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。     

Diagnosis of subacute ruminal acidosis (SARA) by continuous reticular pH measurements in cows

The objective of this study was to determine whether subacute ruminal acidosis (SARA) could be diagnosed by continuous measurements of the reticular pH, as compared with the ruminal pH, using healthy cows fed a control diet and SARA cows fed a rumen acidosis-inducing diet. The reticular and ruminal pH were measured simultaneously by a radio transmission pH measurement system. The mean reticular pH at 1-h intervals decreased gradually from the morning feeding to the next feeding time in both healthy and SARA cows, though the decrease in the ruminal pH was observed to be more drastic as compared with that observed in the reticular pH. The threshold of the 1-h mean pH in the reticulum for a diagnosis of SARA was considered to be 6.3, and a significant positive correlation was observed between the reticular and ruminal pH. No differences in the concentrations of lactic acid, ammonia nitrogen, and volatile fatty acids were noted between the reticular and ruminal fluids in SARA cows. These results demonstrate that the reticular pH can be used to detect SARA in cows, as opposed to using the ruminal pH.     

Effects of endotoxin infusion on circulating levels of eicosanoids, progesterone, cortisol, glucose and lactic acid, and abortion in pregnant cows

The effects of Escherichia coli endotoxin infusions (1.0 or 2.5 micrograms kg-1 over 6 h) on pregnancy were investigated in cows in the first, second and third trimester of gestation. Endotoxin increased the plasma levels of prostaglandins (PGs), thromboxane B2 and cortisol, and decreased progesterone. The severity of the clinical signs and the magnitude of the increases in plasma PGs, thromboxane B2 and cortisol tended to depend on the dose of endotoxin, but were independent of the gestation period. There was hyperglycemia followed by hypoglycemia and lactic acidemia. Hyperglycemia and lactic acidemia were significant only at the high dose of endotoxin. Endotoxin infusion at both doses caused a preferential mobilization of oleic acid from adipose tissue, and also had some effects on the mobilization of palmitic and stearic acids during the post-infusion period. The cows in the first trimester of gestation were more sensitive to the abortifacient effect of endotoxin than cows in the second and third trimester of gestation. The results of this study indicate that the mechanism of endotoxin-induced abortion in cows initially involves a prolonged release of PGF2 alpha and its subsequent stimulant effect on uterine smooth muscle contraction and luteolytic effect leading to a gradual decline in the plasma levels of progesterone. It was concluded that pregnancy terminates in the absence of an adequate level of progesterone, especially during the first trimester of gestation, when progesterone of extraluteal origin is not yet available, coupled with the PGF2 alpha-induced propulsive contraction of the uterus. In addition, the metabolic and circulatory failures in severe cases of endotoxemia, especially at the high dose of endotoxin, resulting either directly or indirectly via the release of various autacoids, catecholamines and cortisol, may also contribute to the termination of pregnancy at any stage of gestation.     

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.     

牛瘤胃酸中毒的血液学及生化指标变化

瘤胃酸中毒是由于牛过量采食含可溶性糖类物质的精饲料,瘤胃内急剧产生、积聚并吸收大量乳酸等物质所致的一种急性消化性酸中毒,危及牛的健康。本文分析了24例病牛的临床表现、血液学和生化指标变化情况。结果表明,病牛主要临床表现为轻症者食欲减退,瘤胃收缩力降低;中度病牛精神迟钝,食欲废绝,呼吸急促;重症病牛陷入昏迷状态,呼吸浅表而快,最后衰竭而死亡。血液学检测结果为病牛的RBC、Hb、Pcv均显著高于健康牛(P<0.05),且随着瘤胃酸中毒的加剧而升高;WBC总数上升,嗜中性白细胞增加而淋巴细胞减少。生化指标检测结果为随病情加重,其血浆二氧化碳结合力及钾、氯、钙等离子不同程度下降;尿素氮含量高于健康牛;轻度酸中毒阶段血糖含量不断增加,但病情严重时则下降。通过本研究,以期为反当动物瘤胃酸中毒的防治提供参考依据。     

Assessment of acid-base status and plasma lactate concentrations in arterial,mixed venous,and portal blood from dogs during experimental hepatic blood inflow occlusion

