Ruminal lactic acidosis in sheep and goats.

The clinical findings in 37 sheep and goats with acute ruminal lactic acidosis included a disturbed general condition characterised by anorexia, apathy, teeth grinding and muscle twitching, ruminal stasis, and the excretion of soupy or watery faeces. The ruminal fluid of affected animals was milky, had a sour odour and a low pH. There was a predominance of Gram-positive bacteria in smears of ruminal fluid. In comparison with 10 control animals, the rumen fluid of 23 sheep with ruminal lactic acidosis had higher lactic acid and lower volatile fatty acid concentrations. In addition, the affected animals often had haemoconcentration and metabolic acidosis. Treatment included single or repeated transfer of ruminal fluid from healthy cows and, depending on the severity, the administration of antacids, yeast and chlortetracycline, and the intravenous infusion of isotonic sodium chloride and 5 per cent sodium bicarbonate solutions. Of the 37 treated sheep and goats, four died within 24 hours, and three others were euthanased after one, two and three days because their condition rapidly deteriorated. Thirty animals were discharged one to nine days after treatment. Twenty-nine of them (78.4 per cent) recovered completely but one was euthanased later.     

Retrospective evaluation of the prognostic utility of plasma lactate concentration,base deficit,pH, and anion gap in canine and feline emergency patients

Objective

To determine the association of plasma lactate concentration, pH, base deficit (BD), and anion gap (AG) in dogs and cats on presentation to an emergency room with outcome, and to compare the prognostic significance of hyperlactatemia with a concurrent metabolic acidosis with that of hyperlactatemia and a normal metabolic acid–base balance.

Design

Retrospective study.

Setting

University teaching hospital.

Animals

Five hundred sixty‐six dogs and 185 cats that had venous blood gas analysis performed.

Interventions

None.

Measurements and Main Results

Medical records were reviewed for plasma lactate concentrations, electrolyte concentrations, and acid–base parameters obtained on emergency room admission, clinical diagnosis, and in‐hospital mortality. The primary outcome measure was all‐cause mortality for the hospitalized visit. Median plasma lactate concentration and AG were higher, BD was more negative, and pH was lower, in non‐survivor dogs and cats. The prevalence of hyperlactatemia was 53% in dogs and 30% in cats. Lactic acidosis was present in 42% and 80% of hyperlactatemic dogs and cats, respectively. Multivariate regression analyses revealed that plasma lactate concentration, BD, and pH, but not AG, were independent predictors of mortality in dogs, and that only plasma lactate concentration was an independent predictor of mortality in cats. Mortality was highest for animals with lactic acidosis, at 59.8% in dogs and 49% in cats. Mortality in dogs with lactic acidosis was significantly higher than dogs with hyperlactatemia and a normal acid–base status (P < 0.0001).

Conclusions

The presence and magnitude of hyperlactatemia on presentation to the emergency room may help identify dogs and cats with high likelihood of in‐hospital mortality, and the presence of lactic acidosis specifically may help identify dogs with yet higher risk of in‐hospital mortality.     

绵羊实验性乳酸酸中毒研究——Ⅱ.血气和阴离子隙对乳酸酸中毒的诊断价值

12只2～(?)岁健康绵羊被分为Ⅰ组(3只)、Ⅱ组(?)只)和Ⅲ组(3只),分别按2.5,5.0,10.0g/kg瘤胃内注入50%D-L消旋体乳酸溶液.Ⅱ组羊在恢复期因过度代偿而导致代谢性碱中毒。各实验绵羊血液pH值与HCO3-、BEB、TCO2、BEECF和SB成正相关,可作为绵羊乳酸酸中毒的可靠诊断依据。计算AG能反映绵羊酸中毒的程度。绵羊瘤胃内注入乳酸10.0g/kg体重,AG升高到35mmol/L时,绵羊处于休克状态,AG35mmol/L可作为乳酸酸中毒预后不良的监测指标。     

