Effects of NaHCO3 loading on acid-base balance, lactate concentration, and performance in racing greyhounds.

This investigation examined the effects of NaHCO3 loading on lactate concentration ([La]), acid-base balance, and performance for a 603. 5-m sprint task. Ten greyhounds completed a NaHCO3 (300 mg/kg body weight) and control trial in a crossover design. Results are expressed as means +/- SE. Presprint differences (P < 0.05) were found for NaHCO3 vs. control, respectively, for blood pH (7.47 +/- 0.01 vs. 7.42 +/- 0.01), HCO-3 (28.4 +/- 0.4 vs. 23.5 +/- 0.3 meq/l), and base excess (5.0 +/- 0.3 vs. 0.2 +/- 0.3 meq/l). Peak blood [La] increased (P < 0.05) in NaHCO3 vs. control (20.4 +/- 1.6 vs. 16.9 +/- 1.3 mM, respectively). Relative to control, NaHCO3 produced a greater (P < 0.05) reduction in blood base excess (-18.5 +/- 1.4 vs. -14.1 +/- 0.8 meq/l) and HCO-3 (-17.4 +/- 1.2 vs. -12.8 +/- 0.7 meq/l) from presprint to postexercise. Postexercise peak muscle H+ concentration ([H+]) was higher (P < 0.05) in NaHCO3 vs. control (158.8 +/- 8.8 vs. 137.0 +/- 5.3 nM, respectively). Muscle [H+] recovery half-time (7.2 +/- 1.6 vs. 11.3 +/- 1.6 min) and time to predose values (22.2 +/- 2.4 vs. 32.9 +/- 4.0 min) were reduced (P < 0.05) in NaHCO3 vs. control, respectively. No differences were found in blood [H+] or blood [La] recovery curves or performance times. NaHCO3 increased postexercise blood [La] but did not reduce the muscle or blood acid-base disturbance associated with a 603.5-m sprint or significantly affect performance.

Resveratrol promotes atherosclerosis in hypercholesterolemic rabbits.

The hypothesis was tested that resveratrol, a compound in red wine, would inhibit atherosclerotic development in rabbits fed 0.5% cholesterol for 60 days. Rabbits were supplemented with or without oral resveratrol. During the study, body weights and food consumption were similar for the two groups. The lack of differences between liver weights and a series of serum parameters indicative of liver disease suggest that liver function was similar in the two groups. The diet produced hypercholesterolemia in both groups, but no differences in lipoprotein-cholesterol concentrations. The electrophoretic mobility of plasma low-density lipoprotein (LDL) and plasma LDL after induced oxidation also was not different between the groups. Staining of atherosclerotic lesions in the control and resveratrol-treated groups revealed that the resveratrol-treated rabbits had significantly more aortic surface area covered by atherosclerotic lesions (P < 0.02). Therefore, resveratrol promoted atherosclerotic development, rather than protect against it, by a mechanism that is independent of observed differences in gross animal health, liver function, plasma cholesterol concentrations, or LDL oxidative status.

Hepatic lipid profiles in miniature pigs after alcohol feeding.

Changes in lipid profiles have not been reported for the known increases in total lipid content in livers of alcoholics. We have reported a lowering of the beta-oxidative capacity of alcoholic livers, and therefore would expect a lower turnover of fatty acids in these livers, and thus a change in lipid profile. The percentage composition of saturated and unsaturated fatty acids in the liver of alcohol-fed miniature pigs versus the controls, as well as the function of distance from the main hepatic vein, have both been determined in this study involving the feeding of ethanol for one year. Livers of alcohol-fed miniature pigs contained more total lipids than those of controls. Results also indicated significantly higher percentages of free fatty acids and triglycerides in the alcohol-fed miniature pigs, and also an increase in percentage total neutral lipids. The effect of distance from the main blood source (and therefore oxygenation) gave a fatty acid profile that showed an increase in the ratio of saturated to unsaturated fatty acids with increasing distance from the right hepatic vein. This change in ratio was independent of alcohol feeding.

Changes in phospholipids of alveolar lining material in calves after aerosol exposure to bovine herpesvirus-1 or parainfluenza-3 virus.