OBJECTIVE: To determine the effects of extended experimental hepatic blood flow occlusion (ie, portal triad clamping [PTC]) in dogs by measuring acid-base status and plasma lactate concentrations in arterial, mixed venous, and portal blood and evaluating the relationship between metabolic and concurrent hemodynamic changes. ANIMALS: 6 healthy Beagles. PROCEDURE: During anesthesia with isoflurane, cardiac output and arterial blood pressure were measured. Arterial, mixed venous, and portal blood samples were collected simultaneously for blood gas analyses and plasma lactate measurements before PTC and at 8-minute intervals thereafter. RESULTS: PTC resulted in severe hemodynamic and metabolic alterations. Eight minutes after PTC, significant decreases in cardiac index from a baseline value of 3.40 +/- 0.27 to 1.54 +/- 0.26 L/min/m2 and in mean arterial blood pressure from a baseline value of 74 +/- 6 to 43 +/- 6 mm Hg were recorded. After PTC, results indicative of lactic acidosis were found in portal blood at 16 minutes, in mixed venous at 32 minutes, and in arterial blood at 48 minutes. Significant differences in measured variables were also found between arterial and portal blood samples, between mixed venous and portal blood samples, and between arterial and mixed venous blood samples after PTC, compared with differences at baseline. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of mixed venous blood is preferable to analysis of arterial blood in the assessment of metabolic derangement. In a clinical setting, occluded portal blood is released to the systemic circulation, and the degree of reperfusion injury may depend on the metabolic status of pooled portal blood.     

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.     

Comparison between pre- and postnatal acid-base status of calves and their perinatal mortality

The acid-base status of 58 calves (all in normal anterior presentation) was determined from venous blood samples before the onset of traction and immediately after vaginal delivery. Calves were assigned to one of three groups according to their blood pH value: group 1 - normal, pH greater than 7.2; group 2 - acidotic, pH 7.2 to 7.0; group 3 - severely acidotic, pH less than 7.0. Before the onset of traction (i.e. during the 30 minutes following the appearance and rupture of the membranes), 43 calves (74.1%) had normal acid-base values, 14 (24.1%) had slight acidosis, and only 1 (1.7%) had severe acidosis. At birth the three groups of calves showed the following distribution: 23 (39.7%) were normal, 29 (50%) had slight acidosis, and 6 (10.3%) had severe acidosis. Seven calves (12.1%) died during birth or within 48 hours after birth; 2 were normal shortly before birth, 4 were acidotic shortly before birth, and 1 was severely acidotic even before the onset of traction. Traction was significantly longer for cows that delivered severely acidotic calves compared to cows in the other two groups.     

Comparison between pre‐ and postnatal acid‐base status of calves and their perinatal mortality

Summary

The acid‐base status of 58 calves (all in normal anterior presentation) was determined from venous blood samples before the onset of traction and immediately after vaginal delivery.

Calves were assigned to one of three groups according to their blood pH value: group 1 ‐ normal, pH >7.2; group 2 ‐ acidotic, pH 7.2 to 7.0; group 3 ‐ severely acidotic, pH < 7.0. Before the onset of traction (i.e. during the 30 minutes following the appearance and rupture of the membranes), 43 calves (74.1%) had normal acid‐base values, 14 (24.1%) had slight acidosis, and only 1 (1.7%) had severe acidosis. At birth the three groups of calves showed the following distribution: 23 (39.7%) were normal, 29 (50%) had slight acidosis, and 6 (10.3%) had severe acidosis.

Seven calves (12. 1%) died during birth or within 48 hours after birth; 2 were normal shortly before birth, 4 were acidotic shortly before birth, and 1 was severely acidotic even before the onset of traction. Traction was significantly longer for cows that delivered severely acidotic calves compared to cows in the other two groups.     

