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Biomedical subjects

M Johnson

Publications and source records attributed to M Johnson.

At least 829 records · Page 46Linked to original sources
PubMed1975

Failure to confirm a vascular cause of muscular dystrophy.

The vascular hypothesis of the cause of muscular dystrophy suggests that ischemia is responsible for the muscle fiber necrosis. A xenon 133 clearance study of muscle blood flow in Duchenne and other muscular dystrophies showed no obvious difference between the response to exercise and arterial occlusion compared with control subjects. Radioautographic study of distribution of 4-125l-antipyrine in skeletal muscle of mice with muscular dystrophy showed no abnormal areas of ischemia. A statistical examination was also made of the grouping of damaged fibers, one of the observations on which the vascular hypothesis was based. Only 0.9% of fibers undergoing phagocytosis occurred in groups of four or more fibers in greater frequency than would have been expected by chance, and 70% of such fibers were isolated. These studies argue strongly against the vascular hypothesis of the cause of muscular dystrophy.

Adult↗
PubMed1975

Energized endocytosis in human erythrocyte ghosts.

The mechanism of endocytosis in resealed human erythrocyte ghosts was studied. The energy for endocytosis or micropinocytosis appears to be derived from Mg-ATP, and membrane internalization is preceded by activation of a membrane-associated Ca,Mg-ATPase and by the active efflux of Ca. Endocytosis, Ca,Mg-ATPase activity, and active Ca efflux all require the presence of Mg. Furthermore, these three phenomena, endocytosis, Ca,Mg-ATPase activity, and active Ca extrusion, all have a concentration dependence on Ca such that low concentrations stimulate and higher concentrations inhibit the phenomena. The optimal concentration of Ca is identical for endocytosis, active Ca efflux, and Ca,Mg-ATPase. Morphologic studies indicated that while active Ca efflux and activation of the Ca,Mg-ATPase activity occurred promptly upon onset of incubation, there was a significant time delay before endocytosis occurred, which suggests that endocytosis additionally involved a more slowly functioning mechanicochemical mechanism. Ruthenium red, a specific inhibitor of Ca,Mg-ATPase and Ca transport, inhibited endocytosis in a concentration-related manner. Prostaglandins E1 and E2 had no measurable effect on ghost endocytosis, active Ca efflux, or Ca,Mg-ATPase activity.

Adenosine Triphosphatases↗
PubMed1975

Cardiovascular and platelet responses in the dog to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid.

The monoenoic prostaglandin precursor, dihomo-gamma-linolenic acid (DGLA), in a single dose intravenously (2.0 mg/kg) in dogs, produced a biphasic alteration in systemic arterial pressure (SAP) with a predominant and marked depressor effect. This SAP response is approximately equidepre-sor to the effect of PGE1 5 mug/kg. DGLA had a positive inotropic effect, causing a greater increase in myocardial contractility than PGE1 in an equidepressor dose. The effect of DGLA on MC was not altered by ganglion blockade or beta-adrenergic blockade. Aspirin blocked the sustained depressor response to DGLA but not an initial drop in SAP and increase of MC of very short duration. Aspirin had no effect on PGE1 or PGF1 alpha responses. DGLA caused no thrombocytopenia, but caused a decrease in sensitivity to platelet aggregation. Control fatty acid injections produced variable effects with no resemblances to DGLA responses. It is concluded that DGLA produces direct depressor and positive inotropic responses as well as responses which may be due to conversion to an endoperoxide formed in the biosynthesis of prostaglandins. In contrast, in equidepressor doses, arachidonic acid (AA), the bisenoic prostaglandin precursor, produces a delayed, single-phase depressor effect which may be due to endoperoxide formation alone. Further, the effect of AA on MC is reflex and is blocked by hexamethonium.

8,11,14-Eicosatrienoic Acid↗
PubMed1975

Effects of ganglionic and beta-adrenergic blockade on cardiovascular responses to the bisenoic prostaglandins and their precursor arachidonic acid.

Arachidonic acid (AA) 300 mug/kg, and PGE2, 5 mug/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF2alpha, 5 mug/kg, produced a pressor response. All three compounds increased myocardial contractile force, but the magnitude of the change following AA was less prominent. After ganglionic blockade, the depressor response to AA and PGE2 persisted and the pressor response to PGF2alpha was augmented. Myocardial contractile force did not increase following AA in ganglion-blocked animals indicating that the cardiac responses observed before hexamethonium were mediated by the baroreceptor reflexes. A much larger dose of AA (900 mug/kg) resulted in a small positive inotropic effect on the heart. This possibly represents a direct cardiac effect of AA, or may be indicative of increased biosynthesis of an intermediate endoperoxide, or PGE2 and PGF2alpha. Both PGE2 and PGF2alpha have a direct positive inotropic effect on the heart. The persist cardiac effects of PGE2 and PGF2 after beta-adrenergic blockade suggests that these compounds may not interact with the beta-receptors of the myocardium.

Adrenergic beta-Antagonists↗
PubMed1975

The effect of arterial PO2 on relative retinal blood flow in monkeys.

The relationship of blood oxygenation to retinal blood flow has been studies in rhesus monkeys. Constriction of major retinal arteries and veins during hyperoxia and dilation during hypoxia are demonstrated. Together with mean circulation times based on the technique of fluorescein densitometry curves, these data allow an estimation of retinal blood flow, which increases considerably in hypoxia and shows a moderate decrease in hyperoxia. These findings indicate that the retinal circulation parallels that of the brain in adjusting to changes in arterial PO2 with compensatory changes in blood flow.

Animals↗