Pulmonary lavage samples were collected from 90- to 130-day-old calves before and 6 days after aerosol inoculation with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI3) virus. Alveolar lining material was separated from lavage fluids by high-speed centrifugation and phospholipids were extracted from alveolar lining material and analyzed by high-performance liquid chromatography. Phosphatidylcholine and phosphatidylethanolamine were 74.2 +/- 6.5% and 13.3 +/- 2.8%, respectively, of the total phospholipid content in the surfactant obtained from calves before virus inoculation. Other phospholipids were represented by substantially lower percentages. Infection with either of the 2 viruses caused a significant (P less than or equal to 0.05) decrease in the percentage of phosphatidylcholine to 66.0 +/- 8.0% and 65.1 +/- 10.8% in the calves inoculated with BHV-1 and PI3 virus, respectively. A significant (P less than or equal to 0.05) increase in the percentage of phosphatidylethanolamine to 18.1 +/- 2.2% and 17.8 +/- 4.5% developed in calves inoculated with BHV-1 and PI3 virus, respectively. Infection with BHV-1 also induced an increase (not significant) in the percentage of phosphatidylinositol from 5.5 +/- 2.8% to 7.8 +/- 2.2%. A similar, but not significant, increase in the percentage of phosphatidylinositol was also seen in the calves inoculated with PI3 virus. Less substantial changes in the percentage of other phospholipids were detected after virus infection.

Alterations in the phospholipid composition and morphology of ovine erythrocytes after intravenous inoculation of Corynebacterium pseudotuberculosis.

Corynebacterium pseudotuberculosis produces a sphingomyelin-specific phospholipase D exotoxin that is a major determinant in the pathogenesis of caseous lymphadenitis. The effect of this exotoxin on erythrocytes was assessed during experimentally induced infection of sheep. Blood was drawn at timed intervals, and the phospholipid composition of erythrocytes was determined by use of high-performance liquid chromatographic analysis of membrane extracts. Erythrocyte morphology was determined by use of transmission electron microscopy. Significant (P less than or equal to 0.05) decreases in erythrocyte membrane sphingomyelin content and significant (P less than or equal to 0.05) increases in phosphatidylglycerol content were observed 30 minutes after IV inoculation of C pseudotuberculosis. The concentration of other phospholipids remained unchanged. Initially, spherostomatocytes were formed that later became pitted at the cell surface. These pits or invaginations appeared as numerous vacuoles at the periphery of thin-sectioned cells. Pitting became progressively worse, leading to an extensive scalloped cell surface. Alterations in the phospholipid composition and morphology of ovine erythrocytes may contribute to pathophysiologic findings in sheep with acute infection induced by C pseudotuberculosis.

High-performance liquid chromatography determination of erythrocyte membrane phospholipid composition in several animal species.

High-performance liquid chromatography (HPLC) was used to determine the phospholipid (PL) composition of ovine, equine, bovine, porcine, and canine RBC membranes. Procedural modifications of established techniques provided for separation of 7 PL within a 15- to 20-minute sample run. Significant (P less than 0.05) differences were detected in RBC membrane PL composition among the various species. The concern for physiologic properties associated with hemolysis and/or sedimentation rate must include evaluation of differences in the PL bilayer structure.

Changes in ovine erythrocyte morphology due to sphingomyelin degradation by Corynebacterium pseudotuberculosis phospholipase D.

Corynebacterium pseudotuberculosis produces a sphingomyelin-specific phospholipase D exotoxin that is a major determinant in the pathogenesis of caseous lymphadenitis. We assessed the changes induced in the morphology and sphingomyelin concentration of ovine erythrocytes after incubation with broth culture filtrates or purified exotoxin. Sphingomyelin was hydrolysed nearly in parallel with shape change. Morphologically, spherostomatocytes were seen initially, and later these contained numerous vacuoles at the periphery. Vacuoles seen in thin sections with transmission electron microscopy appeared as pits with scanning electron microscopy. Pitting became progressively worse with time, leading to extensive scalloping of the membrane surface. Chemically, significant decreases (P less than or equal to 0.05) in erythrocyte membrane sphingomyelin content and significant increases (P less than or equal to 0.05) in the content of glycerophospholipids (i.e. phosphatidylglycerol) were observed in erythrocytes incubated with broth culture filtrates or purified exotoxin. These alterations may contribute to the pathophysiology of acute infections induced by C. pseudotuberculosis.

Effect of Pasteurella haemolytica (A1) capsular polysaccharide on sheep lung in vivo and on pulmonary surfactant in vitro.

