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Biomedical subjects

S Guerrero

Publications and source records attributed to S Guerrero.

At least 37 records · Page 2Linked to original sources
PubMed1987

Electrophysiological characteristics of cardiac pacemaker cells of the frog Caudiverbera caudiverbera.

1. The cardiac pacemaker cells of the frog Caudiverbera caudiverbera are centrally located in the sinus venosus. These cells are rounded, smaller than contractile fibres and have large nuclei. 2. Intracellular recording confirmed the existence of primary and transitional pacemaker cells. 3. Action potentials from primary cells were resistant to blockade by tetrodotoxin (TTX), but were abolished by verapamil suggesting that their bioelectric activity is dependent on a slow inward current. 4. Transitional cells appeared to have two different inward currents contributing to the upstroke: a fast TTX-sensitive and a slow verapamil-sensitive current.

Action Potentials↗
PubMed1987

Electrophysiological effects of bupivacaine on transitional pacemaker cells of the frog heart.

The effects of bupivacaine, a long-acting local anesthetic, were studied on action potentials of spontaneously beating sinus venosus of the frog Caudiverbera caudiverbera. The study was accomplished by recording transmembrane potentials of pacemaker transitional cells. Action potentials of these cells are known to have both a fast and a slow ionic component. Bupivacaine (1 X 10(-5) M to 1 X 10(-4) M) caused a reversible negative chronotropic effect accompanied by decrease of diastolic depolarization rate and prolongation of sinus cycle length. This drug also markedly depressed rate of rise [(dV/dt)max] of action potentials. Tetrodotoxin (TTX) (1 X 10(-7) M) induced similar effects than bupivacaine. In atropine-treated sinus venosus the effect of bupivacaine on spontaneous rate of firing was less intense. However, in cells exposed to both drugs, a greater depression of (dV/dt)max and of other electrophysiological parameters such as action potential amplitude, overshoot and maximum diastolic potentials was observed. Depression of phase 4 depolarization seems difficult to be explained in view of the complex nature of the ionic currents underlying pacemaker depolarization. Reduction of (dV/dt)max caused by bupivacaine and mimicked by TTX was ascribed to blockade of sodium channels. It was concluded that bupivacaine by decreasing (dV/dt)max of transitional cells and by depressing diastolic depolarization slows down conduction of impulses arising from primary cells and that this action may contribute to its cardiac toxicity.

Action Potentials↗
PubMed1986

The effect of 4-aminoquinoline on frog atrial myocardium depolarized by potassium.

Intracellular recording was used to examine the effects of 4-aminoquinoline (4-AQ) on action potentials of frog atrial myocardium depolarized by potassium. Elevating [K+]0 to 12.5 mM resulted in decrease of resting membrane potential from 83 mV (normal Ringer) to 56 mV (P less than 0.001). Under these conditions, verapamil diminished amplitude, overshoot and duration of action potentials, whereas 4-AQ depressed overshoot and prolonged action potential duration (P less than 0.02). Action potentials recorded in 20 mM K+ (isoproterenol added) exhibited a mean resting potential of 38 mV and also a reduced amplitude and duration. Verapamil caused a rapid blockade of the electrophysiological response, suggesting that action potentials were mediated by a current carried by calcium ions. 4-AQ applied in two concentrations (0.25 and 0.5 mM) on atrial trabeculae exposed to 20 mM K+-isoproterenol partially restored resting membrane potential and significantly (P less than 0.001) increased amplitude, overshoot and duration of action potentials. These effects were attributed to an enhanced Ca2+ entrance induced either by a direct action upon voltage-sensitive calcium channels, or resulting from a prolonged action potential due to blockade of potassium conductance.

Action Potentials↗
PubMed1986

Physical growth and bone age of survivors of protein energy malnutrition.

