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At least 1,207 records · Page 67Linked to original sources
PubMed1979

[Effects of calcium, ethanol and hyperosmolarity on the distribution of intervals between MEPP's].

Distributions of intervals between MEPP's, recorded from the frog sartorius muscle in various experimental conditions, were compared, graphically and by X2, with the exponential distributions expected for a Poisson process. For each experiment, 200 intervals were measured. In isotonic Ringer solutions containing no Ca++, MEPP's fitted an exponential distribution; by adding Ca++ (1 mM, 2,5 MM, 15 mM), the fit between empirical and expected distributions became poorer, with an excess of short intervals. MEPP's showed the tendency to occur in bursts, and this was particularly evident at 15 mM Ca++. In the presence of 0,5% ethanol, also at high Ca++ the intervals between MEPP's showed a fair fit to the exponential distribution. In Ringer solutions made hypertonic by the addition of 50 mM sucrose, the fit was poor and there was a relative lack of short intervals. These different patterns of MEPP distribution could be explained by supposing that Ca++, ethanol and hypertonicity activate different mechanisms of transmitter release.

Animals↗
PubMed1975

Histochemical development of myofibres in neonatal piglets.

The periodic acid-Schiff (PAS) reaction and tests for glycogen phosphorylase, oxidative enzymes and acid-stable and alkali-stable adenosine triphophatase (ATPase) were used to determine the degree of histochemical differentiation between myofibres of sartorius muscles from neonatal piglets. Within 24 h of birth, the ratio of myofibres with acid-stable ATPase to those with acid-labile ATPase was 1:21-0. By 10 days the ratio had changed to 1:5-2. Mean minimum myofibre diameters (all histochemical types combined) increased steadily after birth although diameters of myofibres with acid-stable ATPase showed no increase until 6 days. By 10 days, consistent differentiation was observed with the alkali-stable ATPase and glycogen phosphorylase reactions but not with the PAS reaction. During the 10 day neonatal period, all types of myofibres contained large or moderate numbers of mitochondria.

Adenosine Triphosphatases↗
PubMed1987

Nicotinic acetylcholine receptor ion channel blockade by cocaine: the mechanism of synaptic action.

The action of cocaine on neuromuscular transmission of the frog has been studied to unveil the molecular site upon which this agent acts to block synaptic function. Indirectly elicited twitches of the sciatic nerve-sartorius muscle were reduced at greater than or equal to 50 microM cocaine. The electrically evoked action potentials of muscle membrane were inhibited at 200 microM cocaine, in a manner consistent with a local anesthetic effect. At the synaptic region, the quantal release of transmitter from the nerve terminal was not affected by cocaine at concentrations up to 100 microM. The most potent action of cocaine was the blockade of the ion channel of the nicotinic acetylcholine receptor. Transient membrane depolarization induced by microiontophoresis of acetylcholine was reduced to 7% of control at 50 microM cocaine in a dose-related manner; receptor desensitization was affected to a lesser extent by cocaine at all concentrations tested. The decay time constants of endplate currents were reduced at concentrations greater than or equal to 10 microM. The single channel conductances remained unchanged whereas the channel lifetimes were greatly reduced at 25 and 50 microM of the drug. Unblocking could not be discerned from the observed kinetics of either endplate current decay or single channel closed durations. However, with a combination of 10 microM cocaine and 0.4 M ethanol the endplate currents became biphasic. This suggested a blocking of open ion channels of the nicotinic receptor by cocaine followed by dissociation of acetylcholine from the blocked channel (in the absence of ethanol).

Acetylcholine↗
PubMed1988

Acetylcholinesterase reactivators modify the functional properties of the nicotinic acetylcholine receptor ion channel.

