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Biomedical subjects

C I Lin

Publications and source records attributed to C I Lin.

At least 73 records · Page 4Linked to original sources
PubMed1983

Role of calcium in the inotropic effects of caffeine in cardiac Purkinje fibers.

The inotropic effects of caffeine (1-3 mM) were studied in the presence and absence of strophanthidin in canine Purkinje fibers perfused in vitro. Caffeine (1 mM) induced a similar initial increase in contractile force in different calcium solutions (+22, +23 and +24% in 0.54, 2.7 and 8.1 mM calcium, respectively) and when propranolol (3.4 X 10(-6) M) was present. Also, caffeine increased contractile force in high potassium (16.2 mM) at a time when the slow action potentials were unaltered. After the increase, 1 mM caffeine decreased force by about 50%, and the decrease was larger when caffeine (3 mM) or [Ca]0 (8.1 mM) was higher. In the presence of caffeine, strophanthidin (3 X 10(-7)-1 X 10(-6) M) increased force (+302%) if caffeine (0.3 mM) and Ca concentrations (0.54 mM) were low. If either caffeine or calcium was increased, strophanthidin had no effect or decreased force. Strophanthidin alone increased force and then decreased it; caffeine increased force in the first stage and decreased it during the second stage. The positive inotropic effect (+224%) of low sodium (78.4 mM versus 149.4 mM in Tyrode solution) was also abolished by caffeine (-24%). In ventricular muscle fibers, caffeine increased force more (+59%) and reduced force less in the presence of strophanthidin. The results indicate that caffeine increases force initially by releasing calcium from intracellular stores. The caffeine-induced decline in force is modulated by calcium in that it is exaggerated by agents or procedures which increase cellular calcium (strophanthidin, high calcium, low sodium solutions) and is reversed in a low calcium solution.

Animals↗
PubMed1983

Calcium overload and strophanthidin-induced mechanical toxicity in cardiac Purkinje fibers.

In cardiac Purkinje fibers, strophanthidin increases and then decreases contractile force. The relationship between the decrease in force and calcium overload was studied by recording the electrical and mechanical activity under conditions known to increase calcium overload or its effects. Inhibitors of oxidative phosphorylation reduced the positive inotropy of strophanthidin and enhanced the decrease in force. These inhibitors also reduced the inotropic effect of high calcium. Increasing intracellular calcium by decreasing extracellular sodium concentration also resulted in a decrease in the strophanthidin inotropy. When arrhythmia was delayed, strophanthidin induced contracture and this was favored by blockers of glycolysis and by enhancing cellular calcium. Some of these effects were also observed in ventricular muscle fibers but at higher strophanthidin concentrations. The results suggest that the decline in contractile force during strophanthidin exposure is related to calcium overload, although it is made clear that in Purkinje fibers contractile force and resting force may be independently affected under suitable conditions.

Animals↗
PubMed1982

Synthesis of the proteins of complex III of the mitochondrial respiratory chain in heme-deficient cells.

The presence of several proteins of complex III of the respiratory chain has been demonstrated in mitochondria from a mutant of Saccharomyces cerevisiae lacking 5-aminolevulinic acid synthase and, hence, devoid of heme. The two 'core' proteins, apocytochrome b and the iron-sulfur protein, were observed in equal amounts in the heme-deficient and heme-sufficient cells with antiserum against complex III and the sensitive immuno-transfer technique. In addition, three other bands were detected with the complex III antiserum in the mitochondria from the cells lacking heme. One of these has a molecular weight similar to that reported for a precursor form of cytochrome c1. By contrast, when mitochondria from the heme-deficient cells were solubilized with mild detergents and treated with the complex III antiserum, almost no immunoprecipitation was obtained above that obtained with control serum. The presence of only one major labeled band with a molecular weight similar to subunit I was observed after gel electrophoresis. These results suggest that heme may be necessary for proper processing of the apoprotein of cytochrome c1 and for the assembly into the membrane of the subunits of complex III, rather than for the synthesis of the proteins.

Electron Transport Complex III↗
PubMed1982

Adrenergic receptors and increased reactivity of aortic smooth muscle in renal hypertensive rats.

