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Biomedical subjects

G Raymond

Publications and source records attributed to G Raymond.

At least 109 records · Page 6Linked to original sources
PubMed1986

The voltage-dependent blocking effect of phalloidin on the delayed potassium current of voltage-clamped frog skeletal muscle fibres.

The effects of phalloidin (10(-14)-10(-6) M) were tested on voltage-clamped isolated frog muscle fibres. The toxin reversibly blocked the potassium current similarly in both detubulated and intact fibres. Neither the reversal potential nor the activation curve of the current were affected by the toxin (10(-8) M). The inactivation curve was shifted toward negative values at holding potentials more than +20 mV from the reference potential. This shift enhanced the potential-dependent facilitation of the current block observed between -40 and +40 mV from the reference holding potential (the higher the depolarization, the greater the blocking effect, which reached 100% at +40 mV). Contrary to what was seen with the current, hyperpolarization did not relieve the mechanical block. The effect of phalloidin did not seem to be frequency-dependent.

Animals↗
PubMed1986

The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers.

Slow outward potassium currents were recorded in isolated frog skeletal muscle fibres using the double mannitol-gap voltage-clamp technique. Detubulated fibres failed to generate a slow outward current, and apamin had no effect on the remaining current. The maximum blocking effect of organic and inorganic Ca2+-channel blockers on the slow outward channels of intact fibres was larger than that of apamin. Apamin failed to induce an additional block when applied after Ca2+-channel blockers. In a low-Ca2+ solution (OCa, EGTA 1 mM) the slow outward current was slightly increased and the blocking effect of apamin was enhanced. A Ca2+-rich solution (Ca2+ X 10) increased the slow outward current and the blocking effect of apamin was drastically reduced. It is concluded that the apamin-sensitive current which is a component of the slow outward K+ current is located in the tubular membrane. Its activation seems barely dependent on the Ca2+ influx via the slow inward Ca2+ current. Apamin-receptor binding appears to be dependent on the extracellular Ca2+ concentration. Blockade of slow outward current by Ca2+-channel blockers is likely to be the result of a direct action on the slow K+ permeability rather than a consequence of Ca2+ channel inhibition.

Animals↗
PubMed1986

Bay K 8644 enhances slow inward and outward currents in voltage-clamped frog skeletal muscle fibres.

In isolated frog skeletal muscle fibre slow inward calcium current and slow outward potassium current were recorded by means of a double mannitol-gap device. Bay K 8644, the so-called Ca-channel activator, shifted the activation threshold of the slow inward calcium current (recorded in Cl-free, Ca-rich solution), towards negative potential by 15 mV. It increased the peak current amplitude in a dose-dependent manner (from 10(-11) to 10(-7) M; EC50 approximately equal to 10(-9) M). Apamin, the bee venom toxin which is known to specifically block a class of calcium-dependent potassium channels, failed to block the slow inward calcium current and slowed down its declining phase. This effect exhibited a potential dependence: the more the membrane was depolarized, the more the current decay was slowed down. Bay K 8644 (10(-7) M) transiently decreased the slow outward potassium current, which then progressively increased to stabilize at 135% of the control value. This effect seemed to be more pronounced at potentials above the reversal potential for inward ICa. The results suggest that the increase of the slow outward current is due to a direct action of Bay K 8644 on the slow K channel, rather than an indirect action via potentiation of slow inward calcium current. Moreover, results obtained with apamin indicated that the slow outward potassium current is unlikely to flow through Ca-channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

The strontium-induced calcium-release process and its implication in contractility of skeletal muscle of Rana ridibunda.

The electrical and mechanical activities of isolated frog muscle fibres have been recorded simultaneously under conditions (chloride-free saline containing 78.5 mM strontium acetate substituting for NaCl and CaCl2) that allow the development of a tubular strontium permeability. Under voltage-clamp conditions a large part of the contraction is due to the slow inward ISr since both are inhibited by Ni (10 mM). The remaining component of contraction, which seems to be potential-dependent, is not abolished by tetracaine (40 microM) which blocks the current-dependent component. A cumulative effect of strontium, which is not observed in the presence of Ni, leads to a 60-80% reduction in contractility for an estimated [Sr]i near 3 X 10(-4) M while the ending of the contraction observed when Sr is replaced by Ba is never obtained. In contrast no cumulative effect is observed when Ca substitutes for Sr. The first evoked inward current following a caffeine contracture fails to elicit a contraction, but in Ringer 78.5 Sr, contractility is progressively restored by successive depolarizations up to an amplitude which corresponds to 25-40% of the maximum activity. In the presence of Ca instead of Sr, the restoration of contractility reaches 100%. This recovery does not occur when the inward current is blocked by Ni. After strontium loading, a calcium entry fails immediately and reversibly to induce a mechanical response while barium ions induce a progressive and irreversible block of contractility. These results suggest that the strontium entry during successive depolarizations leads to a progressive replacement of intrareticular calcium by strontium. When all the calcium ions have been substituted for by strontium ions, the contractile apparatus remains capable of being activated by intrareticular strontium.

