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Physical and biochemical energy balance during an isometric tetanus and steady state recovery in frog sartorius at 0 degree C.

Frog sartorius muscle stimulated isometrically for 3 s every 256 s to attain a steady state in which initial heat (QI), recovery heat (QR), rate of O2 consumption (JO2), and isometric force (PO) generated are constant for each cycle. For a 3-s tetanus given every 256 s, JO2 was 0.106 mumol/(min . g blotted weight), approximately 71% of the maximum rate observed, whereas lactate production was negligible under these conditions. QI, QT(= QI + QR), and QT/QI were 88.2, 181.5, 2.06 mJ/g blotted weight, respectively. The high-energy phosphate breakdown (delta approximately P) breakdown during the first 3-s tetanus was not different from that during a contraction in the steady state and averaged 1.1 mumol/g blotted weight. Less than half of the initial heat could be accounted for in terms of the extent of the known chemical reactions occurring during contraction. From the stoichiometry of the theoretical biochemical pathways, the amount of ATP synthesized in the steady state exceeds delta approximately P during contraction by more than twofold, corresponding to an apparent ADP:O ratio of 1.5. If it is assumed that carbohydrate oxidation is the only net chemical reaction in the steady state, the total heat production can be explained on the basis of the measured JO2. Under this assumption, heat production during recovery was less than that expected on the basis of the oxygen consumption and delta approximately P during contraction. These observations support the hypothesis that the unexplained enthalpy production and low apparent ADP:O ratio are causally related, i.e., that the reaction(s) producing the unexplained heat during contraction is reversed during the recovery period.

Adenosine Triphosphate↗

Pre- and postjunctional blocking effects of aminoglycoside, polymyxin, tetracycline and lincosamide antibiotics.

The effects of seven antibiotics (streptomycin, amikacin, polymyxin B, lincomycin, clindamycin, tetracycline and oxytetracycline) were compared with those of magnesium, tubocurarine and lignocaine in the frog sciatic nerve--sartorius muscle preparation, using intracellular recording techniques. All compounds except tubocurarine decreased end-plate potential quantal content. The prejunctional effects of magnesium, streptomycin, amikacin, polymyxin B and oxytetracycline (but not the other drugs) were well reversed by increasing the calcium concentration. At concentrations which depressed quantal content, only magnesium, tetracycline and oxytetracycline did not reduce postjunctional sensitivity. Further postjunctional effects of the drugs were revealed by alterations in the time-courses of end-plate potentials. All the drugs tested except magnesium, tubocurarine and lincomycin produced changes in muscle action potentials. None of the compounds had anticholinesterase activity. The results confirm that aminoglycoside, polymyxin, tetracycline and lincosamide antibiotics produce neuromuscular block by a combination of both pre- and postjunctional actions.

Action Potentials↗

Important considerations in the design and construction of groin flaps.

A method for constructing groin flaps is presented which the author has used successfully. The flap is elevated medial to the sartorius muscle. The lateral femoral cutaneous nerve is preserved. The muscular branch is carefully divided to avoid damage to the superficial circumflex iliac artery. Near the femoral artery, the important draining vein, which often diverges from the cutaneous artery, must be preserved. One side of the flap is cut longer than the other and diagonal closure of the donor site and the flap are performed. This diagonal closure increases the circumference of the tube at the base of the flap, thereby reducing the risk of vascular compression. Diagonal closure also produces a spiral in the tube. The direction of the spiral can be controlled to facilitate closure of defects on the palm or dorsum of the hand.

Fascia↗

The free or pedicled saphenous flap.

The saphenous flap described by Acland is a septocutaneous artery flap based on the saphenous vessels and great saphenous vein. The use of this flap in 2 patients who required soft tissue coverage is reported herein. The saphenous flap has the advantages of thin and pliable skin, a long and large pedicle, and the technical possibility of combination with the sartorius muscle, sensory nerve, and the femur or tibia. Donor defects are usually closed directly and cause no functional limitations. This flap is useful for the coverage of thin defects that require mobility, especially in the extremities or the intraoral region. It also could be used for the reconstruction of various types of organ losses (e.g., as a motor providing musculocutaneous flap, an osteocutaneous flap involving the femur or the tibia, and/or a vascularized nerve graft).

Aged↗

Nitroprusside inhibits neurotransmitter release at the frog neuromuscular junction.

Sodium nitroprusside (SNP), when applied at concentrations ranging from 0.01 microM to 1.0 mM, reduced endplate potentials in sartorius muscle fibers of the frog (Rana pipiens) by a mean of 57% (range 37-79%). Using quantal analysis, this reduction was shown to be predominantly, if not exclusively, due to a reduction in neurotransmitter release rather than a decrease in postsynaptic sensitivity. Inhibition of neuromuscular transmission was not observed if the preparation was pretreated with bovine hemoglobin prior to the addition SNP nor if 'old' SNP solutions, in which the SNP had decomposed for at least 24 h, were applied. These results suggest that nitric oxide inhibits the evoked release of neurotransmitter at the frog neuromuscular junction.