Acute response of urine pH following ammonium chloride administration to dogs

To test the acidifying ability of the distal portion of the nephrons in healthy dogs, 0.2 g of NH4Cl/kg of body weight was given PO. Samples for venous blood gas analysis and urine pH were taken hourly for 6 hours. Systemic acidemia developed, as evidenced by a statistically significant (P less than 0.05) decrease in blood pH 1 hour after NH4Cl administration. Four hours after administration, mean urine pH decreased to a low of 5.16 +/- 0.1 and was less than 5.5 3 hours after administration. Changes in urine pH 2 hours after administration were statistically significant (P less than 0.05). In human beings, NH4Cl loading is used to detect patients with distal renal tubular acidosis (defective hydrogen ion secretion by the distal nephrons) and normal acid/base values. Distal renal tubular acidosis is diagnosed if urine pH fails to decrease to less than 5.5 after NH4Cl administration. On the basis of the findings of this study, a similar value would be valid for dogs.     

Venous blood gas and lactate values of mourning doves (Zenaida macroura), boat-tailed grackles (Quiscalus major), and house sparrows (Passer domesticus) after capture by mist net, banding, and venipuncture

Blood gas partial pressures, pH, and bicarbonate and lactate concentrations were measured from the basilic vein of mourning doves (Zenaida macroura) and the jugular vein of boat-tailed grackles (Quiscalus major) and house sparrows (Passer domesticus) to assess immediate impacts of mist net capture and handling for banding and venipuncture. Mourning doves and house sparrows exhibited mild acidemia (median [minimum-maximum] venous blood pH(41 degrees C) = 7.394 [7.230-7.496] and 7.395 [7.248-7.458], respectively), relative to boat-tailed grackles (Quiscalus major; 7.452 [7.364-7.512]), but for different reasons. Mourning doves exhibited relative metabolic acidosis (lower venous blood pH, higher lactate concentrations, lower bicarbonate, and no significant differences in partial pressure of CO2 (pCO2) or partial pressure of O2 (pO2) compared with boat-tailed grackles). House sparrows exhibited relative respiratory acidosis (lower venous blood pH, higher pCO2, lower pO2, and no significant differences in bicarbonate and lactate concentrations compared with boat-tailed grackles). All birds captured by mist net and handled for banding and venipuncture experienced some degree of lactic acidemia; and values were greater in mourning doves (lactate, 7.72 [3.94-14.14] mmol/L) than in boat-tailed grackles (5.74 [3.09-8.75] mmol/L) and house sparrows (4.77 [2.66-12.03] mmol/L), despite mourning doves resisting least and being easiest to disentangle from the mist net. House sparrows were more susceptible to respiratory acidosis, warranting particular care in handling birds <30 g to minimize interference with ventilation. The different sample collection site for mourning doves may have affected results in comparison with the other two species, due to activity of the wing muscles. However, despite the higher lactate concentrations, pCO2 was relatively low in doves. The metabolic, respiratory, and acid-base alterations observed in this study were minor in most cases, indicative of the general safety of these important field ornithology techniques. The effect of other adverse conditions, however, could be additive.     

Endotoxin and Arachidonic Acid Metabolites in Portal,Hepatic and Arterial Blood of Cattle with Acute Ruminai Acidosis

Andersen, P. Haubro, M. Hesselholt and N. Jarlev: Endotoxin and arachidonic acid metabolites in portal, hepatic and arterial blood of cattle with acute ruminai acidosis. Acta vet.scand.1994,35,223-234.– Ruminai acidosis was induced experimentally with 70 g barley / kg body weight in 2 rumen fistulated cows with chronic indwelling catheters in the portal vein, in a hepatic vein and the carotid artery. The cows were followed for 24 and 20h after the overfeeding and evaluated clinically and by clinical chemistry. The 2 cows exerted different responses to the treatment. Both cows showed signs of severe ruminai acidosis. Both cows had endotoxin in portal and hepatic vein blood, but only 1 of the cows convincingly developed a systemic endotoxaemia. A pre-hepatic release of the stable prostacyclin and thromboxane metabolites, 6-ketoprostaglandin F_lα and thromboxane B₂ was demonstrated in this cow. The results of the present study show that endotoxin and arachidonic acid metabolites of pre-hepatic origin may be factors involved in the pathogenesis of ruminai acidosis, and that investigation of the factors affecting translocation of ruminai endotoxin and subsequent clearing in the liver, will be of importance.     