寡果糖诱导瘤胃急性酸中毒对山羊瘤胃发酵、蹄组织结构及炎症因子、金属蛋白酶表达的影响

本试验旨在研究寡果糖诱导瘤胃酸中毒对山羊瘤胃发酵、蹄组织结构、蹄部炎症因子及金属蛋白酶表达的影响。采用随机区组设计,将8头健康装有永久性瘤胃瘘管的波杂山羊(波尔山羊×长江三角洲白山羊)随机分为对照组和诱导酸中毒的试验组,每组4头。其中试验组山羊瘤胃寡果糖灌注量为21 g/kg BW。分别于灌注前(0 h)和灌注后4、8、12、24和48 h采集瘤胃液,同时分别在0、4、8、24和48 h通过颈静脉采集血液,灌注后48 h屠宰2组山羊,采集蹄组织。结果表明:与对照组相比,试验组山羊瘤胃液p H、挥发性脂肪酸浓度平均值显著降低(P0.05),血液和瘤胃液中乳酸和脂多糖浓度平均值显著提高(P0.05);组织形态学结果显示,与对照组相比,试验组山羊蹄组织中次级表皮蹄小叶和次级真皮蹄小叶的长度变短,蹄小叶形状不规则;实时定量PCR检测结果显示,较对照组比较,试验组山羊蹄组织中基质金属蛋白酶组织抑制物-1的mRNA的相对表达量显著降低(P0.05),白细胞介素-6、膜型基质金属蛋白酶-1和基质金属蛋白酶-2的mRNA的相对表达量显著升高(P0.05)。结果提示,寡果糖诱导山羊急性瘤胃酸中毒可导致山羊瘤胃发酵紊乱,提高瘤胃液和血液中脂多糖与乳酸浓度,导致山羊蹄组织相关炎症因子与金属蛋白酶表达改变,最终引发山羊急性蹄叶炎。     

奶山羊过食玉米中毒的血液学研究

20只假定健康奶山羊进行了玉米中毒的研究,现仅将血液学研究报道于后:一次经瘤胃瘘管给予40、60、80g/kgwt王米粉,分别可致奶山羊中毒、出现严重症状和病亡;内毒素及乳酸中毒是本病的本质,中后期尚有氨的作用;pH下降,乳酸增加,白细胞总数及血小板减少,内毒素检测及血浆鱼精蛋白副凝集试验阳性,是本病在血液学方向的主要特征。     

D-Lactic acidosis in calves as a consequence of experimentally induced ruminal acidosis

In order to test the hypothesis that ruminal drinking in calves can lead to D-lactic metabolic acidosis, ruminal acidosis was induced in nine calves by intraruminal application of untreated whole milk via a stomach tube. The amount of the daily force-fed liquid was 3 x 1 l. The experimental design called for an end of intraruminal applications if two or more of the following signs were observed: severe depression, estimated degree of dehydration >10%, absence of sucking reflex, lack of appetite for two consecutive feedings, severe metabolic acidosis with calculated Actual Base Excess (ABE) <-15 mmol/l. The procedure was scheduled to be discontinued on the 17th day of experiment. The onset of ruminal acidification occurred rapidly, and mean pH value fell from 6.70 (+/-0.48) to 4.90 (+/-0.38) after the first application. The following days the pH values varied between 4 and 5. Rumen acidity was characterized biochemically by a significant increase in both isomers of lactic acid. The effects of the intraruminal administration on the calves were detrimental; eight of nine calves showed an acute disease process. According to the pre-established clinical standard, seven of nine calves were removed from the intraruminal feeding schedule. All but one of the calves developed severe systemic acidosis. The increase in anion gap demonstrated the net acid load. In all the calves D-lactate levels were found to show a significant and rapid increase. On the contrary, L-lactate never deviated from physiological levels. These observations confirm that, in young calves as in adult cattle, ruminal acidosis may lead to a clinically manifested D-lactic metabolic acidosis.     

Characterization of acid-base disturbances and effects on calcium and phosphorus balances of dietary fixed ions in pregnant or lactating does

Effects of fixed cation-anion balance on acid-base status and calcium and phosphorus balances were examined. Pregnant and lactating goats were fed a diet of alfalfa hay, concentrate and minerals to vary the cation-anion balance [meq sodium (Na) + meq potassium (K)-meq chloride (Cl)]/100 g diet dry matter (DM) over the range found in ruminant feeds. Small but significant effects on ruminal pH, fermentation and dilution rate were observed. Metabolic acid-base status of pregnant and lactating goats was normal when (Na + K - Cl) balance was 40 to 50 meq/100 g DM. The other treatments drastically altered plasma electrolyte concentrations, causing metabolic acid-base disturbances and profound changes in calcium and phosphorus metabolism. Subclinical hypernatremic, hypochloremic metabolic alkalosis was induced by a dietary fixed cation excess (Na + K - Cl) of greater than 85 meq/100 g DM (typical of buffered, alfalfa diets) and caused hypocalciuria, diminished calcium and phosphorus absorption, and possibly diminished dietary calcium absorption and resorption of calcium from bone. Subclinical hyperchloremic, hyponatremic metabolic acidosis from a diminished dietary fixed cation-anion balance (Na + K - Cl) of less than 10 meq/100 g DM (typical of nonbuffered corn silage or grain diets) caused hypercalciuria, enhanced calcium and phosphorus absorption and apparently enhanced calcium resorption from bone. Apparent effects on absorption and resorption depended on calcium and phosphorus intakes. Alterations in goats performance were not demonstrable. Dietary excesses of fixed cations over anions (meq Na + K - Cl/100 g diet DM greater than 50) cause metabolic alkalosis in ruminants, whereas fixed anion excesses (meq Na + K - Cl/100 g diet DM less than 40) cause metabolic acidosis. Content of electrolytes in diets should be reported in all nutrition trials with ruminants for assessment of metabolic acid-base status.     

