Effects of halothane sensitivity on mobility status and blood metabolites of HAL-1843-normal pigs after rigorous handling.

The objective of this study was to determine if HAL-1843-normal pigs that respond abnormally to halothane anesthesia were more likely to become nonambulatory (NA) when subjected to rigorous handling than pigs that exhibit a normal response to halothane. After a 1,100-km transport, pigs exhibiting low (HS-L; n = 33), intermediate (HS-I; n = 10), and high (HS-H; n = 47) sensitivity to halothane were moved through a 36.6-m long aisle that was 2.1 m wide at each end and 0.6 m wide in the middle 18.3 m. Ten groups of 8 pigs were briskly moved down the aisle and back 4 times, receiving a minimum of 1 electrical prod per pass (8 prods/pig). Before testing, rectal temperature was measured, open-mouth breathing and skin discoloration were visually evaluated, and a blood sample was collected from each pig. After the test, the pigs were returned to their pens, and the same measurements were taken immediately posttest and 1 h posttest (no blood at 1 h posttest). Pigs that were HS-H were more prone to becoming NA compared with HS-L pigs (P < 0.02). Regardless of halothane status, a greater number of pigs exhibited open-mouth breathing and skin discolorations immediately posttest than at the pretest or 1 h posttest times (P < 0.05). No differences were observed in blood metabolites between the different halothane sensitivity categories. However, pigs that became NA had elevated blood levels of creatine phosphokinase, lactate, glycerol, nonesterified fatty acids, ammonia, and urea nitrogen before testing (P < 0.05). Collectively, these data suggest HS-H pigs are more susceptible to becoming NA than HS-L. The elevated pretest blood metabolites of NA pigs suggest that they were in a hypermetabolic state that predisposed them to becoming NA.

Metabolic responses of lactating dairy cows to 14-day intravenous infusions of glucagon.

Twenty cows were assigned at parturition to two groups to study metabolic effects of continuous intravenous infusions of glucagon. Groups were control cows and cows treated with glucagon at 10 mg/d for 14 d starting at d 21 postpartum. Daily blood samples and nine liver biopsies were taken from d 7 to 49 postpartum. Plasma glucagon increased six- to seven-fold during infusions of treated cows. Plasma insulin was increased heterogeneously by glucagon infusions. Plasma glucose increased 11.5 and 9.0 mg/dl during wk 1 and 2 of glucagon infusions. No other plasma metabolites tested (nonesterified fatty acids, beta-hydroxybutyrate, and urea N) were affected by glucagon infusions. Liver glycogen decreased by d 2 of glucagon infusion but was repleted to preinfusion values by d 7 and increased to 169% of the preinfusion baseline values at 3 d after cessation of glucagon. Milk production decreased transiently during glucagon infusions. Both milk production and milk protein percentage decreased during glucagon infusion, which could imply a decreased availability of amino acids for milk protein synthesis. Feed intakes did not increase during glucagon infusions, which was in contrast to the control group. Results indicated that glucagon infusions caused liver glycogenolysis initially and probably enhanced gluconeogenesis but glucagon did not appear to increase lipolysis from adipose tissue in these early lactating dairy cows.

Metabolic responses of dairy cows and heifers to various intravenous dosages of glucagon.

To evaluate the ability of glucagon to improve carbohydrate status in dairy cows without an increase in blood lipids, glucagon was infused intravenously for 48 h into lactating cows and spayed heifers in three crossover experiments. During Experiment 1, glucagon (5 and 20 mg/d) was infused into four midlactation cows. Experiment 2 involved the infusion of 0, 2.5, 5.0, or 10 mg/d of glucagon into eight heifers; each heifer received two of the dosages. In Experiment 3, four early lactation cows were treated with 5 and 10 mg/d of glucagon. Glucagon consistently increased plasma glucose concentrations in a dose-dependent fashion throughout the 48-h periods. Plasma insulin was increased in a nondose-dependent manner by glucagon in Experiment 1. Plasma urea N was increased when glucagon was administered at 5 mg/d during Experiment 2 and tended to be decreased during Experiment 3. Nonesterified fatty acids in plasma were, in most cases, not affected; however, they were increased by glucagon at 10 mg/d during Experiment 2. Concentrations of beta-hydroxybutyrate were increased only by the 20-mg/d dosage. During Experiment 1, liver glycogen concentrations decreased by 2.1% (wet weight basis) for both dosages of glucagon, and concentrations of total lipid in the liver were increased by 0.6% (wet weight basis) by 20 mg/d of glucagon. Milk fat percentage was increased by glucagon, but milk volume and milk protein production were decreased during Experiment 1. Glucagon improved carbohydrate status over the 48-h periods in all experiments but did not increase plasma nonesterified fatty acids except at the 10-mg/d dosage in Experiment 2.

Alleviation of fatty liver in dairy cows with 14-day intravenous infusions of glucagon.