Capsular polysaccharide (CP) of Pasteurella haemolytica (type A1) was first deposited by fiberoptic bronchoscopy into the lungs of sheep to examine lesions and changes in bronchoalveolar lavage cell populations and, later, was mixed with pulmonary surfactant to investigate alterations in physical properties or surface tension. At 22 hours after deposition, minimal lesions were seen in the lungs only at and contiguous to the site of CP deposition in 2 of 4 sheep. Microscopically, alveoli and interlobular septa were filled with edema fluid. Terminal airways and alveoli contained a moderate amount of neutrophils that varied between sheep. Significant differences in number or type of bronchoalveolar lavage cells were not observed in the weekly lavages between each group or among sheep within each group, either before or after deposition of CP or physiologic saline solution. After 6 hours of incubation at 37 C, CP-surfactant mixtures were examined with a surface tensiometer and centrifuged in sucrose gradients. The CP bound to surfactant, resulting in formation of a precipitate with a surface tension of 31.6 +/- 0.1 dynes/cm and a density of 1.07 to 1.08 g/ml. Lipopolysaccharide of P haemolytica, used as a control, also bound to surfactant, resulting in a complex with a surface tension of 57.7 +/- 0.4 dynes/cm and a density of 1.06 to 1.10 g/ml. Surfactant alone had a surface tension of 32.6 +/- 0.2 dynes/cm and density of 1.05 to 1.06 g/ml. The CP appears by itself not to be a direct major factor in the lung damage that develops in cases of pneumonic pasteurellosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic obstructive pulmonary disease in a dog.

Chronic obstructive pulmonary disease was diagnosed in a 3-year-old Basset Hound that was referred to the hospital because of respiratory distress. Results of radiography, bronchoscopy, and pulmonary function tests indicated lung hyperinflation, airflow restriction, and loss of elastic recoil of the lungs. Because of the poor response to treatment, the dog was euthanatized. Postmortem findings revealed emphysema, bronchiectasis, and bronchitis, which comprise chronic obstructive pulmonary disease.

Adaptation of lipogenesis and lipolysis to dietary ethanol.

The effect of dietary ethanol on metabolic fates of glucose and ethanol, and activities of lipoprotein lipase and hormone-sensitive lipase in several tissues of miniature pigs were determined in vitro. Ethanol and glucose were used at similar rates for fatty acid synthesis in liver and brain and CO2 production in liver. Ethanol was preferred over glucose for fatty acid and CO2 production in ileal mucosal cells. Glucose was the preferred substrate for lipogenesis and oxidation to CO2 in adipose tissue and skeletal muscle, and for oxidation to CO2 in brain. Dietary ethanol decreased glucose and ethanol conversion to fatty acids in ileal mucosa and brain, respectively. Dietary ethanol had no effect on the capacity of liver, adipose tissue, and skeletal muscle to convert either glucose or ethanol to long-chain fatty acids. The capacity to oxidize ethanol, but not glucose, to CO2 in liver was increased by dietary ethanol. No dietary ethanol effect was observed in other tissues. The capacity for removal of plasma triglycerides (based on lipoprotein lipase activity) tended to increase in adipose tissue and skeletal muscle of pigs fed ethanol. Mobilization of long-chain fatty acids from adipose tissue (based on hormone-sensitive lipase activity), triglyceride concentration in plasma, and percentage of lipid in liver remained unchanged when ethanol was fed. Livers of ethanol-fed pigs, however, were larger than livers of control pigs. Our results indicate that feeding miniature pigs 21-37% of total caloric intake as ethanol causes significant metabolic adaptations of lipid metabolism in liver and ileal mucosa, but not in adipose tissue, skeletal muscle, and brain. The ethanol feeding, however, did not cause fatty livers or hyperlipidemia.

Allergy and pulmonary impairment in Iowa veterinarians.

If small animal practice exposure, including the laboratory animal situations encountered in academic and other research pursuits, is more detrimental to veterinarians than large animal practice exposure for induction of allergic respiratory disease, then preventive measures such as increased ventilation, use of high efficiency particulate filters, and wearing of masks should be encouraged to reduce allergen exposures. Migration from large animal practice, likewise, should be discouraged. Failure to migrate to low occupational allergy risk situations early enough in a veterinary career can have severe and even fatal results. If the observed respiratory disease in veterinarians is in fact due to exposure, then unfortunately, it may in some cases be progressive and not just chronic. Data which could provide criteria for predicting occupational allergy and possible related respiratory disease outcome is scant at this time and career counselling is difficult. If the veterinary occupational animal allergy data should be proven correct such results can be used to help others.

Alveolar phospholipids of 17-day-old pigs exposed to microorganisms of nonpulmonic origin.