Osmolal and anion gaps in dogs with acute endotoxic shock

Serum osmolalities, biochemical concentrations, osmolal and anion gaps, blood lactate concentrations, and acid base status were evaluated in anesthetized, healthy control dogs and in dogs with endotoxic shock. The osmolal gap was not affected by endotoxemia. Compared with control dogs, dogs with endotoxic shock had mildly, though insignificantly, increased anion gaps and significantly increased blood lactate concentrations. The anion gap in dogs with endotoxic shock was positively (r = 0.77) and significantly correlated with the blood lactate concentration. Therefore, the blood lactate concentration of a dog in endotoxic shock may be estimated by use of the equation: lactate = 0.27 (anion gap) - 1.46. Confidence limits for this estimation were calculated. Dogs with endotoxic shock developed a lactic acidosis and hyperchloremic metabolic acidosis, with hyperventilation.     

维吉尼亚霉素对于奶牛乳酸中毒及瘤胃发酵的调控综述

维吉尼亚霉素作为常用饲用抗生素能够抑制瘤胃乳酸发酵菌,改善瘤胃内不良发酵,提高饲料利用率,在高精日粮条件下可对奶牛乳酸中毒起到一定预防作用。本文总结了国内外关于维吉尼亚霉素的相关试验与文献;从奶牛酸中毒机制着手,综述其对于酸中毒的调控;并总结与分析了维吉尼亚霉素对奶牛瘤胃发酵的影响。为今后在奶牛日粮中的合理使用,实现奶牛安全饲养提供理论依据。     

Effect of acute acidemia on blood biochemical variables in healthy ponies

L-Lactic acid and D,L-lactic acid infusion in ponies resulted in metabolic acidosis with high anion gap (AG). Increased AG was explained entirely by increased blood L- and D-lactate concentrations. Hydrochloric acid infusion caused metabolic acidosis with decreased AG. Saline (NaCl) infusion caused mild metabolic acidosis, with no significant change in AG. Plasma K+ concentration was decreased by all types of infusions, with a maximum of 0.50, 0.25, 0.40, 0.50 mmol/L below baseline at the end of infusion in the L-lactic acid-, D,L-lactic acid-, HCl-, and NaCl-infused ponies, respectively. Only hydrochloric acid had a tendency to increase plasma K+ concentration. Hypophosphatemia developed in NaCl- and HCl-infused ponies, but not in the D,L-lactic acid-infused ponies. Serum inorganic phosphate concentration in L-lactic acid-infused ponies increased initially, but was significantly (P less than 0.05) lower than values in the other ponies at 4 hours after onset of infusion. In ponies, the effect of acidemia on plasma K+ and serum inorganic phosphate concentrations was similar to that reported for other species. Changes were small in magnitude and depended on the nature of the acid anion. Results indicate that large changes in plasma K+ and serum inorganic phosphate concentrations during acidosis are probably not a direct result of acidemia.     

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.     

Changes in the profile of liver enzymes in newborn calves induced by experimental,subclinical acidosis in pregnant cows and osmotic diarrhoea

Experimental, subclinical acidosis was induced by oral administration of sacharose during the last 2 months of pregnancy in 15 cows. Seven cows and their newborn calves were used as a control group. The liver enzyme activities in the serum and the blood acid-base status were determined in the 15 calves from the cows in the experimental group. Mannitol was administered orally to 8 calves from the experimental group to induce osmotic diarrhoea. It was concluded that subclinical acidosis in pregnant cows alters the biochemical liver profile of their newborn calves, affecting the aspartate aminotransferase, alanine transaminase, beta glucuronidase, glutamate dehydrogenase and bilirubin activities in the serum, which are associated with oedematous changes to the hepatocytes. Diarrhoea was accompanied by an increase in the alkaline phosphatase and gammaglutamyl transferase activities and a decrease in the total protein concentration in the serum. These changes were apparently related to the numerous necrotic foci in the liver and the proliferation of the Kuppfer cells. It would appear from these results that the liver damage in the newborn calves was associated with the subclinical, metabolic acidosis in their dams and that osmotic diarrhoea occurring in the neonatal period additionally impaired the liver function.Abbreviations ALP alkaline phosphatase - ALT alanine transaminase - AST aspartate aminotransferase - GR betaglucuronidase - bw body weight - ELISA enzyme-linked immunosorbent assay - GD glutamate dehydrogenase - GGT gammaglutamyl transferase - IU international unit     