Twenty multiparous cows were fed additional concentrate during the final 30 d prepartum to cause susceptibility to fatty liver. From 14 to 42 d postpartum, all cows were subjected to a protocol to induce fatty liver and ketosis. To test glucagon as a treatment for fatty liver, either glucagon at 10 mg/d or excipient was infused via the jugular vein from 21 to 35 d postpartum. All cows had fatty liver at 14 d postpartum and became ketonemic and hypoglycemic during the induction of ketosis. Glucagon increased plasma glucose to 142% of that of controls throughout the 14-d treatment. The hypoinsulinemia present in cows with fatty liver was not affected by glucagon. Plasma beta-hydroxybutyrate and nonesterified fatty acids were decreased by glucagon. At 6 d postpartum, liver triacylglycerol averaged 12.9% of liver (wet weight basis). Glucagon had decreased triacylglycerol content of livers by 71% at d 35. Glycogen was 1.0% of the wet weight of livers at 6 d in milk, but it was decreased by glucagon to 0.5% at 2 d after glucagon began. Glycogen then increased in cows treated with glucagon until at 38 d in milk liver glycogen was 3.7% versus 1.6% in controls. Our results document that glucagon decreases the degree of fatty liver in early lactation dairy cows, which also decreases the incidence of ketosis after alleviation of fatty liver.

The effect of narasin on apparent nitrogen digestibility and large intestine volatile fatty acid concentrations in finishing swine.

The effect of narasin on apparent nitrogen and dry matter digestibilities and large intestine VFA concentrations in finishing swine was investigated. The study used 21 crossbred barrows averaging 72 kg. Seven blocks were formed on the basis of pretreatment dry matter digestibility, and barrows were randomly assigned to three treatments in each block. Treatments consisted of a control (C) and narasin (N15 and N30) applied at 15 and 30 ppm, respectively. Fecal and urine samples were collected. Upon the completion of the digestibility work, intestinal samples were taken from three locations, and VFA concentrations for each animal were measured. Weight gains for the N15 and N30 treatments were increased 3.0 and 6.0% (not significant), respectively, over control. Fecal nitrogen was decreased (P < .05) in the narasin-fed barrows, and apparent nitrogen digestibility was increased (P < .05). Neither nitrogen retention nor urinary nitrogen excretion was altered (P > .05) due to narasin. There were no increases (P > .05) in apparent dry matter digestibility due to narasin. Analysis of pooled colon samples showed an increase (P < .05) in the concentration of propionic acid in relation to acetic and butyric in the narasin-fed barrows. Butyric acid was reduced (P < .05) in the transverse colon of narasin-fed barrows. In summary, narasin administration to finishing barrows resulted in improved apparent nitrogen digestibility, thus decreasing fecal nitrogen, and increased relative concentrations of propionic acid in the large intestine.

Through the looking glass: children's perceptions of growing up with cystic fibrosis.

This qualitative study used a grounded theory approach to explore the unfolding of the chronic illness experience for children during middle childhood. A purposive sample of 20 children (6-12 years) with cystic fibrosis (CF) were interviewed. Discovering a sense of difference was found to be the central phenomenon that described the experience of having CF during the middle childhood years. Four central themes emerged in the stories of these children: (a) puzzling out the diagnosis, (b) being teased and picked on, (c) telling others, and (d) keeping up. The study concluded that interventions must focus on the psychosocial demands made on children with CF along their course of development. By designing interventions around meaningful outcomes in their daily lives, we will help children with CF find ways to feel normal while adhering to treatment regimens, thereby helping to improve the quality of their lives.

Effect of exercise on postural sway in the elderly.

Fifty female subjects, aged 72-92 (mean 82) years, were enrolled in a 12-week (36 classes) exercise program aimed at increasing postural stability. Subjects were residents of sheltered apartments, rest homes or nursing homes, well enough and mobile enough to participate in the classes. The subjects were randomized into an exercise or a control group. Their postural sway, standing at rest on a force platform, was measured with eyes open and eyes closed. The groups were well matched in all respects. The results showed no improvement in the postural sway as a result of the exercise program. We hypothesize that increasing postural sway in the elderly represents a deterioration in, for the most part, the nervous system and may at this extreme of life indicate an irreversible loss of function. For this reason no improvement in postural sway may be possible.

Administration of monensin in self-fed (salt limiting) dry supplements or on an alternate-day feeding schedule.

Two series of trials were conducted to evaluate alternative methods of administering monensin to pasture cattle. In a series of five trials, monensin was incorporated into supplements at 440 mg/kg to provide an average intake of 200 mg X head-1 X d-1 for growing cattle on pasture. Comparisons were made between daily and alternate-day feeding of the supplements. A control treatment consisting of unmedicated supplement fed daily also was included. Monensin at 200 mg/d and 400 mg on alternate days increased gain by .077 (P less than .01) and .082 (P less than .01) kg/d above control-cattle gains (.54 kg daily). Nine pasture trials were conducted to compare the effectiveness of monensin in increasing the daily gain of growing cattle when hand-fed daily in a supplement or self-fed in supplements that contained salt to regulate supplement intake. Desired supplement intakes were approximately .454 kg X head-1 X d-1 in six trials, .68 kg/d in one trial and 1.81 kg/d in two trials. Monensin produced gain increases of .09 kg daily (P less than .01) with both feeding systems. The daily gains of cattle that were hand-fed and self-fed were equal (P greater than .10). Self-fed treatments containing monensin required fewer changes in salt level than self-fed treatments not containing monensin, and the salt levels required to limit intake were generally 25 to 50% lower when monensin was in the supplement.