高精料诱导的SARA对泌乳期山羊血液和瘤胃液中皮质醇的影响

选择7只装有永久性瘤胃瘘管的泌乳中期山羊,2×2拉丁方设计,分别饲喂精粗比为6∶4和4∶6的饲料,通过饲喂精粗比6∶4饲料建立泌乳期山羊瘤胃亚急性酸中毒(subacute ruminal acidosis, SARA)模型,研究SARA时山羊血液和瘤胃液中皮质醇浓度、肝脏皮质醇受体(glucocorticoid receptor, GR)mRNA表达及其他相关指标的变化。结果表明,精粗比6∶4日粮饲喂2周后成功诱导SARA状态(SARA组),采食后瘤胃液pH值低于5.8持续时间约6 h,而精粗比为4∶6组山羊瘤胃液pH均高于6.0 (对照组)。高精料日粮处理对瘤胃pH和乳酸以及瘤胃液和血浆内的脂多糖、皮质醇浓度有显著性影响(P<0.05),采食前SARA组山羊瘤胃液中乳酸浓度显著高于对照组(P<0.05),采食后0~4 h乳酸含量下降,6~10 h时逐渐增加并极显著高于对照组(P<0.01);2组间瘤胃液中脂多糖浓度无显著性差异(P>0.05),SARA组血浆脂多糖浓度在采食前和采食后6 h均显著高于对照组(P<0.05);采食前SARA组山羊血液中皮质醇浓度高于对照组(P=0.05),但采食后6 h两组间无显著差异(P>0.05); 2组山羊瘤胃液中皮质醇浓度在采食后2,4和6 h分别显著高于对照组(P<0.05),但在采食前和采食后10 h无显著差异(P>0.05)。Real-time PCR结果显示,SARA组山羊肝脏中GR mRNA表达显著下调(P<0.05)。本研究结果显示,泌乳期山羊发生SARA时糖皮质激素水平升高,负反馈下调肝脏GR的表达水平,提示SARA时机体处于应激状态,可能引起肝脏的物质代谢和营养物质重分配的改变。     

Effects of the acid-tolerant engineered bacterial strain Megasphaera elsdenii H6F32 on ruminal pH and the lactic acid concentration of simulated rumen acidosis in vitro

The aim of this study was to examine the effects of the acid-tolerant engineered bacterial strain Megasphaera elsdenii H6F32 (M. elsdenii H6F32) on ruminal pH and the lactic acid concentrations in simulated rumen acidosis conditions in vitro. A mixed culture of ruminal bacteria, buffer, and primarily degradable substrates was inoculated with equal numbers of M. elsdenii H6 or M. elsdenii H6F32. The pH and lactic acid concentrations in the mixed culture were determined at 0, 2, 4, 6, 8, 10, 12, 14, 16, and 18 h of incubation. Acid-tolerant M. elsdenii H6F32 reduced the accumulation of lactic acid and increased the pH value. These results indicate that acid-tolerant M. elsdenii H6F32 could be a potential candidate for preventing rumen acidosis.     