Animals↗
PubMed1985

Effects of phalloidin on electrical and mechanical activity of frog muscle fibres.

The effects of phalloidin (10(-15) to 10(-5) M) on isolated muscle fibres of the frog were investigated under current or voltage clamp conditions in a double mannitol gap device coupled to a mechanoelectric transducer which allowed the estimation of isometric tension. The toxin significantly increased the action potential duration and the amplitude of the associated contraction. Under voltage-clamp conditions, for a concentration range of 10(-14) to 10(-8) M, phalloidin reversibly decreased (up to 42.7% +/- 3.1) the fast outward potassium current responsible for the delayed rectification. For concentrations from 10(-8) to 10(-5) M, the toxin irreversibly reduced (up to 43.3% +/- 2.9) the amplitude of the contractile response. It is concluded that, in skeletal muscle fibre of frog, phalloidin acts at two different levels, one which may be located at the outer face of the surface membrane while the other may be located deeper within the cell.

Action Potentials↗
PubMed1985

Barium inhibition of the tonic component of frog atrial contraction.

Barium ions are able to substitute for calcium as charge carriers for the slow inward current of cardiac membrane. The effects of such a substitution on the mechanical activity of voltage-clamped frog atrial trabeculae have been investigated using the double mannitol gap device coupled with a mechano-electric transducer. In the presence of barium, the 'tonic' phase of the contraction is suppressed and the remaining contraction is correlated to the influx of barium ions via the slow inward channel. Since a Na-Ca exchange regulates the tonic contraction, the present results suggest that barium ions cannot substitute for calcium in this mechanism.

Animals↗
PubMed1985

Concentrations of fusidic acid, cloxacillin, and cefamandole in sera and atrial appendages of patients undergoing cardiac surgery.

The concentrations of cefamandole, cloxacillin and fusicid acid were measured in the serum and heart tissue of 100 recipients of these drugs before cardiac surgery. During cardiopulmonary bypass, mean (+/- standard deviation) peak concentrations in serum of all patients were 63.0 +/- 34.0 micrograms of cefamandole per ml, 30.8 +/- 17.7 micrograms of cloxacillin per ml, and 32.4 +/- 10.8 micrograms of fusidic acid per ml. Mean (+/- standard deviation) concentrations in atrial appendages taken 1 h (+/- 15 min) after infusion were 21.3 +/- 11.0 micrograms of cefamandole per g, 23.8 +/- 17.3 micrograms of cloxacillin per g, and 10.7 +/- 4.2 micrograms of fusidic acid per g. No cloxacillin could be detected in 5 of 39 heart specimens. Mean tissue-to-serum ratios at 1 h for cefamandole, cloxacillin, and fusidic acid were respectively 0.35, 0.73, and 0.33. Fusidic acid, a drug which is highly effective in vitro against both methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis, was detectable in heart tissue in concentrations which were 12 times higher than the MICs of this agent against these resistant microorganisms.

Adult↗
PubMed1984

Blue-sensitive cones in the primate retina: microspectrophotometry of the visual pigment.

Direct absorbance and bleaching absorbance-difference spectra were obtained using a photon-counting microspectrophotometer from the outer segments of ten blue-sensitive cones of macaque monkeys. The peak wavelength (lambda max) of the direct measurements was 426 +/- 3.4 nm, whereas the lambda max of the bleaching difference was 434 +/- 6.6 nm. We consider these values to be upper and lower bounds since both measurements may be shifted in opposite directions by wavelength-dependent effects. Therefore, the true peak sensitivity must be close to 430 nm.

Animals↗
PubMed1984

Effects of apamin on the outward potassium current of isolated frog skeletal muscle fibres.

The effect of apamin, a polypeptidic toxin from bee venom which is a specific blocker of certain Ca2+-dependent K+ channels, has been tested (50-100nM) on voltage clamped single skeletal muscle fibres of the frog. The results have shown the existence of an inhibitory effect of the toxin on the slow outward K+ current which suggests the existence of a Ca2+-sensitive component of the slow K+ permeability in the plasma membrane of the frog muscle fibre.

Animals↗
PubMed1984

Triamterene kinetics and dynamics in cirrhosis.