Alveolar lining material was obtained from gnotobiotic pigs; gnotobiotic pigs exposed to aerobes, anaerobes, or mixtures of both microorganisms; and conventional farm-raised pigs. Alveolar lining material concentrations of phosphatidylcholine, sphingomyelin, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylglycerol, and lysolecithin were determined. Seventy-four pigs were allotted to the following groups: 1--gnotobiotes (n = 13), 2--gnotobiotes with aerobes (n = 6), 3--gnotobiotes with anaerobes (n = 31), 4--gnotobiotes with anaerobes and aerobes (n = 2), 5--gnotobiotes with facultative anaerobes (n = 9), and 6--conventionally farm-farrowed (n = 13). The conventionally raised pigs had lysolecithin, sphingomyelin, and phosphatidylinositol concentrations that were significantly different from those of all other groups of pigs. Phosphatidylethanolamine was significantly decreased in group 6 pigs when compared with that in all other groups. There were also statistically significant differences between the gnotobiotic (group 1) and the exposed gnotobiotic (groups 2, 3, 4, 5) pigs, although the differences were less pronounced. Since intestinal microbes produce alveolar lining material phospholipid differences, studies need to be concerned with phospholipid changes that occur after exposure to lung-specific microorganisms and with physiologic changes in lung function associated with the phospholipid changes.

Pulmonary and hematologic changes in swine with Mycoplasma hyopneumoniae pneumonia.

Studies were made of the physiologic changes in the lung of young growing pigs intratracheally inoculated at 5.5 to 6 weeks of age with Mycoplasma hyopneumoniae. Hematologic changes also were studied. Studies were performed at the 4th, 5th, and 6th weeks after inoculations were done. The inoculated pigs had a marked decrease in body weight gain. There were no significant changes in the heart rate, respiratory rate, and rectal temperature, even though at necropsy the apical, cardiac, and diaphragmatic lobes of the lungs of inoculated pigs had scattered, but well-demarcated, pneumonic lesions. The lungs were edematous and increased in weight, compared with those of control (noninoculated) pigs. There were several changes in respiratory functions in the inoculated animals, including significant increases in esophageal pressure negativity, expiratory flow rate, tidal and minute volumes, and work of breathing and significantly less oxygen consumption. Inspiratory flow rate and airway resistance were markedly increased. The elasticity of infected lungs was reduced, as shown by notable decreases of dynamic lung compliance. According to blood gas analyses, acid-base balance had changed in the inoculated pigs. Arterial blood pH, arterial partial pressures of O2 and CO2, and arterial concentration of HCO3- decreased. To some degree respiratory acidosis indicated by a significant decrease of base excess was evident in the blood of inoculated pigs. As a result, inoculated animals required hyperventilation (compensatory respiratory alkalosis) to maintain the pH of arterial blood near a physiologically normal value. The pigs with mycoplasmal pneumonia showed no drastic hematologic changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Beneficial effects of exercise on l-isoproterenol induced myocardial infarction in male rats.

The effect of exercise on the severity of isoproterenol-induced acute myocardial infarction was studied in male rats. Thirty-three 100-day-old Sprague-Dawley rats were subjected to moderate treadmill exercise (65% VO2max) for 13 wk. Exercise consisted of running 15 m/min for 30 min on an 8 degree incline for 5 d/wk. Sixty-three sedentary control animals of equal age were housed with the exercising animals throughout the experiment. Growth rates of the sedentary rats (SD) were matched to exercising rats (EX) by reducing food intake. Cardiac hypertrophy was not evident after exercise training, yet significantly lower heart rates (386-421/min) were observed in EX rats. Resting arterial blood pressure was not significantly altered by exercise. In response to l-isoproterenol stress (70 mg/kg), EX and SD rats exhibited significant increases in heart rate (EX: 19%, SD: 9%), respiratory rate (EX: 39%, SD: 15%), and cardiac contractility (EX: 48%, SD: 54%). EX and SD rats exhibited severe reductions in aortic pressure (EX: 92/63 mmHg, SD: 74/48 mmHg) resulting in large declines in the double product (HR X SAP). No EX rat died from l-isoproterenol injection, but 24% of the SD rats died. Exercise was beneficial in the reduction or prevention of induced infarction and this occurred without cardiac hypertrophy.

Effects of ethanol on brain sialic acid and 2-deoxyribose in young rats.

Young rats, on a nutrient-fortified liquid diet containing 7% ethanol, showed decreases in brain sialic acid and 2-deoxyribose within 2 weeks; action on both compounds was delayed in forebrain, but decreases were apparent there after 6 weeks.