Effect of ionophore antibiotics on experimentally induced lactic acidosis in cattle

Salinomycin, a new ionophore antibiotic, was tested and compared with lasalocid and monensin for preventing experimentally induced lactic acidosis. Five rumen-fistulated adult cattle were used in a 5 X 5 Latin square design, and the treatments were as follows: no treatment (control), 0.11 mg of salinomycin/kg of body weight (S1), 0.22 mg of salinomycin/kg (S2), 0.66 of lasalocid/kg, and 0.66 mg of monensin/kg. Acidosis was induced by intraruminal administration of a ground corn-corn starch mixture (50:50, 12.5 g/kg) once a day for up to 4 days. Antibiotics were administered along with grain-starch mixture. Rumen and blood samples were obtained before and at 6, 12, and 24 hours after each carbohydrate-antibiotic dosing to monitor acid-base status. Control and S1-treated cattle became ruminally acidotic within 54 hours, whereas cattle treated with S2, lasalocid, and monensin resisted acidosis for up to 78 hours after dosing. Cattle treated with S2, lasalocid, or monensin had higher rumen pH and lower L(+)- and D(-)-lactate concentrations than did control or S1-treated cattle. Rumen pH decrease to below 5.0 in S2-, lasalocid-, and monensin-treated cattle was not due to lactic acid, but to increased production of volatile fatty acids. Rumen propionate proportion increased initially in antibiotic-treated cattle, but after 48 hours, butyrate proportion increased significantly. Despite low rumen pH and high lactate concentration, lacticacidemia was not evident, and the systemic acid-base disturbance was mild in control cattle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of clinical observations and blood chemistry values for predicting clinical outcomes in dairy goats with pregnancy toxaemia

Background

Pregnancy toxaemia (PT) is a disease that affects pregnant goats during their last month of gestation and is characterized by a high case fatality rate. This study involved 32 does maintained on a commercial dairy goat farm that were diagnosed with PT. A physical examination was performed on and haematology parameters obtained from each doe, at the time of diagnosis. The data from the 24 PT goats that died was compared with the corresponding data from the 8 PT goats that survived.

Results

Polypnea, swollen limbs, anorexia with absence of ruminal motility, recumbency, nervous signs and drooping ears were the most frequently observed clinical manifestations. Nineteen out of 21 recumbent goats died. Sixteen out of 17 goats with anorexia and absence of ruminal motility died. Mean beta-hydroxybutyric acid (BHBA) values in the goats that died were not significantly different from those in goats that survived. The blood values for pH and pCO₂ (p?<?0.005) as well as for HCO₃ ^?, BE and K⁺ (p?<?0.001) were significantly lower in the goats that died than in those that survived.

Conclusions

The clinical signs most indicative of a poor prognosis are anorexia with absence of ruminal motility and recumbency. Among the blood parameters to be considered, hypokalaemia and metabolic acidosis are the most relevant. Goats with PT have a high mortality and their condition can deteriorate very fast. Based on the authors’s experience, a good strategy to minimize the economic losses caused by PT is to focus on the offspring survival rate since an early decision (induction of kidding or caesarian surgery) can increase the number of alive kids.

     

Tolerance of goats to experimental grain engorgement and intraruminal lactic acid injection

Grain overfeeding and intraruminal lactic acid injection was carried out in goats in order to induce signs of grain engorgement or laminitis. Twelve female goats of the small East African breed divided into three equal groups were either overfed with coarsely ground maize meal for 14 days or injected with an 85% syrup of lactic acid intraruminally at a single dose rate of 0.5% bodyweight, while others acted as a control. No clinical differences in the haematological picture, rumen pH, respiration and pulse rates could be observed between the treatment groups and the control. The postmortem and histopathological examinations of the claws showed no pathological changes commonly associated with laminitis. It is concluded that goats can tolerate large amounts of carbohydrates or lactic acid without any injurious effects, which may indicate a superior activity as compared to sheep and cattle.     

