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Biomedical subjects

J B Harris

Publications and source records attributed to J B Harris.

At least 127 records · Page 7Linked to original sources
PubMed1976

Emetine myopathy in the rat.

1 (-)Emetine (0.25-2.0 mg/kg i.p.) was administered to rats for up to 220 days. 2 At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small reduction in both the resting membrane potential and in the maximum rate of rise of the action potential. There was no atrophy or loss of muscle fibres although in the occasional muscle, hyaline fibres, necrotic fibres and split fibres were observed. There was a focal loss of myofibrillar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) in Type II and Type III fibres, but no such loss in Type I fibres. 3 The animals receiving 2.0 mg/kg of (-)emetine gained weight slowly for up to 20 days but then rapidly lost weight and by 30 days they were weak and emaciated. The muscles from these animals were severly atrophied and the total muscle wet weight was reduced by almost 20%. 4 The strength of the muscles from these animals was measured in vitro using direct stimulation. They were weaker than normal both in absolute terms and when expressed in terms of tension developed/unit wet weight. 5 There was no evidence of either functional or structural denervation but surgically denervated muscles from animals in this group were indistinguishable from denervated muscles from normal rats. 6 Severe structural damage was obvious in the fibres of both extensor digitorum longus and soleus. Necrotic, hyaline and splitting fibres were common and the focal loss of myofibrillar ATPase and NADH-TR activity was extensive and occurred in Type I fibres as well as in Type II and Type II fibres. 7 It is concluded that the muscular weakness induced by (-)-emetine is due to a direct effect on the muscle fibres and that this occurs at a subcellular level. There is no evidence that functional or structural denervation plays any role in the aetiology of emetine myopathy in the rat.

Animals↗
PubMed1976

Role of oxalacetate in lipoate effect on frog gastric mucosa.

The mechanism of action of lipoate on frog gastric mucosa was investigated. Oxalacetate (OAA) reversed lipoate-inhibited QO2 and QH+ of chambered mucosas by 70 and 40%, respectively. Pyruvate or glucose produced similar effects. Neither activity was affected by OAA when added after glucose, pyruvate, decanoate, butyrate, or lipoate-propionate-inhibited mucosa. Lipoate-treated or lipoate-propionate-treated mucosa did not respond to histamine; OAA addition prior to histamine restored responsiveness. Tracer and chromatographic techniques showed that lipoate reduced and pyruvate increased OAA formation. Preincubation of mitochondrial extracts of gastric mucosa with 2 mM lipoate increased pyruvic dehydrogenase activity 110%. Pyruvic carboxylase (PC) activity was primarily in the mitochondrial fraction of the gastric mucosa. The PC preparation was shown to have an absolute requirement for CoASAc, contained biotin, was not inhibited by lipoate, and had an apparent Km approximately equal to 3.6 X 10(-4) M for pyruvate. The results suggest that OAA concentration is regulated by PC activity and is one of the factors controlling QO2 and QH+ in the frog gastric mucosa.

Animals↗
PubMed1975

An electrophysiological and morphological study of normal and denervated chicken latissimus dorsi muscles.

1. Some electrophysiological and morphological properties of 'fast' (singly innervated) and 'slow' (multiply innervated) muscle fibres were studied in normal and denervated posterior and anterior latissimus dorsi muscles of the young chickens. 2. Normal singly and multiply innervated muscle fibres are capable of generating action potentials which in all qualitative respects are similar. 3. The action potentials of multiply innervated muscle fibres are of lower amplitude and slower maximum rate of rise than action potentials in singly innervated muscle fibres. 4. Denervation causes the resting membrane potential and the maximum rate of rise of the action potential to fall. The changes are greater in singly innervated than in multiply innervated fibres, but in neither case are as great as in mammalian skeletal muscle fibres after surgical denervation. 5. In neither singly nor multiply innervated muscle fibres do the action potentials generate any 'resistance' to tetrodotoxin as a result of denervation. 6. The diameter of multiply innervated fibres is increased after denervation, but it is reduced in singly innervated fibres. The number of myofilaments increases in multiply innervated fibres, but decreases in single innervated fibres. In both types of muscle fibre the volume fraction of myofibrils is decreased. 7. In the singly innervated muscle fibres there is an increase in the volume fraction of mitochondria. 8. In the singly innervated muscle fibres, there is some rearrangement of the membrane systems in that some of the transversely orientated triads are replaced by longitudinally orientated dyads.

Action Potentials↗
PubMed1975

Lipoate effect on carbohydrate and lipid metabolism and gastric H+ secretion.

Acid secretion (QH+) and oxygen consumption (Qo2) by frog gastric mucosae in vitro were sharply stimulated by lipoate. A rapid decline followed stimulation, subsequently falling below control values. Addition of only glucose or lactate had no effect on Qo2 or QH+. Pyruvate caused slight significant stimulation of Qo2. Any one of these compounds added to lipoate-treated mucosae increased the stimulatory effect of lipoate and markedly slowed the rate of decline subsequent to maximum stimulation. Various fatty acids had a moderate-to-high stimulatory effect on Qo2 and QH+. Lipoate added prior to the addition of fatty acids decreased the stimulatory effect of buryrate (minus 56%), decanoate (minus 87%), and palmitate (minus 60%). Propionate became an inhibitor in the presence of lipoate. Lipoate increased (plus 100%) the amount of glycogen oxidized and decreased (minus 69%) the amount of triglycerides oxidized. Lipoate-treated mucosae did not respond to histamine. Addition of glucose restored responsiveness. The results indicate that beta-oxidation of fatty acids plays a major role in the acid secretory process and is centrally involved in cyclic AMP and histamine stimulation of QH+.

Animals↗