The contractile responses of aortic smooth muscle and the dissociation constant (Ka) of the norepinephrine (NE) acting on alpha-adrenergic receptors in isolated thoracic aorta from normotensive and renal hypertensive rats were studied. Male Wistar rats were made hypertensive by uninephrectomy with figure-of-eight ligatures around the contralateral kidney. Two to three weeks after operation, the arterial systolic pressure for sham-operated rats was 123 +/- 2, and that for hypertensive rats was 164 +/- 4 mm Hg. Spontaneous rhythmic contractions of aortic rings, which were potentiated by low [Na]o and abolished by nifedipine (10(-6) - 10(-5) M), were observed in 4 out of 18 hypertensive rats. Aortic rings from normotensive rats showed no spontaneous rhythmicity. Although rhythmic phasic contractions could be induced in normotensive tissues by NE or caffeine in the presence of NE, tissues of hypertensive rats responded more readily. Furthermore, the threshold and the ED50 for tonic contractile response to NE was lower in hypertensive aortic rings than in the rings obtained from normotensive aortas. The Ka of NE acting on alpha-adrenergic receptors was derived from concentration-response data for NE before and after irreversible blockade of a fraction of the receptors with dibenamine (1-2 X 10(-7) M) in the presence of cocaine and propranolol. Mean Kas obtained were 5.58 +/- 0.42 X 10(-7) and 2.12 +/- 0.28 X 10(-7) M for normotensive and hypertensive rats, respectively. The increased contractile responses of the hypertensive aorta may be explained, at least partially, by a higher resting [Ca]i and a greater affinity of NE acting on the alpha-adrenergic receptors.

Acetylcholine↗
PubMed1981

Orientation of complex III in the yeast mitochondrial membrane: labeling with [125I] diazobenzenesulfonate and functional studies with the decyl analogue of coenzyme Q as substrate.

Mitochondria (or mitoplasts) and submitochondrial particles from yeast were treated with [125I] diazobenzenesulfonate to label selectively proteins exposed on the outer or inner surface of the inner mitochondrial membrane. Polyacrylamide gel analysis of the immunoprecipitates formed with antibodies against Complex III or cytochrome b revealed that the two core proteins and cytochrome b were labeled in both mitochondria and submitochondrial particles, suggesting that these proteins span the membrane. Cytochrome c1 and the iron sulfur protein were labeled in mitochondria but not in submitochondrial particles, suggesting that these proteins are exposed on the cytosolic side of the inner membrane. The steady-state reduction of cytochromes b and c1 was determined with succinate and the decyl analogue of coenzyme Q as substrates. Addition of the coenzyme Q analogue to mitochondria caused reduction of 15-30% of ;the total dithionite-reducible b and 100% of the cytochrome c1: Addition of the coenzyme Q analogue to submitochondrial particles led to the reduction of 70% of the total dithionite-reducible cytochrome b but insignificant amounts of cytochrome c1. A model to explain the topography of Complex III in the inner membrane is proposed based on these results.

Diazonium Compounds↗
PubMed1980

The antiarrhythmic effect of potassium and rubidium in strophanthidin toxicity.

The effect of potassium and rubidium on the electrical and mechanical activity of canine Purkinje fibers were studied in vitro in the presence and absence of strophanthidin. High (5.4mM) K or 2.7 Rb decreased the force of contraction. In the presence of these ions, strophanthidin increased the force of contraction as usual but the onset of arrhythmias was delayed. During the toxic stage of strophanthidin, high K or Rb increased the force of contraction, abolished the arrhythias and improved markedly the action potential. In the presence of calcium overload induced by exposure to a K-poor or Na-free solution, K and Rb induced an increase in force of contraction. And in ventricular muscle these ions relaxed the contracture induced by strophanthidin. It is concluded that K and Rb (in addition to other mechanisms) exert an antiarrhythmic action by increasing potassium conductance and by reducing the calcium overload induced by strophanthidin.

Animals↗
PubMed1979

Effect of calcium on strophanthidin-induced electrical and mechanical toxicity in cardiac Purkinje fibers.

The role of calcium in the electrical and mechanical toxicity induced by strophanthidin (10(-6) M) was studied in canine Purkinje fibers perfused in vitro. Strophanthidin caused an increase in contractile force ("therapeutic effect") followed by a subsequent decrease and by the onset of arrhythmias ("toxic effects"). The onset of arrhythmias occurred sooner in low- and later in high-calcium solutions with respect to the normal calcium. The positive inotropic (therapeutic) effect of strophanthidin was reduced or prevented by caffeine (1 mM) or by high calcium. The late (toxic) decline in force during exposure to strophanthidin was temporarily reversed by decreasing [Ca]o to a low value. Similarly, the contractile force decreased when [Ca]o was increased from 8.1 to 16.2 mM and this decline was transiently reversed when [Ca]o was reduced to a low value. It is concluded that in Purkinje fibers 1) electrical toxicity may occur independently of an intracellular calcium accumulation, and 2) the mechanical toxicity may be due to an excessive accumulation of calcium in the fiber.

