHg) (1 mmHg=0.133 kPa) elicited significant increases in V(AMP) (of approximately 92 %) and f(V) (of approximately 18 %) as well as decreases in fh (of approximately 64 %), V.(b) (approximately 29 %) and arterial blood pressure (of approximately 11 %); R(S) did not change significantly. Denervation of the branchial branches of cranial nerves IX and X to the pseudobranch and each gill arch eliminated all cardiorespiratory responses to hypercarbia. Prior administration of the muscarinic receptor antagonist atropine also abolished the hypercarbia-induced ventilatory responses and virtually eliminated all CO(2)-elicited cardiovascular adjustments. Although the atropinized dogfish displayed a hypercarbic bradycardia, the magnitude of the response was significantly attenuated (36+/-6 % decrease in fh in controls versus 9+/-2 % decrease in atropinized fish; means +/- s.e.m.).Thus, the results of the present study reveal the presence of gill CO(2) chemoreceptors in dogfish that are linked to numerous cardiorespiratory reflexes. In addition, because all cardiorespiratory responses to hypercarbia were abolished or attenuated by atropine, the CO(2) chemoreception process and/or one or more downstream elements probably involve cholinergic (muscarinic) neurotransmission.
成年太平洋刺鲨（Squalus acanthias）被置于急性（约20分钟）高碳酸血症环境中，同时我们监测动脉血压、全身血管阻力（R(S)）、心输出量（V(b)）和频率（fh）以及通气幅度（V(AMP)）和频率（f(V)）。对对照鱼、阿托品化（100 nmol kg(-1)）鱼和鳃去神经支配的鱼进行了一系列单独实验，以研究鳃上假定的CO(2)化学感受位点及其与自主神经系统和心肺反射的联系。在未处理的鱼中，中度高碳酸血症（水CO(2)分压；Pw(CO2)=6.4±0.1 mmHg）（1 mmHg = 0.133 kPa）引起V(AMP)显著增加（约92%）和f(V)增加（约18%），同时fh降低（约64%）、V.(b)降低（约29%）和动脉血压降低（约11%）；R(S)无显著变化。切断第九和第十对脑神经至假鳃和每个鳃弓的鳃支神经，消除了对高碳酸血症的所有心肺反应。预先给予毒蕈碱受体拮抗剂阿托品也消除了高碳酸血症诱导的通气反应，并几乎消除了所有由CO(2)引起的心血管调节。虽然阿托品化的刺鲨表现出高碳酸血症性心动过缓，但反应幅度明显减弱（对照组fh降低36±6%，而阿托品化鱼降低9±2%；均值±标准误）。因此，本研究结果揭示了刺鲨鳃中存在与多种心肺反射相关的CO(2)化学感受器。此外，由于阿托品消除或减弱了对高碳酸血症的所有心肺反应，CO(2)化学感受过程和/或一个或多个下游元件可能涉及胆碱能（毒蕈碱）神经传递。