Early postnatal malnutrition produces delay in growth and developmental processes, and children from a low socioeconomical level where undernutrition is prevalent are shorter than those from higher socioeconomic levels. We examined the effects of severe and early protein energy malnutrition on growth and bone maturation. We studied 40 preschool children who had been admitted to hospital in infancy with protein energy malnutrition and 38 children from the same socioeconomic level, paired for age and sex, who had never been malnourished. Growth measurements were made over a period of 4-6 years, and bone age was determined in a subgroup through wrist roentgenograms. Results showed a correlation between protein energy malnutrition, birth weight of infants, and mother's height and head circumference. The group with protein energy malnutrition showed a significant delay in stature after four years, especially the girls (p less than 0.001). Weight:height ratio was reduced in boys compared with controls but not in girls. Both groups showed a delay in bone maturation, but there were no significant differences between them. We found a positive correlation between bone age and arm fat area in control boys and between bone age and height for age in boys with protein energy malnutrition. The finding that rehabilitated children were shorter than the control group but had similar bone age at follow up suggests that genetic or prenatal factors were important in their later poor growth, and this suggestion is supported by their smaller birth size and the smaller size of their mothers.

Age Determination by Skeleton↗
PubMed1985

Effects of cholinergic drugs and 4-aminopyridine on cat ciliary muscle contractility.

The effects of some cholinergic agents and 4-aminopyridine (4-AP) on neurally mediated contractions of in vitro cat ciliary muscle preparations were studied. The contractile response to trains of stimuli was enhanced by eserine and completely blocked by tetrodotoxin or atropine. Low concentrations of carbachol did not modify muscle resting tension but clearly attenuated contractile response to electrical stimuli, while higher concentrations increased the resting tonus leading to contracture which did not respond to further stimulation. 4-AP is known to be a potassium-channel blocking drug that increases neurotransmitter release at nerve terminals during the action potential. This substance exhibited a dose-related potentiation of the evoked ciliary muscle contractions without changing resting tension. The eventual reducing effect of 4-AP on the accommodative convergence/accommodation ratio (AC/A) is discussed in relation to its potential clinical application in certain strabismus patients.

4-Aminopyridine↗
PubMed1984

Inhibitory effect of acetylcholine on muscular tonus of the small intestine of a lizard.

The present report concerns the effects of cholinergic agonists on the isometric tension of "in vitro" preparations of the esophagus and distal part of the small intestine of the lizard Liolaemus gravenhorsti. Acetylcholine (Ach) and carbachol elicited a dose-related increase of isometric tension in the esophagus, whereas the small intestine was slowly relaxed by these drugs. Eserine induced a synergistic action on the cholinergic responses of both organs, and atropine completely antagonized the respective effects. The esophagus and the intestine showed different thresholds for the cholinergic evoked responses, the former being about 30 times more sensitive than the intestine. Assessment of cholinesterase activity revealed that Ach is hydrolyzed at a significant lesser speed in the intestine than in the esophagus. The results do not provide information about the nature of the chemical mediator causing the inhibitory effect observed in the intestine. The eventual role of an adrenergic mechanism mediated by muscarinic receptors is under study in our laboratory.

Acetylcholine↗
PubMed1984

Comparison of the electrophysiological effects of 4-aminoquinoline, quinidine and lidocaine on frog atrial contractile fibres.

Standard microelectrode techniques were used to study the electrophysiological effects of 4-aminoquinoline (4-AQ), a 4-aminopyridine analogue, on frog atrial contractile fibres and the effects compared with those of quinidine and lidocaine. The effects of 4-AQ (250 and 500 microM) were: reduction of action potential amplitude, overshoot and maximum upstroke velocity (Vmax) and increase of action potential duration. These effects were reversible after washing. No change in membrane resting potential was observed with these drug concentrations. Quinidine (27 and 54 microM) caused no statistically significant changes of resting potential and overshoot but dose-dependently decreased Vmax. Action potential duration (APD) was shortened or unchanged at 60% repolarization, whereas at 90% repolarization APD was increased by the higher concentration of this drug. Quinidine (54 microM) also depressed action potential amplitude. Lidocaine (17 microM) induced a slight decrease of action potential amplitude and a marked reduction of Vmax as well as of APD without changing membrane resting potential or overshoot. Comparison of these results indicate that 4-AQ and quinidine share most electrophysiological effects such as depression of upstroke velocity, action potential total amplitude and repolarization rate at phase 3 of the transmembrane potential. Lidocaine and 4-AQ share only the capability of decreasing Vmax, whereas the effect upon repolarization was the opposite. Consequently, this study together with a previous one of our laboratory (Guerrero, 1982) suggest that 4-AQ is a drug having some quinidine-like properties.