Triamterene is extensively metabolized by the liver and undergoes important presystemic elimination in normal subjects after oral doses. We examined triamterene disposition in eight healthy controls and seven patients with cirrhosis and ascites. A specific and sensitive HPLC assay was used to measure concentrations of triamterene and of its major metabolite p-hydroxy-triamterene sulfate (OH-T-S). Apparent oral clearance of triamterene in controls averaged 1617 +/- 219 ml/min. Plasma concentration of OH-T-S was 7.2 +/- 1.1 times that of the parent compound (estimated by the ratio AUCOH -T-S/ AUCtriamterene ). Urinary recovery of OH-T-S accounted for 45% of the triamterene dose. There was 92% reduction in apparent oral clearance of triamterene (134 +/- 42 ml/min) in patients with cirrhosis. The ratio AUCOH -T-S/ AUCtriamterene fell to 0.55 +/- 0.2, and urinary recovery of OH-T-S accounted for only 15% of the dose. These changes in triamterene kinetics in patients with cirrhosis resulted in prolongation of its natriuretic effect, which lasted for up to 48 hr, whereas it was only 8 hr in the controls. These observations reinforce the concept that cirrhosis is associated with a markedly impaired disposition of drugs that have a large first-pass effect.

Adult↗
PubMed1983

[Permeability to strontium ions and excitation-contraction coupling in skeletal muscle of frogs].

Electrical and mechanical activities of frog skeletal muscle fibres were simultaneously investigated under conditions which allow the development of a strontium permeability. It was shown that the contraction elicited by a long lasting Sr response depends upon two mechanisms: a potential dependent one, and a mechanism which is related to the entry of Sr ions into the cell through the tubular membrane.

Animals↗
PubMed1983

[Pharmacokinetics and metabolism of acetaminophen in normal, alcoholic and cirrhotic subjects].

It is well known that a chemically reactive metabolite of acetaminophen formed in the liver can cause hepatic necrosis. The amount of cysteine and N-acetylcysteine derivatives excreted in the urine is an index of the amount of reactive metabolite produced. We have examined the pharmacokinetics and the pattern of acetaminophen metabolites in the urine, in 6 healthy controls, in 9 alcoholic subjects without liver disease, and in 11 patients with alcoholic cirrhosis but abstaining from alcohol. In alcoholics, oral clearance of the drug was similar to that of control subjects, but the amount of cysteine and N-acetylcysteine conjugates excreted in urine was significantly increased. In cirrhotics, the clearance of acetaminophen was decreased by 50 p. 100, but the pattern of urinary metabolites was unchanged. These results support previous anecdotal reports of increased acetaminophen hepatotoxicity in alcoholic subjects.

Acetaminophen↗
PubMed1982

Effect of auditory rhythm on muscle activity.

the changes in the electromyogram patterns of two antagonist muscles were studied when female subjects performed a motor task with and without an auditory rhythm. During the performance of the motor task without the rhythm, the subjects demonstrated a common and consistent personal tempo and a common electromyogram pattern. With the imposed timing of an even or uneven rhythm, the initiation and duration of the electromyograms changed significantly for subjects in both rhythm groups. Variations of electromyograms decreased significantly for subjects inthe even-rhythm group and increased significantly for subjects in the uneven-rhythm group. The authors suggest specific ways in which rhythm can be used in rehabilitative techniques to modify the onset, duration, and inconsistency of muscular activity.

Adolescent↗
PubMed1982

Existence of a sodium-induced calcium release mechanism of frog skeletal muscle fibres.

1. The electrical and the mechanical activity of isolated frog muscle fibres have been simultaneously recorded in a physiological solution which allows the development of a large tubular sodium current. 2. Under such experimental conditions, fibres develop long-lasting action potentials and strong mechanical responses. 3. In voltage-clamp experiments a slow inward current is revealed for depolarizations higher than +20 mV from the resting potential. This current increases until +40 to +50 mV and then decreases to reverse near +90 mV. The amplitude of the mechanical response increases with the potential to reach an optimum value between +40 and +50 mV and then decreases to stabilize when the depolarization is near +90 mV. 4. In the presence of picrotoxin the slow inward current is reversibly inhibited and the tension-depolarization curve has an S-shape as found in normal physiological conditions. 5. The dependence of a part of the contraction upon the slow inward current is reinforced by the fact that in a 50% sodium solution the amplitude of the current and that of the contraction are reduced in the same proportion. 6. Detubulated fibres failed to generate such a sodium inward current. 7. When sodium ions are replaced by lithium ions a slow inward lithium current develops but it does not induce a mechanical response. 8. Tetracaine reversibly inhibits the current-dependent component of the contraction without affecting the potential-dependent one. 9. It is concluded that the contraction recorded in the present experimental conditions is the sum of two components: one is potential-dependent and the other depends on a sodium-induced calcium release mechanism.

Action Potentials↗