Interactions of the oximes pyridine-2-aldoxime (2-PAM) and 1-(2-hydroxyiminomethyl-1-pyridino)-3-(4-carbamoyl-1-pyridino++ +)-2-oxapropane dichloride (HI-6), reactivators of phosphorylated acetylcholinesterase enzyme, with the nicotinic acetylcholine receptor-ion channel complex were studied using electrophysiological techniques. Single channel studies revealed that both oximes increased the opening probability of channels that were activated by acetylcholine. The oximes reduced mean channel open time and burst time in a concentration- and voltage-dependent manner. End-plate current amplitude was increased by 2-PAM (10-100 microM) and HI-6 (1 microM) but depressed at higher concentrations of these agents. The oximes decreased the time constant of end-plate current decay, particularly at hyperpolarized membrane potentials. HI-6 depressed indirect twitch response of the sartorius muscle, whereas 2-PAM caused a facilitation followed by depression. Both agents directly hydrolyzed acetylthiocholine, in addition to weakly inhibiting acetylcholinesterase. Our study demonstrates a direct molecular interaction of the oximes HI-6 and 2-PAM with the natural agonist molecule and with the acetylcholine receptor-ion channel complex. These effects can explain the excitatory and inhibitory actions of both agents, and may form the basis for their antidotal effectiveness against organophosphorus poisoning. The quantitative differences between the effects of 2-PAM and HI-6 on the above parameters are important in view of their differential antidotal efficacies.

Acetylcholinesterase↗
PubMed1978

The increase in spontaneous transmitter release produced by beta-bungarotoxin and its modification by inorganic ions.

The excitatory phase of the biphasic action on transmitter release of the neurotoxin, beta-bungarotoxin (beta-BuTX; 0.5 microgram ml-1), was studied on miniature end-plate potentials (MEPPs) at frog sciatic nerve-sartorius muscle junctions. The most common type of excitatory response was characterized by a continuous increase in MEPP frequency that reached a plateau; a less common form was characterized by irregular episodic bursts of firing. There was a direct relationship between toxin activity and [K+]O (2.5-10.0 mM) with virtually no effect of the toxin at normal [K]O+ at the concentration of toxin used. In the absence of Mg++, there was a paradoxical inverse relationship between toxin activity and [Ca++]O (0.5-4.0 mM) at higher [K+]O. However, in the presence of 1.0 mM Mg++ the increased MEPP frequency produced by beta-BuTX was independent of [Ca++]O. The action of beta-BuTX was very sensitive to blockade by Mg++. Toxin activity was demonstrated in a Sr++-containing, Ca++-free solution, but not in a Mg++-containing, Ca++-free solution. It is probable that beta-BuTX causes a slight depolarization of the nerve terminals by a mechanism not sensitive to blockade by tetrodotoxin and that the ability of beta-BuTX to depolarize the terminals can account for the enhancement of the response by raising [K+]O and the depression of the response by Mg++. Alternatively, beta-BuTX could be producing its effects by some, as yet undefined, direct action on the release process.

Action Potentials↗
PubMed1989

[The development of desensitization during rhythmic activity of the synapse and in the course of generating a single signal].

The possibility of desensitization (DS) development under the rhythmic activity and during the generation of the single response to acetylcholine was studied in the frog sartorius muscle by voltage-clamp technique. It was revealed, that under conditions promoting DS (hyperpolarization, muscle warming, rise of calcium concentration as well as treatment by the DS--potentiating agent--proadifen) decrease of the postsynaptic membrane sensitivity to the acetylcholine can develop after few multiquantal end-plate currents--and when acetylcholinesterase is inhibited--during the response to a single quantum of acetylcholine.

Animals↗
PubMed1985

Triphenylmethylphosphonium blocks the nicotinic acetylcholine receptor noncompetitively.

Triphenylmethylphosphonium (TPMP) blocked the nerve-elicited twitch tension of frog sartorius muscles by 50% at a concentration of about 20 microM. This neuromuscular blockade by TPMP, which originated at the level of the nicotinic receptor, was due in part to the ability of the drug to block the quiescent receptor by degrees that depended on the TPMP concentration and on membrane potential. In addition, the blockade was markedly enhanced when the receptor was activated by acetylcholine. Finally, TPMP shortened the lifetimes of ACh-activated ion channels. These findings were interpreted as follows. Under resting conditions, TPMP shifted the equilibrium of the receptor channel complex toward the desensitized state. TPMP united with the activated ion channel to shorten channel lifetime and to deepen the blockade. High concentrations (greater than or equal to 50 microM) of TPMP altered muscle action potentials and often increased, by about 30-fold, the frequency of miniature endplate potentials.

Acetylcholine↗
PubMed1986

[Effect of cholinergic compounds on spontaneous quantal mediator release at the neuromuscular synapse of the frog].

