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Results for “PECTORALIS MUSCLES”

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At least 1,405 records · Page 78Linked to original sources
PubMed1978

Characterization of glycogen in selected tissues of turkey poults with spontaneous round heart disease and furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults 2--5 weeks after hatching to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. From EKG data obtained at weekly intervals, poults were selected for sacrifice at 5 and 10 weeks of age. Poults were sacrificed by cervical dislocation and appropriate samples of tissue from the left ventricle, liver, pectoralis and tibialis cranialis muscles were removed for glycogen assays. Character of glycogen, as determined by percent of branching and number of glucose units per segment, was not significantly altered in poults with spontaneous round heart disease or FZ-induced cardiomyopathy. This suggests that the glycogen accumulation noted in these conditions most closely resembles type II glycogenosis.

Animals↗
PubMed1981

Inhibition of programmable demand pacemaker by pacemaker-induced myopotentials.

Pacemaker-induced myopotentials caused inhibition of a demand pacemaker in two cases in which the unipolar partially encapsulated pacemaker flipped over in its pocket and directly stimulated the muscles of the chest wall. This pacemaker-induced muscular stimulation, possibly combined with afterpotential sensing or T-wave sensing (or both), caused the rate of the demand pacemaker to fall when the output of the programmable pacemaker was set to deliver high energy charges. By programming the unit to deliver a lower charge (shorter width of pulse), the rate rose appropriately to the programmed rate. Likewise, manual rotation of the unipolar pacemaker into proper orientation with the active uninsulated surface directed towards the skin also solved the problem temporarily.

Aged↗
PubMed2000

Eimeria acervulina infection elevates plasma and muscle 3-methylhistidine levels in chickens.

To assess muscle breakdown during avian coccidiosis, the level of the nonmetabolizable amino acid 3-methylhistidine (3MH) was determined in muscle, plasma and excreta from chickens infected with Eimeria acervulina. The changes in 3MH levels during infection were assessed at 1-29 days postinoculation (DPI) in animals given 5 x 10(5) oocysts per bird. The effect of levels of parasitism were evaluated at 8 DPI in birds receiving 5 x 10(3), 5 x 10(4), 5 x 10(5) or 1 x 10(6) oocysts each. The 3MH levels of plasma, muscle, and excreta samples were determined by high-pressure liquid chromatography after derivatization with fluorescamine. Weight gains, breast muscle weight, eviscerated weight, plasma carotenoid levels, dry weight of muscle, and gross lesion scores were also determined. Infected birds had significantly elevated plasma and muscle 3MH at 4 and 8 DPI following a single dose of E. acervulina. The increase in 3MH levels had an inverse relationship with the time course of weight gain and plasma carotenoid levels. Plasma and muscle 3MH levels returned to control values by 15 DPI and remained unchanged from control values through the remainder of the experiment (29 DPI). Breast weight was decreased in infected birds, but the ratio of breast weight to eviscerated body weight was unchanged. Excretion of 3MH decreased relative to controls at 4 and 8 DPI and returned to control levels on 15 DPI. The plasma and muscle levels of 3MH were related to severity of infection; however, levels of excreted 3MH were not. The results suggested that muscle breakdown, as assessed by plasma and muscle levels of 3MH, increased during the acute stage of E. acervulina infection. The underlying causes for this muscle breakdown was unclear but could involve a physiological response to anorexia and decreased food intake during the acute phase of infection. Levels of excreted 3MH did not increase during infection and this may be the result of decreased excreta output during infection. Plasma and muscle levels of 3MH were correlated with severity of E. acervulina infections but may not be as sensitive an indicator of infection as plasma carotenoid levels or other physiological parameters.

Animals↗
PubMed1984

Spontaneous rotation of permanent pacemaker--a cause of muscle stimulation and myopotential inhibition.

In 5 of 192 patients who received their first pacemaker during a 17-month period, severe pectoral muscle stimulation was caused by spontaneous rotation of the pacemaker in the pocket, so that the uncoated side faced backwards. All five patients were women with abundant, loose subcutaneous tissue which allowed increased mobility of the pacemaker. This causal mechanism of muscle stimulation seems to be related to the reduced size and the coating of modern pacemakers. Reprogramming of the pacemaker to a lower output solved the problem in three cases, but reoperation was necessary in two. These cases stress the need to secure the pacemaker to the fascia during implantation, particularly in patients at enhanced risk. For such patients, use of a pacemaker equipped with suture holes may be advisable.

Aged↗
PubMed1975

Effect of arginine deficiency on normal and dystrophic chickens.

Normal and genetically dystrophic chickens were fed diets deficient in arginine or further aggravated by the addition of lysine. Growth of dystrophic chicks is depressed less by a deficiency of arginine than that of normal chicks. Muscular ability of dystrophic chicks was improved by feeding them an arginine deficient diet but this effect may be related to the size of the bird. The total creatinine content of the pectoral muscle of dystrophic chicks was reduced more with a deficiency of arginine than was that of normal chickens.

Amino Acids↗
PubMedDate not supplied

Reduction of pacemaker-induced pectoral muscle stimulation using an insulating patch.

An 82-year-old female patient was admitted for replacement of her pulse generator battery which had reached an end-of-life situation. The old unipolar leads were retained. Pectoral muscle stimulation began shortly after implantation. Though complete abolition of muscle stimulation was not achieved, an insulating patch placed between the muscle and the pacemaker can reduced stimulation.

Aged↗
PubMed1976

Interference with function of unipolar pacemaker due to muscle potentials.

One hundred and seventy-three unipolar pulse generator systems were tested in 169 patients to determine the incidence of sensing of muscle potentials. One hundred and twenty-two implants in the pectoral region were suitable for assessment and 60 (49 per cent) demonstrated sensing. Ventricular-inhibited units sensed muscle potentials in 69 per cent (47 of 78), with 9 patients complaining of related symptoms. Ventricular-synchronous units sensed in 30 per cent (13 of 34) with no patient manifesting symptoms.

Action Potentials↗