Action Potentials↗
PubMed1984

Electrophysiological effects of 4-aminoquinoline on frog atrial contractile fibres.

The effects of 4-aminoquinoline (4-AQ), a drug structurally related to 4-aminopyridine, were studied on atrial contractile fibres from the amphibian Caudiverbera caudiverbera by means of intracellular electrodes. In concentrations that did not change resting potential, 4-AQ (0.25-1.5 mM) reduced upstroke velocity, action potential amplitude (APA) and overshoot in a dose-dependent manner. 4-AQ also prolonged action potential duration (APD) and the fibre effective refractory period (ERP), making the ratio ERP/APD greater than one. These effects were reversible by washing. The drug-induced reduction of upstroke velocity was frequency-dependent. This effect and increase of APD were more intense at higher values of resting potential. All effects produced by 4-AQ remained constant in either high or low external K+ concentrations. The depressant effects of this compound on upstroke velocity, overshoot, APA as well as increase of APD were antagonized by doubling the extracellular Na+ concentration. Data presented support the view that 4-AQ exerts its effects on the frog heart by blocking both sodium and potassium channels, thus causing quinidine-like actions.

Action Potentials↗
PubMed1982

Facilitatory effects of 4-aminopyridine on strontium-mediated evoked and delayed transmitter release from motor nerve terminals.

The effect of 4-aminopyridine (4-AP) on Sr-mediated evoked and delayed transmitter release at the frog neuromuscular junction was examined using conventional electrophysiological techniques. 4-AP (5-50 microM) increased transmitter release evoked in response to conducted nerve impulses or to electrotonic depolarization of tetrodotoxin (TTX)-treated motor nerve terminals. Spontaneous quantal transmitter release was not affected by the drug as judged by the lack of effect on miniature end-plate potentials (MEPPs) frequency. However, 4-AP (10-20 microM) markedly enhanced the frequency of MEPPs appearing during conducted low rate repetitive nerve impulses or single electrotonic depolarization of TTX-blocked nerve terminals. The results suggest that 4-AP increases the influx of Sr2+ into nerve terminals in a way that modifies its sequestration and removal by the subcellular elements of the terminal.

4-Aminopyridine↗
PubMed1982

Effects of 4-aminoquinoline on action potentials of the frog sinus venosus.

The electrophysiological effects of 4-aminoquinoline (4-AQ), a drug structurally related to 4-aminopyridine, were studied on the sinus venosus of the frog Caudiverbera caudiverbera with standard microelectrode techniques. 4-AQ in concentrations (0.01-1.5 mM) that did not modify membrane resting potential, reversibly depressed pacemaker activity and the rate of diastolic depolarization. These effects were not prevented by atropine. 4-AQ also reduced maximum diastolic potential, whereas action potential amplitude, overshoot and dV/dtmax remained unaffected. Action potential duration was prolonged by 4-AQ in a concentration-related manner by slowing down the repolarization phase. The effects upon repolarization and on diastolic depolarization were abolished by doubling extracellular calcium concentration. They were not suppressed, however, by electrically pacing sinus preparations at the pre-drug frequency. A plausible interpretation of the data is that 4-AQ effects are the consequence of a direct inhibition of potassium conductance at the cell membrane.

Action Potentials↗
PubMed1980

Effects of 4-aminopyridine on pacemaker activity of frog sinus venosus.

The effects of low concentrations of 4-aminopyridine (4-AP) were studied on the frog sinus venosus by means of intracellular microelectrodes. 4-AP depressed spontaneous automaticity. This effect was not reversed by atropine. 4-AP also prolonged the sinus action potential repolarization and slowed the rate of diastolic depolarization. These effects are attributed to blockade of potassium conductance.

Aminopyridines↗