The action of cholinergic drugs on spontaneous quantal transmitter release has been investigated in the frog sartorius muscle. Acetylcholine and carbacholine decreased the miniature end-plate potential frequency. These presynaptic effects had no dependence on the potassium concentration in the bath solution. Nicotinic agonists--nicotine, tetramethylammonium and suberyldicholine had a similar effect, while muscarinic agents--methylfurmetide, oxotremorine and F-2268 (L- and D-stereoisomers) did not affect the transmitter release. The presynaptic effects of carbacholine and acetylcholine were abolished neither by atropine nor by d-tubocurarine and bensohexonium. It is suggested that there are nicotinic receptors on the frog motor nerve terminals that modify spontaneous quantal transmitter release and differ pharmacologically from nicotinic end-plate, ganglionic and presynaptic receptors of higher vertebrates.

Acetylcholine↗
PubMed1987

[Muscarinic agonists do not alter the process of spontaneous quantum secretion of the mediator from motor nerve endings in the frog].

The action of carbacholine (Cch) and muscarinic agonists--methylfurmethide, oxotremorine, metacholine, L- and D-F-2268 isomers on spontaneous quantum transmitter release was investigated in experiments on the frog sartorius muscle of R. temporaria. Cch decreased the frequency of miniature and plate potentials (mEEP) by 48%. The muscarinic agonists at a wide concentration range had no effect on mEEP frequency both in normal ionic medium and with potassium concentration increase to 10 mmol/l. The data obtained confirm the assumption that the inhibitory action of Cch on spontaneous transmitter release is unrelated to its muscarinic activity. It was concluded that muscarinic cholinoreceptors controlling spontaneous transmitter release are absent in the frog motor nerve terminals.

Acetylcholine↗
PubMed1985

[Tetanic potentiation of miniature end-plate potential frequency at frog neuromuscular junction in manganese solutions].

Using a sciatic nerve-sartorius muscle preparation of the frog, we have studied the effect of Mn on the increase in miniature end-plate potential (MEPP) frequency that occurs during tetanic stimulation (50 Hz, 2-3 min) of the nerve in nominally Ca2+-free, Mn2+ and Mg2+ solutions. During stimulation the frequency increased over the first minutes to reach an asymptote. The time course for the increase was analyzed following the model proposed by Barton, Cohen and Van der Kloot (1983). The ratio of the Ca2+ bound to the receptor at intervals during the tetanus, b, to the Ca2+ bound before stimulation was begun, b0, was calculated from MEPP frequencies. b/b0 indicates changes in intraterminal Ca2+ concentration produced by the tetanus. In solutions made with no added Ca2+ but containing 1 mM MgEGTA, the increase in b/b0 during stimulation showed a linear or convex time course. Similar time courses were obtained in solutions containing Mn2+ or Mg2+ as the sole divalent cation. On the other hand, when solutions contained Ca2+, the time course for the increase followed a sigmoidal curve. The present results suggest that Mn2+ enters the nerve terminal during stimulation and raises the intracellular Ca2+ concentration, which in turn promotes transmitter release.

Animals↗
PubMed1987

Potentiation of aminoglycoside-induced neuromuscular blockade by protons in vitro and in vivo.

pH-dependent effects of 100 microM streptomycin and various aminoglycosides were examined at frog (Rana pipiens pipiens) sciatic sartorii in vitro by using the intracellular microelectrode recording technique. pH-dependent effects of streptomycin were also examined on indirectly elicited (nerve-stimulated) and directly elicited sartorius muscle twitches in vitro. Furthermore, in vivo effects of systemic pH alterations on neomycin-induced mortality were examined in Sprague-Dawley rats. There was a direct correlation between aminoglycoside potency and the number of basic groups per drug molecule (r = 0.95). At pH 7.2 and 9.0, the effect of pH on aminoglycoside potency correlated inversely with the pKa of the aminoglycoside (r = -0.98). At 0.7 and 2.2 pH units below 7.2, however, aminoglycoside-induced inhibitions of quantal content, end-plate potential amplitude and the indirectly elicited muscle twitch were potentiated by a pH-dependent mechanism that was independent of the pKa of the aminoglycoside. At these pH values, qualitatively similar drug effects were not observed on miniature end-plate potential amplitude and frequency or the directly elicited muscle twitch. Potentiation of aminoglycoside action was observed on mortality of rats, however, when the pH was 0.1 pH unit below 7.4. Thus, potentiation of aminoglycoside-induced neuromuscular blockade by protons in vitro and in vivo was demonstrated and appears to involve the pH-dependent activity of a prejunctional membrane component that regulates voltage-dependent, Ca++-mediated transmitter release.