Animals↗

Extensile medial approach to the femur.

A proposed extensile medial approach to the medial surface of the shaft of the femur was studied on 30 cadaver thighs. The incision is made along a line extending from the mid inguinal point to a point one-third the distance from the adductor tubercle to the medial side of the patella. After mobilizing the sartorius muscle posteromedially, the medial femur is exposed by a three-step technique. Step I involves bluntly defining the internervous plane distally between the vastus medialis muscle and the adductor magnus tendon until limited proximally by the distal end of the vastoadductor membrane at an average of 9 cm from the adductor tubercle. In step II blunt dissection between the vastus medialis and the adductor longus muscles is carried from proximal to distal until limited by the proximal end of the vastoadductor membrane. Now the well-defined vastoadductor membrane area ("danger zone") measuring 6 cm in length on average is safely dealt with (step III) and the medial femur is exposed. Distal extension can be made to expose the knee joint. The approach can be extended proximally to the lesser trochanter between the vastus medialis and both the adductor brevis and pectineus muscles. Anatomic measurements in relation to the adductor tubercle and cross-sections of the thigh were made to better describe anatomic constants and variables in this rather unfamiliar medial thigh area.

Cadaver↗

Repair of a huge defect of the gluteal region by rotation of a combined tensor fasciae latae-sartorius myocutaneous flap.

Although the tensor fasciae latae myocutaneous flap is convenient for covering some defects in the gluteal region, it is not suitable to repair a huge defect because of its limited area. Based on the close relationship of the sartorius and the tensor fasciae latae at their origins and blood supply, the authors designed a myocutaneous flap containing both the tensor fasciae latae and the sartorius muscles and their skin territories with an area exceeding 800 cm2. Two successfully repaired patients are reported. The flaps provide normal sensitivity. The vascular pedicle has a reliable anatomy, being easily dissected, and averages 4.6 to 5.8 cm in length. Both muscles are expendable. There is little functional difficulty for hip joint after the operation.

Aged↗

Lateral femoral cutaneous nerve: an anatomic study.

The purpose of our study was to determine the location of the lateral femoral cutaneous nerve and its branches at the inguinal ligament and proximal thigh. We think that further defining the location of the nerve and its branches based on certain measurements from known anatomic landmarks would enable us to determine a danger zone that could aid in preventing iatrogenic injury to the lateral femoral cutaneous nerve. The anatomic course of the lateral femoral cutaneous nerve was studied in 29 cadaver specimens and distances from various landmarks were recorded. In addition, the branching pattern of the nerves was recorded. We observed variability in the course and branching patterns of the lateral femoral cutaneous nerve. The lateral femoral cutaneous nerve was found to potentially be at risk as far as 7.3 cm medial to the anterior superior iliac spine along the inguinal ligament and as much as 11.3 cm distal on the sartorius muscle from the anterior superior iliac spine. As many as five branches of the lateral femoral cutaneous nerve were found and in 27.6% of cases the lateral femoral cutaneous nerve branched before traversing the inguinal ligament. We used this information to describe a danger zone, which could be used as a guide to help prevent unnecessary injury during certain procedures.

Adult↗

Modified radical inguinal lymphadenectomy for carcinoma of the penis: technique and results.

PURPOSE: Modified radical inguinal lymphadenectomy for carcinoma of the penis is presented that satisfies the requirement for complete groin dissection, while significantly decreasing postoperative complications. MATERIALS AND METHODS: Eight patients with squamous cell carcinoma and 2 with leiomyosarcoma of the penis underwent bilateral modified inguinal lymphadenectomy, including removal of the superficial and deep inguinal lymph nodes. To avoid damage to the vessels of the groin region that run parallel to the inguinal ligament and lie in the fat of the superficial layer of the superficial fascia dissection is done beneath this layer. The proper cleavage plane is just above the membranous layer of the superficial fascia, beneath which the superficial inguinal lymph nodes are located. The saphenous vein is preserved and the sartorius muscle is left in situ, so as not to disturb collateral lymphatic drainage. RESULTS: At a followup of 6 to 104 months no skin necrosis, infection or deep venous thrombosis occurred. In 2 patients early moderate lymphedema of the lower extremities resolved with time, 2 had scrotal edema and 3 had a transient lymphocele. CONCLUSIONS: As described, modified radical inguinal lymphadenectomy decreases the morbidity associated with groin dissection, while removing superficial and deep inguinal lymph nodes.

Adult↗

Free microdissected thin groin flap design with an extended vascular pedicle.