LIVER METABOLISM DURING MALIGNANT HYPERTHERMIA IN THE PIETRAIN PIG

Liver function was systematically investigated in 7 malignant hyperthermia (MH) susceptible Pietrain pigs (mean weight 67 kg ± 7 kg SEM) to determine the contribution of hepatic metabolism to circulating substrates (Hall, Lucke, Lovell and Lister 1978). It was considered that the progressive lactic acidosis observed in MH may be a result, not only of impaired hepatic uptake of lactate but also production of lactate by the liver as is said to occur in Type II lactic acidosis (Cohen and Simpson 1975). These authors suggested that as the enzyme pyruvate decarboxylase is pH sensitive, and because it is rate limiting in the gluconeugenic pathway of lactate to glucose, under conditions of severe acidosis (pH 7.1) hepatic lactate uptake will be inhibited and there will be production of lactate by the liver. Pigs were prepared with hepatic vein, right ventricle and common carotid artery cannulae. Control measurements were made before inducing MH by ventilating with 1% halothane for 10 minutes together with intravenous injection of 1 mg suxamethonium chloride per kg body weight. Paired arterial and hepatic venous samples were collected at 10 minute intervals for the following estimations: pH, oxygen content, glucose, potassium, lactate, pyruvate, alanine, free fatty acids and glycerol. Hepatic blood flow was estimated by continuous infusion of Indocyanine green (Lucke and Hall 1978). All pigs developed MH with a rise in mean muscle temperature from 37.8°C to 41.5°C after 40 minutes. Mean hepatic blood flow decreased to 25% of control value but, because there was a concomitant increase in oxygen extraction by the liver, hepatic oxygen consumption did not change significantly. At 20 minutes after MH there was a 7-fold increase in glucose efflux from the liver with an arterial glucose concentration of 12.6 mmol/1. There was a massive efflux of 1.1 mmol K+/min early in the response showing that the characteristic hyperkalaemia is not only due to potassium loss from muscle but mainly hepatic in origin. The mean lactate uptake by the liver increased from the control 0.21 mmol/min to 1.19 mmol/min after 10 minutes MH. Even in the presence of gross acidosis (mean pH 6.75) and hepatic blood flow 25% of control, hepatic lactate uptake was still 3 times that recorded in the resting state. It is important to note, however, that although hepatic lactate uptake was increased under these conditions, it was still insufficient in the presence of gross muscle stimulation with a mean arterial lactate concentration of 19.3 mmol/l. It is concluded that the lactic acidosis in porcine MH is due to peripheral overproduction with some impairment of hepatic uptake. The gluconeugenic capacity of the liver was never completely inhibited despite the severity of the metabolic acidosis and hyperthermia and at no stage was there production of lactate by the liver.     

The acid-base equilibrium and carbohydrate metabolism during infection with Eperythrozoon suis

Following on from clinical observations which point to severe metabolic disturbances in association with acute Eperythrozoon (E.) suis infection, the parameters of acid-base balance (pO2, pCO2, pH, actual bicarbonate, standard bicarbonate, base excess) as well as the glucose-, lactate- and pyruvate levels, were measured in venous blood during the course of eperythrozoonotic infection. Glucose consumption was investigated in in vitro experiments with differing numbers of pathogens. Acute E. suis infection is accompanied by a severe acidosis and hypoglycaemia. In vitro experiments showed that a rapid breakdown of glucose follows in E. suis infected blood. No significant reduction in glucose concentration was established in control blood in a comparable time period. The results give rise to the assumption that E. suis is capable of independent glucose breakdown. Both the increase in lactate concentration (metabolic component) and a disturbance of pulmonary gaseous exchange (respiratory component) are regarded as the cause of the acidosis.     

Correlation between anion gap, blood L lactate concentration and survival in horses

Blood L lactate concentration and anion gap were measured in 32 horses suspected of having metabolic acidosis. There was good linear correlation between these variables (r = 0.90791, P less than 0.0001) and both were good prognostic indicators. Anion gap was a good indicator of the presence but not the severity of L lactic acidosis and was a slightly better prognostic indicator. The ability to predict survival was not improved by the measurement of L lactate in addition to anion gap.     

Effects of acute lactic acidosis on some hemodynamic and hematologic values in three cows

Some hemodynamic and hematologic effects of acute experimental lactic acidemia in 3 healthy cows are presented. Lactic acidemia was induced by intravenous infusion of a 10% solution of racemic lactic acid. The prominent features of the acidification of the blood were increases in carotid artery blood pressure and responses to intravenously injected norepinephrine, slight bradycardia and slight hyperventilation. Intravascular hemolysis with hemoglobinuria was a constant finding. Otherwise, no adverse effects of the acidemia were noted. These changes were paralleled by a progressive fall in arterial blood pH, base excess and PCO2 and increasing venous blood L (+)-lactate concentrations A reasonable explanation for the hemodynamic effects of the acidemia is peripheral vasoconstriction elicited by either stimulation of the sympathetic nervous system or increased sensitivity of vasoconstrictive receptors. The results are discussed with special reference to primary lactic acidosis encountered in grain engorgement in ruminants and to the secondary lactic acidosis of shock. These conditions are characterized by hemoconcentration and hypovolemia. Therefore, the results of this study of healthy normovolemic cows may not be valid in the severely dehydrated, hemoconcentrated and acidemic cow as hypotension is reported in the literature in connection with ruminal acidosis in sheep.     

