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Biomedical subjects

M S Hudecki

Publications and source records attributed to M S Hudecki.

33 records · Page 2Linked to original sources
PubMed1984

In vivo effects of three calcium blockers on chickens with inherited muscular dystrophy.

Genetically homozygous Line 413 dystrophic chickens were given in separate trials daily i.p. injections of aqueous solutions of the calcium blocker drugs, diltiazem, verapamil, or nifedipine. At a dosage of 20 mg/kg/day, drug therapy in each case significantly prolonged the functional ability of the dystrophic chickens as quantitated regularly by a standardized test for righting ability. Enhanced functional ability, however, was not generally accompanied by a decrease in the usually high plasma creatine kinase activity. In addition, there was no change in the pectoralis muscle mass or protein with any of the drug treatments. Moreover, no significant reduction in the abnormally high total muscle calcium was found with calcium blocker treatment. Also, there was no marked change in the histopathology of muscle from the drug-treated dystrophic chickens. We concluded that drugs with calcium entry blocker activity offer only limited benefit in retarding dystrophic symptoms expressed in the chicken (viz., short-term enhancement in righting ability).

Animals↗
PubMed1983

Limited benefit to genetically dystrophic chickens from a synthetic proteinase inhibitor: Ep475.

Chickens with inherited muscular dystrophy (Line 413) were treated in two separate trials with daily intraperitoneal injections of 10% DMSO-water solutions containing the proteinase inhibitors, Ep475 and E64. Drug therapy in each case significantly prolonged the functional ability of the treated chickens. Diluent control chickens around day 35 ex ovo characteristically reached a maximum ability to right from the supine position in a standardized functional test for muscle weakness. Subsequently, the control chickens were found to decline progressively in their ability to right. Treatment with the proteinase inhibitors had no effect on the typically elevated levels of plasma creatine kinase activity. In a histological analysis of the affected pectoralis major muscle, drug treatment had no effect on the relative distribution of degenerating, and vacuolated fibers, inflammatory cells, and abnormal fiber diameters. An exception was seen in decreased necrotic fibers of chickens treated with high doses of Ep475. Moreover, both inhibitors had positive effects on two biochemical abnormalities common to the dystrophic pectoralis muscle: increase in noncollagen protein, and reduction in total calcium.

Animals↗
PubMed1981

In vivo effects of protease inhibitors on chickens with hereditary muscular dystrophy.

Beginning on day 4 ex ovo, and every 3 d thereafter, genetically dystrophic Line 413 chickens were given intraperitoneal injections (4 mg/kg body wt) of a protease inhibitor, leupeptin, pepstatin, or antipain. Experimental chickens received protease inhibitors dissolved in a water:ethanol:dimethyl sulfoxide solution (50:40:10, vol:vol:vol). Control untreated animals received diluent injections. Untreated dystrophic chickens typically reach around day 30 ex ovo a maximum ability to right from the supine position in a standardized functional test for muscle weakness. After day 30 ex ovo, the dystrophic chickens are found to decline progressively in their ability to right, compared with normal, nondystrophic controls, which have an unimpaired ability to right. Concomitantly, dystrophic chickens exhibit characteristically high levels of plasma creatine phosphokinase enzyme activity. In addition, an increased frequency of degenerating, regenerating, and vacuolated myofibers, and inflammatory cells appear in the affected pectoralis major muscles from the dystrophic chicken. Throughout the duration of the trial, there was no major enhancement in the functional righting ability of dystrophic chickens receiving any one of the protease inhibitors tested. However, there was a significant reduction in the abnormally high levels of plasma creatine phosphokinase in the treated chickens. Also, there was an apparent reduction in the mean number of vacuolated fibers in the pectoralis muscle from the protease inhibitor-treated birds. No significant reductions were observed in the relative frequency of degenerating and regenerating myofibers or inflammatory cells. In addition to the plasma creatine phosphokinase decrease, however, therapeutic benefit was seen in 31.0, 30.5, and 14.8% increases in the wet weight (and total noncollagen protein) of pectoralis muscle from dystrophic chickens receiving leupeptin, pepstatin or antipain, respectively.

Animals↗
PubMed1980

Screening of antiserotoninergic drugs with the genetically dystrophic chicken.