Aminoglycosides↗
PubMed1988

Diagnosis and management of vulvar carcinoma.

With the steady increase in life expectancy, invasive cancer of the vulva is now becoming more prominent among gynecologic malignancies. Early, careful examinations and informed patients can aid in early diagnosis. Carcinoma in situ, verified by biopsy, is best treated with wide local excision. Invasive vulvar carcinoma should be treated with radical vulvectomy and bilateral groin node dissection. The major source of morbidity is wound breakdown. The use of modified incision techniques and sartorius muscle transplantation have significantly decreased these postoperative complications. The clinical staging system for vulvar carcinoma is approved by the International Federation of Gynecology and Obstetrics (FIGO). The disease usually spreads systematically from the vulva to superficial groin nodes, to deep groin nodes, and then to pelvic nodes. Survival rates of 84% for stage I disease can be achieved. Evidence of positive groin nodes indicates a poor prognosis. However, even patients with advanced disease can be surgically cured by radical surgery. Five of ten patients (50%) with stage IV disease were alive and free of disease at five years with exenterative surgery. Any patient who is a reasonable medical risk, with a vulvar lesion that is resectable, should be treated surgically. Otherwise, the patients not only die, but they die in abject misery.

Female↗
PubMed1988

A new scheme for hierarchical classification of anastomosing vessels.

A new scheme is presented for hierarchical classification of vessels in anastomosing networks. The scheme is based on topological information, i.e. on patterns of vessel interconnection, not on vessel dimensions. As an illustration, this ordering scheme is applied to the anastomosing arteriolar network in cat sartorius muscle. Vascular segments are classified and the frequency distribution of segment length is determined for each order. In addition, vascular loops are classified, and the area, perimeter, and number of segments per loop are determined.

Animals↗
PubMed1986

Effects of phencyclidine and its analogs on the end-plate current of the neuromuscular junction.

The interactions of the hallucinogenic drug PCP [1-(1-phenylcyclohexyl)piperidine] and some of its analogs with the nicotinic acetylcholine receptor-ionic channel complex were studied using electrophysiological techniques. The peak amplitude and the decay time constant of the nerve-evoked end-plate current (EPCs) recorded from the frog sartorius muscle were reduced by all the analogs in a concentration-dependent manner (IC50 between 5 and 90 microM). PCP, TCP [1-[1-(2-thienyl)cyclohexyl]-piperidine] and PCE (N-ethyl-1-phenylcyclohexylamine), among other analogs, caused a negative slope conductance in the current-voltage relationship at hyperpolarized potentials and a voltage- and time-dependent depression of the peak amplitude of the EPC. When the piperidine ring of the PCP molecule was substituted by a morpholino ring, as in 1-(1-phenylcyclohexyl)morpholine and 1-[1-(2-thienyl)-cyclohexyl]morpholine, the potency decreased and the negative conductance was eliminated. The removal of the piperidine ring of PCP in 1-phenylcyclohexylamine and the hydroxylation of the cyclohexane ring in 4-phenyl-4-piperidino-cyclohexanol reduced the potency and produced double exponential decays at potentials between +50 and -50 mV. At -100 mV, the potency for decreasing peak EPC amplitude was well correlated with the potency for reducing the decay time constant for all the analogs. The voltage- and time-dependent depression of the EPC amplitude was reduced by substitution of a morpholino ring and by the elimination of the piperidine ring of PCP. The behaviorally active analogs were the most potent EPC blockers, which suggests a synaptic role for the production of depressant behavioral effects observed with PCP.

Animals↗
PubMed1987

An electronic mechanism in the actions of drugs and other cardinal adsorbents. I. Effects of ouabain on the relative affinities of the cell surface beta- and gamma-carboxyl groups for K+, Na+, glycine and other ions.

