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Biomedical subjects

A Wilde

Publications and source records attributed to A Wilde.

53 records · Page 3Linked to original sources
PubMed1984

Combined effects of hypoxia, hyperkalemia and acidosis on membrane action potential and excitability of guinea-pig ventricular muscle.

The effects of hypoxia (with and without acidosis) on membrane action potentials and recovery kinetics of their upstroke velocity (Vmax) were studied in isolated guinea-pig papillary muscles at various extracellular K+ concentrations. At 5 mM [K+]0, hypoxia (hypoxic and glucose-free perfusate) at pH 7.4 caused a progressive shortening of action potential duration and a slight decrease in Vmax and resting potential. The recovery kinetics of Vmax assessed by premature stimuli were not affected by hypoxia. At high [K+]0 of 10 or 12 mM, hypoxia caused a marked decrease in Vmax, while the shortening of the action potential and the decrease in resting potential were similar to those at 5 mM [K+]0. However, the recovery kinetics of Vmax were markedly slowed by hypoxia. When hypoxia was added in the presence of mild acidosis (pH 6.8), the shortening of the action potential due to hypoxia was appreciably less. However, other hypoxia-induced changes in action potential and in recovery kinetics of Vmax under normal and high [K+]0 were not influenced by the concomitant acidosis. These results show that the depressant effect of hypoxia on the action potential upstroke and on the recovery of excitability of ventricular myocardium is increased when the muscles are partly depolarized at high K+. Slight differences in extracellular K+ in the presence of hypoxia have a marked effect on the time course of recovery of excitability. This inhomogeneity in refractoriness could be important for the occurrence of re-entrant arrhythmias in ischemic myocardium.

Acidosis↗
PubMed1984

Structural and functional characterization of Newcastle disease virus polycistronic RNA species.

Upon infection, the Newcastle disease virus (NDV) genome is transcribed to produce 18S, 22S, and 35S RNAs (M. Bratt , and W. Robinson, J. Mol. Biol. 23:1-21, 1967). The 22S RNA has been shown to contain 18S sequences and is thought to represent polycistronic transcripts generated by transcriptional readthrough of adjacent genes ( Varich et al., Acta Virol. 23:341-343, 1979). With improved extraction procedures, the 22S RNA was found to represent up to 25% of the total transcription in NDV-infected cells. This RNA was resolved into at least five discrete species on formaldehyde-agarose gels. All but one of these molecules contain 3' polyadenylate sequences but not internal polyadenylate sequences. These transcripts are found on polyribosomes of infected cells, suggesting that they are functional mRNAs.

Animals↗
PubMed1975

[Influence of spontaneous collaterals on the fibrillation threshold of the heart following acute coronary occlusion].

Fibrillation threshold (FS) were determined in 27 mongrel dogs by direct electrical stimulation of the myocardium by 50 Hz AC impulses of 0.20-0.28 sec during the vulnerable period. The FS is the current which just suffices to produce ventricular fibrillation. Sinus rhythm was restored 10 sec after onset of ventricular fibrillation by defibrillation. Determinations of FS were carried out for each animal repeatedly before and 3 min after acute ligation of the circumflex ramus respectively the descendens ramus of the left coronary artery. Post mortem selective coronary angiography was performed in all cases and the extent of spontaneous collateral vessels was estimated by the rate of retrograde contrast radiography of the ligated coronary artery. The FS fell appreciably following acute ligation of both the circumflex ramus and the sescendens ramus. Beside the size of the ligated area (the circumflex ramus supplies a larger area of the myocardium in the dog than the ramus descendens) the extent of collateral supply was the determining factor for the reductions of the FS: Following coronary ligation of the circumflex ramus the FS fell on the average from 24.0 mA to 4.1 mA if no collateral vessels were detectable; in the animals with well developed collaterals the FS was reduced from 24.8 to only 14.1 mA. After acute occlusion of the descendens ramus the FS fell from 27.9 mA to 11.5 mA in the group with not sufficient collateral supply and from 31.2 mA to only 21.5 mA in the group with well developed collaterals. The comparison of the different decreases of the FS after coronary occlusion clearly shows that the influence of the in size differing ischemic areas on the decrease of the FS is particularly evident if no collateral vessels are existent. If collateral vessels are well developed this difference is not significant. These results demonstrate that the influence of well developed collaterals on the decrease of the FS after coronary occlusion exceeds the dependence on the size of the ischemic area.

Acute Disease↗