Cardiorespiratory Effects of the Intravenous Administration of Tiletamine-zolazepam to Cats

The hemodynamic and respiratory effects of three doses (9.7, 15.8, and 23.7 mg/kg intravenous [IV]) of a 1:1 combination of tiletamine and zolazepam were studied after isoflurane anesthesia in cats instrumented for the recording of hemodynamic data. Systolic, mean, and diastolic arterial blood pressures were decreased 1 minute after drug administration but then increased above baseline with all three doses. Cardiac output was decreased briefly at 1 minute with the 15.8 and 23.7 mg/kg doses. The rate of development of left ventricular pressure and peripheral vascular resistance decreased at 1 minute but returned to baseline or above by 10 minutes. There were no significant changes in heart rate, central venous pressure, or left ventricular end diastolic pressure. The arterial pH and blood gas measurements reflected the development of respiratory acidosis after administration of 23.7 mg/kg. These results support the conclusions that tiletamine-zolazepam administered intravenously is a useful and comparatively safe anesthetic agent in the cat.     

Impact of lactic acid fermentation in the large intestine on acute lactic acidosis in cattle

Microbial and fermentation changes in the ingesta of the large intestine and their influence on the pathogenesis of acute lactic acidosis were studied in 4 cows fitted with permanent cannulas in the ileum and cecum. Feed mixture containing 65% of maize was infused into the cecum for several days in amounts of 2 and 4 kg per day. The daily amount was divided in 8 equal portions and given with 3 l of warm physiologic saline solution. During the period of ad libitum feeding of hay, the pH values in cecal digesta were 7.4 to 7.6 and the amount of total volatile fatty acids 40-60 mmol/kg with high molar percentage (87-90 mol%) of acetic acid. As to lactic acid only the L(+) lactic isomer was found in a concentration of about 0.4 mmol/kg. Infusion of low amounts of starch induced mild lactic acid fermentation in the cecum associated with a pronounced increase in the concentration of L(+) and D (-) lactic acid to peak levels of 80 +/- 10 mmol/kg and 7 +/- 1 mmol/kg, respectively. Lactic acid fermentation ceased within 2 to 3 days indicating that the gut microflora had adapted to the starch infusion. Slight decreases of blood pH and bicarbonates in blood as well as a moderate increase of netto acid-base excretion in urine indicated mild changes of acid-base balance, but clinically no pathological symptoms were observed. Higher amounts of infused starch caused pronounced lactic acid production in the large intestine which persisted throughout the experiment. Peak L(+) and D(-) lactic acid concentration in cecal digesta reached on the average 137 +/- 16 mmol/kg and 45 +/- 7 mmol/kg respectively. Significant decreases of blood pH values from 7.41 +/- 0.02 to 7.18 +/- 0.08 (P < 0.001), actual bicarbonate from 28.2 +/- 3.2 to 11.0 +/- 2.6 mmol/l (P < 0.001) and base excess from 3.9 +/- 3.6 to -15.2 +/- 3.8 mmol/l (P < 0.001) were observed. D (-) lactic acid concentration in blood increased to 3.2 +/- 0.4 mmol/l, but L(+) lactic acid values remained unchanged under 1 mmol/l. Clear clinical symptoms of indigestion and intoxication characterized by severe inappetence, ruminal stasis and general weakness were also observed. Typical clinical symptoms of disease as well as blood and urine changes in acid-base balance indicated that lactic acid fermentation in the large intestine contributes considerably to the pathogenesis of acute ruminant lactic acidosis.     

Phagocytosis of bovine blood and milk polymorphonuclear leukocytes after ozone gas administration in vitro

To determine the effects of ozone on the phagocytosis of bovine polymorphonuclear leukocytes (PMNs), ozone gas was administered in vitro on the blood and milk of healthy lactating cows, cows with acute mastitis, and cows with milk fever. In the blood of healthy dairy cattle, although there was no significant effect of ozone gas on the viability of the leukocytes, phagocytosis of PMNs significantly decreased. In contrast, ozone gas administration in vitro significantly increased phagocytosis of PMNs from the blood of cows with acute mastitis and milk fever, and from mastitic milk. These findings showed that ozone administration in vitro has positive and negative effects on bovine PMN phagocytosis, depending on the health status of the animal.