Vengust M, Stämpfli H, De Moraes A N, Teixeiro-Neto F, Viel L, Heigenhauser G
Firestone Equine Respiratory Research Laboratory, University of Guelph, Ontario, Canada.
Equine Vet J Suppl. 2010 Nov(38):40-50. doi: 10.1111/j.2042-3306.2010.00240.x.
Carbonic anhydrase (CA) catalyses the hydration/dehydration reaction of CO(2) and increases the rate of Cl(-) and HCO(3)(-) exchange between the erythrocytes and plasma. Therefore, chronic inhibition of CA has a potential to attenuate CO(2) output and induce greater metabolic and respiratory acidosis in exercising horses.
To determine the effects of Carbonic anhydrase inhibition on CO(2) output and ionic exchange between erythrocytes and plasma and their influence on acid-base balance in the pulmonary circulation (across the lung) in exercising horses with and without CA inhibition.
Six horses were exercised to exhaustion on a treadmill without (Con) and with CA inhibition (AczTr). CA inhibition was achieved with administration of acetazolamide (10 mg/kg bwt t.i.d. for 3 days and 30 mg/kg bwt before exercise). Arterial, mixed venous blood and CO(2) output were sampled at rest and during exercise. An integrated physicochemical systems approach was used to describe acid base changes.
AczTr decreased the duration of exercise by 45% (P < 0.0001). During the transition from rest to exercise CO(2) output was lower in AczTr (P < 0.0001). Arterial PCO(2) (P < 0.0001; mean ± s.e. 71 ± 2 mmHg AczTr, 46 ± 2 mmHg Con) was higher, whereas hydrogen ion (P = 0.01; 12.8 ± 0.6 nEq/l AczTr, 15.5 ± 0.6 nEq/l Con) and bicarbonate (P = 0.007; 5.5 ± 0.7 mEq/l AczTr, 10.1 ± 1.3 mEq/l Con) differences across the lung were lower in AczTr compared to Con. No difference was observed in weak electrolytes across the lung. Strong ion difference across the lung was lower in AczTr (P = 0.0003; 4.9 ± 0.8 mEq AczTr, 7.5 ± 1.2 mEq Con), which was affected by strong ion changes across the lung with exception of lactate.
CO(2) and chloride changes in erythrocytes across the lung seem to be the major contributors to acid-base and ions balance in pulmonary circulation in exercising horses.
碳酸酐酶(CA)催化CO₂的水合/脱水反应,并提高红细胞与血浆之间Cl⁻和HCO₃⁻的交换速率。因此,长期抑制CA有可能减弱运动马匹的CO₂排出,并导致更严重的代谢性和呼吸性酸中毒。
确定碳酸酐酶抑制对运动马匹CO₂排出以及红细胞与血浆之间离子交换的影响,以及其对有或无CA抑制的运动马匹肺循环(通过肺)中酸碱平衡的影响。
六匹马在跑步机上运动至疲惫,一组未进行CA抑制(对照组),另一组进行CA抑制(乙酰唑胺组)。通过给予乙酰唑胺(10mg/kg体重,每日三次,持续3天,运动前给予30mg/kg体重)来实现CA抑制。在休息和运动期间采集动脉血、混合静脉血和CO₂排出量样本。采用综合物理化学系统方法来描述酸碱变化。
乙酰唑胺组使运动持续时间缩短了45%(P<0.0001)。在从休息过渡到运动期间,乙酰唑胺组的CO₂排出量较低(P<0.0001)。乙酰唑胺组的动脉血PCO₂较高(P<0.0001;平均值±标准误,乙酰唑胺组为71±2mmHg,对照组为46±2mmHg),而跨肺的氢离子(P=0.01;乙酰唑胺组为12.8±0.6nEq/l,对照组为15.5±0.6nEq/l)和碳酸氢根(P=0.007;乙酰唑胺组为5.5±0.7mEq/l,对照组为10.1±1.3mEq/l)差异较对照组更低。跨肺的弱电解质未观察到差异。乙酰唑胺组跨肺的强离子差较低(P=0.0003;乙酰唑胺组为4.9±0.8mEq,对照组为7.5±1.2mEq),这受到跨肺强离子变化的影响,但乳酸除外。
运动马匹肺循环中红细胞内的CO₂和氯离子变化似乎是酸碱和离子平衡的主要贡献因素。