Animals↗
PubMed1979

Sodium lack prevents strophanthidin toxicity in Purkinje fibers.

The effect of strophanthidin on electrical and mechanical activity of canine cardiac Purkinje fibers perfused in vitro was tested in the presence and in the absence of sodium. The following results were obtained: (1) in Tyrode's solution, strophanthidin causes spontaneous fast rhythms; (2) perfusion of a tetraethylammonium (TEA) Na-free solution results in an initial slowing and quiescence followed by the development of spontaneous small potentials; (3) exposure to strophanthidin during the perfusion of the Na-free solution fails to induce an acceleration of spontaneous discharge; (4) on returning from Na-free to Tyrode's solution there is a temporary acceleration of the small potentials and this acceleration is larger and lasts longer when the Na-free solution contains strophanthidin, and (5) in fibers intoxicated with strophanthidin, exposure to Na-free solution stops the fast rhythms. It is concluded that sodium plays an important role in strophanthidin toxicity and no toxicity occurs when sodium is replaced by TEA.

Action Potentials↗
PubMed1978

A system for studying effects of microwaves on cells in culture.

An improved design of the fluid-filled waveguide-exposure chamber is described for studying effects of microwave radiation on cells in vitro. The system with a micropipette sample holder may be used as a prototype to isolate the apparent nonthermal factor of microwave radiation on cells in culture from those effects resulting from cell temperature rise. This system also allows more precise calibration of incident and absorbed microwave energies. Compared with control, somatic cells of the Chinese hamster exhibited a lower rate of growth and difference in morphology after 2450 MHz microwave radiation for 20 min at a power density of 500 mW/cm2.

Animals↗
PubMed1978

Role of sodium in strophanthidin toxicity of Purkinje fibers.

The action of strophanthidin on the membrane potentials and contractile force of canine Purkinje fibers was studied in vitro. Purkinje fibers were exposed to strophanthidin (10(-6) M) until spontaneous fast discharge occurred. In Tyrode solution, strophanthidin increased and subsequently decreased ("mechanical toxicity") contractile force. The onset of spontaneous rhythms ("electrical toxicity") usually occurred when force was declining. In low-Na Tyrode (-71 mM NaCl), force increased: on exposure to strophanthidin, mechanical toxicity occurred sooner and electrical toxicity later. In low-Na low-Ca Tyrode, electrical toxicity developed sooner than in low-Na Tyrode. In high-Na Tyrode (+27 mM NaCl), force increased, and the time to electrical and mechanical toxicities was decreased. Increasing osmolarity (+54 mosM) with either sucrose or choline chloride increased force and shortened the time to the onset of strophanthidin toxicities. In the presence of arrhythmias, lowering [Na]o decreased transient oscillations and led to disappearance of arrhythmias. It is concluded that Na plays a role in strophanthidin-induced electrical toxicity, whereas Ca appears more important for mechanical toxicity.

Action Potentials↗
PubMed1977

Heparin neutralizing activity and coronary artery disease.

It has been previously shown and confirmed in the present investigation that the disaggregation of adenosine diphosphate (ADP)-induced platelet aggregates occurs at a slow rate more frequently in the platelet-rich plasma (PRP) of men with coronary artery disease. ADP-induced platelet aggregation was studied in the citrated PRP of 32 men (21 with and 11 without coronary artery disease) to determine the relation between release of heparin neutralizing activity (HNA) from platelets and the rate of platelet diaggregation. Each of the five PRP with slow (less than 10 per cent) disaggregation were from men with coronary artery disease. Platelets from these five PRP released from 34 to 51 per cent of their content of HNA during ADP-induced aggregation in contrast to the 27 PRP with more rapid disaggregation, only three of which had a detectable release of HNA. Of the latter 27 PRP, 21 had a second phase of aggregation which usually reached a peak of light transmission less than that of the first phase. These data are consistent with (but do not prove) the hypothesis that HNA released during aggreation may be one of the factors tending to prevent disaggregation of ADP-induced platelet aggregates.

Adenosine Diphosphate↗