Line 413 early-onset, genetically homozygous dystrophic chickens were given twice-daily intraperitoneal injections of the antiserotoninergic drugs p-chlorophenylalanine hydrochloride, fluoxetine hydrochloride, ergonovine maleate, nortriptyline hydrochloride, methiothepin maleate, and methysergide bimaleate in combination with penicillamine. Except in one case, treatment with drugs significantly prolonged the righting ability of the treated dystrophic chickens, as measured by a periodic standardized flip-test procedure. Abnormally high levels of plasma creatine phosphokinase, lactate dehydrogenase, and SGOT were found in the untreated dystrophic chickens. However, of the drug-treated dystrophic chickens, in some cases the plasma enzyme activities were reduced whereas in others they were enhanced. In agreement with previous findings, the blood serotonin levels of the dystrophic chickens were found at all age groups to be significantly higher than those in the corresponding normal chickens. This phenomenon may in part account for the improvement in righting ability demonstrated in the dystrophic chickens receiving treatment with antiserotoninergic drugs.

Animals↗
PubMed1976

Erythrocyte surface membrane alterations.

Electrophoretic mobility measurements were made of red blood cells obtained from patients with Duchenne and myotonic muscular dystrophy, from dystrophic mice and chickens, and from corresponding controls. Alterations in the erythrocyte surface electrokinetic properties were found in dystrophic mice and chickens and in many, but not all, patients with muscular dystrophy. The results are consistent with the concept of muscular dystrophy as a systemic membrane disease not limited to muscle.

Adolescent↗
PubMed1976

Retardation of symptoms of dystrophy in genetically dystrophic chickens by chemotherapy.

Chickens homozygous for muscular dystrophy were treated twice-daily with the serotonin antagonist, methysergide. Development of the dystrophic state was monitored by a test of skeletal muscle weakness, and by the characteristic marked evaluation of creatine phosphokinase (CPK) in the serum. The drug treatment prevented the onset of muscle weakness for 45 days ex ovo in all of the test animals, and for more than 60 days in 80% of them, in contrast to the untreated dystrophic animals. The CPK elevation in serum was also markedly reduced in the treated animals. A serotonin-mediated vascular effect or a direct action of serotonin on the muscle, is suggested to be involved in the development of muscle weakness in this form of dystrophy, and to be an appropriate target for chemotherapeutic control.

Aging↗
PubMedDate not supplied

Delayed functional disability in dystrophic chickens receiving chemotherapy.

Line 413 early-onset, genetically homozygous dystrophic chickens were given twice-daily intraperitoneal injections of the antiserotoninergic drug cinanserin, alone or in combination with methysergide. Other trials consisted of penicillamine treatment in combination with either methysergide or cyproheptadine. Chemotherapy significantly prolonged the righting ability of treated dystrophic chickens, as measured by a periodic standardized flip-test procedure. Plasma creatine kinase activities were not affected by any of the various drug treatments. However, the blood serotonin levels of the dystrophic chickens (grand mean 1.47 microgram serotonin/ml blood) were found to be significantly higher (p less than 0.001) than those in the corresponding normal chickens (0.99 microgram/ml). This finding may partially account for the antiserotoninergic drug enhancement in righting ability that was demonstrated in the drug-treated dystrophic chickens.

Animals↗
PubMedDate not supplied

Parenteral branched-chain amino acid treatment and avian dystrophy.

Genetically homozygous line 413 dystrophic chickens were given twice-daily intraperitoneal injections of solutions containing branched-chain amino acids (BCCA-leucine, valine, isoleucine) either alone or in combination; and their alpha-ketoacid analogs (alpha-ketoisocaproic and alpha-ketoisovaleric acids). Another trial consisted of an amino acid mixture containing BCAA. Amino acid supplementation in each case significantly prolonged righting ability measured regularly by a standardized flip-test procedure. Enhanced functional ability was not generally accompanied by a decrease in plasma creatine kinase activity. However, a measurable increase in the affected pectoralis major muscle mass and protein content (female chickens in particular) was found with BCAA therapy. Moreover, the increase in muscle bulk was attended in some cases by a reduction in the relative number of degenerating fibers quantitated microscopically. Contrariwise, the amino acid mixture caused a reduction in pectoralis muscle mass. It is concluded that parenteral BCAA therapy offers limited benefit in retarding dystrophic symptoms in the chickens.

Amino Acids↗