The effects of ouabain on the effectiveness of glycine, Li+, Na+, K+, Rb+, and Cs+ in the external medium in reducing the rate of entry of labeled Cs+ into frog sartorius muscles were studied. The results showed that in the absence of ouabain the effectiveness of glycine and alkali-metal ions in inhibiting labeled Cs+ entry follows the rank order: K+ greater than Cs+, Rb+ greater than Na+, Li+ greater than glycine. Exposure to ouabain in essence reverses this order which then becomes: glycine greater than Li+, Na+ greater than K+, Rb+, greater than Cs+. These results confirm the prediction of the basic electronic interpretation of drug action according to the association-induction hypothesis. In addition, it shows that the action of ouabain on the surface beta- and gamma-carboxyl groups of frog muscle mediating Cs+ entry is quite similar to its action on the cytoplasmic beta- and gamma-carboxyl groups that are the seats of K+ accumulation in the bulk phase cytoplasm as well as to its action on the cell surface beta- and gamma-carboxyl groups responsible for the generation of the resting potential. In all these cases, ouabain acts as an electron-donating cardinal adsorbent (EDC). Finally the marked increase of the binding strength of glycine on the surface beta- and gamma-carboxyl groups was used to explain the primary pharmacodynamic effect of cardiac glycosides in combating heart failure.

Adsorption↗
PubMed1987

[Anatomy and clinical aspects of sartoriusplasty].

According to Mathes and Nahai (1982) the sartorius muscle is supplied in a segmental fashion (Type IV) from six to ten branches arising from the superficial femoral artery. They state that the use of this flap is limited because of the segmental blood supply. In contrast, dissecting 40 cadaver specimens at the Anatomy Department of Munich University a different vascular anatomy was revealed in which only two to four branches from the femoral artery supply the whole muscle. Based on this pattern of intramuscular vascular connections, the most proximal arterial branch provides the blood supply to the whole muscle. Elevated on the proximal vascular pedicle the muscle can cover defects of symphysis, fill the acetabulum following disarticulation of the septic hip joint and osteomyelitic defects of femur.

Arteries↗
PubMed1987

Compound-action potentials of myelinated fibers in the saphenous nerve of the dog: in situ electrophysiologic and behavioral studies.

Compound-action potentials (CAP) were recorded directly from the surface of fascicles of the distal portion of the saphenous nerve (SN) of dogs in situ. Potentials were evoked through needle electrodes and were recorded through bipolar stainless steel electrodes. Stimuli of 10-microseconds duration and of 0.4 +/- 0.15-mA amplitude evoked a monophasic CAP. Sensory conduction velocities of afferent fibers, the action potentials of which contributed to this evoked compound potential, ranged from 62.4 +/- 2.8 m/s for the most rapidly conducting fibers to 30.5 +/- 2.4 m/s for the least rapidly conducting fibers. Stimuli of 25-microseconds duration and of 2.2 +/- 0.8-mA amplitude evoked a second, longer latency CAP in addition to the first CAP. Sensory conduction velocities of afferent fibers, the action potentials of which contributed to this evoked compound potential, ranged from 20.4 +/- 2.9 m/s for the most rapidly conducting fibers to 13.7 +/- 1.0 m/s for the least rapidly conducting fibers. Low-amplitude, negative peaks were recorded between the first and second major potentials elicited by the longer duration stimuli. Stimuli of still longer duration and higher currents induced contractions of the caudal part of the sartorius muscle by current spread in 9 of 12 dogs. In 3 dogs, a third monophasic CAP was evoked, having a maximal conduction velocity of 1.7 +/- 0.2 m/s. After section of the distal portion of the SN on one side in each of 2 dogs, an absence of signs of sensory deficit was found on clinical neurologic examination. The area of cutaneous innervation of the cranial branch of the distal portion of the SN was determined electrophysiologically.

Action Potentials↗
PubMed1979

[Termination of the presynaptic effect of carbacholine by tubocurarine].

The presynaptic action of carbacholine (Cch) was studied in experiments on the frog sartorius muscle neuromuscular preparation. Cch proved to decrease the quantum content of the end plate potential (EPP); this effect was induced by a direct Cch action on the motor nerve endings. d-tubocurarine decreased the sensitivity of the nerve endings to Cch significantly. Both d-tubocurarine and Cch had concurrent antagonistic interrelations in respect to their action on the quantum content of EPP. Atropine in low concentrations had no influence on the presynaptic effect of Cch. It was concluded that Cch decreased the quantum content of EPP through the N-cholinergic structures of the motor nerve endings.

Animals↗