奶山羊实验性过食黄豆的血液学研究

20只装置永久性瘤胃瘘管的假定健康奶山羊进行了过食黄豆对其血液理化性质影响的研究。结果表明,一次给予40、00、80g/kgwt黄豆,分别可导致发病,明显临床症状和死亡;过食黄豆是一个由酸中毒转入以氨中毒为主的代谢性碱中毒的全过程,血氨浓度与黄豆的给予量呈正相关;血液pH值先下降(7.13±0.22,P<0.01)而后上升(7.86±0.25,P<0.01),血浆CO_2CP先降低(12.03±2.73mmol/L,P<0.05)而后升高(22.76±0.76mmol/L,P<0.01),血乳酸先升高(2.07±0.22,P<0.01)后降低(1.23±0.05mmol/L,P<0.01);血氨、血pH值及血浆CO_2CP的升高,是过食黄豆在血液理化性质方面的特征。     

Organic acidemia in a young cat associated with cobalamin deficiency

Objective: To describe a case of severe metabolic acidosis and encephalopathy secondary to cobalamin (Cbl) deficiency in a young cat. Case summary: A 4‐year‐old spayed female domestic short hair cat weighing 2.5 kg, presented with a 2‐day history of neurological signs referable to the cerebrum. The cat was evaluated for similar episodes twice before, however, no definitive diagnosis was made for either visit. On presentation the cat was minimally responsive and had a metabolic acidosis and ketonuria with no apparent reason, such as lactic acidosis or diabetic ketoacidosis. The patient was diagnosed postmortem with an organic acidemia secondary to low Cbl levels. New or unique information provided: The purpose of this report is to alert emergency clinicians to be suspicious of an organic acidemia in any case of metabolic acidosis and ketonuria that cannot be explained. Early identification of inherited organic acidemias in domestic animals may allow prompt and appropriate treatment of these conditions.     

乳酸在奶牛体内的代谢途径及其对奶牛健康影响的研究进展

乳酸（lactic acid）是奶牛瘤胃内重要的中间代谢产物，合理的调节乳酸代谢特征、充分利用及发挥乳酸的有益功能对奶牛健康生产具有重要意义。文章介绍了乳酸的合成途径及主要产酸菌、乳酸的代谢途径及主要利用菌、乳酸在奶牛瘤胃内的代谢方式及影响其代谢的因素，详细阐述了乳酸产生菌与利用菌对乳酸代谢调节的影响，同时介绍了植物提取物对乳酸代谢调节作用及乳酸代谢调节对奶牛胃肠道菌群、泌乳性能和乳房炎的影响。为进一步了解乳酸对奶牛健康的作用机制及相关植物活性物质在生产实践中的应用提供理论依据，为解决高精料饲粮引起的奶牛酸中毒的预防与治疗提供新思路。     

Infusion of sodium bicarbonate in experimentally induced metabolic acidosis does not provoke cerebrospinal fluid (CSF) acidosis in calves

In a crossover study, 5 calves were made acidotic by intermittent intravenous infusion of isotonic hydrochloric acid (HCl) over approximately 24 h. This was followed by rapid (4 h) or slow (24 h) correction of blood pH with isotonic sodium bicarbonate (NaHCO(3)) to determine if rapid correction of acidemia produced paradoxical cerebrospinal fluid (CSF) acidosis. Infusion of HCl produced a marked metabolic acidosis with respiratory compensation. Venous blood pH (mean ± S(x)) was 7.362 ± 0.021 and 7.116 ± 0.032, partial pressure of carbon dioxide (Pco(2), torr) 48.8 ± 1.3 and 34.8 ± 1.4, and bicarbonate (mmol/L), 27.2 ± 1.27 and 11 ± 0.96; CSF pH was 7.344 ± 0.031 and 7.240 ± 0.039, Pco(2) 42.8 ± 2.9 and 34.5 ± 1.4, and bicarbonate 23.5 ± 0.91 and 14.2 ± 1.09 for the period before the infusion of hydrochloric acid and immediately before the start of sodium bicarbonate correction, respectively. In calves treated with rapid infusion of sodium bicarbonate, correction of venous acidemia was significantly more rapid and increases in Pco(2) and bicarbonate in CSF were also more rapid. However, there was no significant difference in CSF pH. After 4 h of correction, CSF pH was 7.238 ± 0.040 and 7.256 ± 0.050, Pco(2) 44.4 ± 2.2 and 34.2 ± 2.1, and bicarbonate 17.8 ± 1.02 and 14.6 ± 1.4 for rapid and slow correction, respectively. Under the conditions of this experiment, rapid correction of acidemia did not provoke paradoxical CSF acidosis.