A method for obtaining swine alveolar macrophages by segmental pulmonary lavage.

A technique for obtaining alveolar macrophages (AM) from anesthetized swine is described. Animals were intubated and segmental pulmonary lavage was performed utilizing a double lumen catheter (DLC). An average of 98% of the initial 100 ml lavage fluid was recovered with a typical yield of 1 x 10(8) free alveolar cells (FAC). AM were then separated from other FAC by their adherence to plastic. The final adherent cell population consisted of greater than 95% macrophage as determined by morphology and non-specific esterase activity. The technique described had no adverse effects on the animals even when repeated on the same animal several days later.

Acutely administered ethanol decreases whole-brain sialic acid and cerebellar 2-deoxyribose.

As a follow-up to a previous study that suggested that acutely administered ethanol could decrease steady-state brain levels of sialic acid (SA), we evaluated the time course of the ethanol effect and tested the influence of route of administration and sex. Compared to the control treatments, ethanol (2 gm/kg) significantly decreased brain SA in each of the four brain regions that were tested. The decrease was evident by 30 minutes after ethanol administration, but peak effect was reached at about 1--2 hours. The decrease occurred with either injection or self-administration, but the greatest decrease occurred in the self-administration group. The SA-induced decrease was greatest in females. An ancillary part of the study included measurement of brain levels of 2-deoxyribose (DR). Ethanol given by either route of administration caused a preferential decrease in DR levels in the cerebellum. Lesser, but statistically significant, decreases in SA and DR occurred in controls, suggesting that these chemicals are sensitive to subtle environmental contingencies associated with the experimental procedures.

Large regional and strain differences in rat brain sialic acid and 2-deoxyribose.

Sialic acid, a very polar component of glycolipids and glycoproteins that is exposed on membrane surfaces, was observed in rat brain to vary in the descending order: forebrain, midbrain, cerebellum and medulla. Levels of 2-deoxyribose were also differentially distributed, with about 3.5 times as much in the cerebellum and nearly equal amounts elsewhere. Similar results were obtained with another genetic strain, but clear quantitative differences were evident for both chemicals.

Biochemical markers of ethanol effects on brain.

Because sialic acid is a potential biochemical marker of membrane development or alteration, we compared acute and chronic ethanol effects on sialic acid. Experiments were conducted with 50 adult male Wistar rats (approximately 400 gm), housed in groups of five. Rats drank ad libitum a vitamin-fortified diet (Nutrament) that was adulterated with ethanol; ethanol intake averaged for each rat 10-18 gm/kg/day. Controls were fed an equal total volume, made isocaloric with sucrose. Rats were sacrificed weekly for four weeks, and an acute challenge dose of ethanol (2 gm/kg, intraperitoneally) was given 45 minutes before sacrifice of both control and ethanol-consuming rats. Some controls were challenged only with saline. We replicated our earlier findings of regional differences in sialic acid and in cerebellar deoxyribose (measured as a necessary adjunct in the autoanalyzer modification of the Warren-Delmotte methods). In the saline-challenged controls, levels of both compounds were higher at four weeks than after one week. Similar increases occurred also in the chronic ethanol-consuming group, but not in the ethanol-challenged controls, which had significantly lower values. Results in saline-challenged controls suggest that the chronic treatment either 1) created a tolerance which protected cells from damage by the challenge dose of ethanol, or 2) killed neurons, thus promoting proliferation of glial cells.

Influence of cations, sialic acid and pH on the expansion of films of canine lung surfactant.

Sialic acid (14.6 mug/mg protein) was quantitated in the non-cellular material removed from the lung of Beagle dogs by lavage. Sialic acid did not affect the dynamic surface tension properties of either the total alveolar lipid removed by lavage or of its major lipids, dipalmitoyl lecithin (DPL) and dipalmitoyl phosphatidyl glycerol (DPG). The presence of divalent cation (Ca2+, Mg2+, Mn2+ and Zn2+) or a lowered pH in the subphase medium lowered the surface tension during the expansion phase of the total alveolar lipid film when it was compressed and expanded on a Wilhelmy trough. Films of DPL behaved similarly, but no pH effect was observed with DPG monolayers. The cation effect manifested itself in the same direction as the value of the individual stability constants (Zn2+ greater than Mn2+ greater than Mg2+ greater than Ca2+) which suggests ionic binding of the cations to the phosphate group of the phospholipids. A physiological advantage of such an effect may lie in the conservation of the energetically favorable low surface tension state achieved during film compression with a minimum of surfactant lipid.