BACKGROUND: The senior author has developed a method of microdissection whereby a thin perforator flap can be elevated accurately in a single-stage procedure. Recently, the authors also applied the microdissection technique to the inguinal area and elevated microdissected thin groin flap. METHODS: In preparation of the flap, the perforator penetrating the fascia of the sartorius muscle is initially detected suprafascially, and then the deep adipose and subfascial layer of the inguinal area is dissected using an operating microscope. After confirming the distribution of the blood vessels in this area, the flap is elevated while dissection is performed between the deep and superficial adipose layers. RESULTS: Six cases of scar contracture or skin defect by general burn, three cases of other types of traumatic tissue defects, and one case of skin loss at the donor site of an extended wraparound flap were successfully reconstructed with these new flaps. CONCLUSIONS: The uniform thinness and long vascular pedicle are distinctive characteristics of this flap compared with the traditional groin flap. Moreover, the buried vessels in the deep adipose layer and fascia can be confirmed by microdissection; this enables prediction of the safe area of the flap.

Adipose Tissue↗

Differential effects of an L-type Ca2+ channel antagonist on activity- and phosphorylation-enhanced release of acetylcholine at the neuromuscular junction of the frog in vitro.

The effects of the selective L-type Ca(2+)-channel antagonist nimodipine on changes in the electrophysiological correlates of acetylcholine release induced by activity in the motor nerve or by inhibition of protein dephosphorylation were studied in the isolated sartorius muscle of the frog. Nimodipine (1 microM) had no effect on basal miniature endplate potential (mEPP) frequency or on the quantal content of the endplate potential (EPP) evoked at 0.33 Hz. Stimulation of the motor nerve at frequencies of 20, 40 and 50 Hz progressively increased the quantal content and at 50 Hz caused an increase in mEPP frequency measured at the end of the train. Nimodipine (1 microM) had no effect on the change in either parameter caused by activity in the motor nerve. The L-channel agonist BAYK 8644 had inconsistent effects, causing at 0.33 Hz an increase in quantal content at 55% of the neuromuscular junctions examined. Application of the phosphatase inhibitor okadaic acid (1 microM) caused an increase in miniature endplate potential and/or current [mEPP(C)] frequency but not in quantal content. The increase in spontaneous frequency was reduced by the Ca(2+)-channel blockers nimodipine (1 microM) and cadmium (75 microM). The amplitude of mEPP(C)s was increased by okadaic acid (1 microM), but neither the decay time constant of miniature endplate currents (mEPC) nor the amplitude of endplate currents evoked by iontophoretic application of carbachol was so altered. The activity of electric eel acetylcholinesterase was unchanged by okadaic acid. The present data do not support the concept that the recruitment of normally silent L-type Ca(2+)-channels contributes to activity-dependent increases in acetylcholine release. The results obtained with okadaic acid suggest that protein phosphorylation and dephosphorylation may regulate the activity of L-type channels and the packaging of acetylcholine.

Acetylcholine↗

ACTIONS OF MECAMYLAMINE, DIMECAMINE, PEMPIDINE AND THEIR TWO QUATERNARY METHO-SALTS AT THE NEUROMUSCULAR JUNCTION.

Mecamylamine, dimecamine and pempidine differed in neuromuscular-blocking activity on the isolated phrenic nerve-diaphragm preparation of the rat from the corresponding methiodides by a factor of less than two. It was concluded that the active component of each amine was the cation acting extracellularly. The finding that the neuromuscular-blocking activity of mecamylamine at pH 6.7 was similar to the activity at pH 7.7 did not refute this conclusion. Mecamylamine, dimecamine methiodide, dimecamine and pempidine, at concentrations insufficient to cause block, could increase the twitch response of the rat diaphragm; the ability to do this increased in the above order. With pempidine (the most active compound) this effect, on the isolated sartorius muscle of the frog, was a direct action. During steady partial block by each of the compounds, the responses to brief tetanic stimulation, to neostigmine and to an increase in calcium concentration were similar to those observed during block by tubocurarine. From indirect evidence, pempidine methiodide appeared both to enhance the release of acetylcholine from motor-nerve terminals and to cause postsynaptic block.

Abdominal Muscles↗

Prostaglandin E1 and noradrenaline at the neuromuscular junction.

The effects of prostaglandin E(1) (PGE(1)) on neuromuscular transmission in the frog nerve-sartorius muscle preparation were studied with intracellular recording techniques. PGE(1) was inactive in all concentrations examined; both spontaneous miniature end-plate potentials and evoked end-plate potentials were unchanged after preparations were bathed in up to 2.2x10(-5)M (8 mug/ml) PGE(1). PGE(1) did not prevent the increase in end-plate potential amplitude which frequently occurred on addition of noradrenaline to the bathing solution.

Animals↗

Barbiturate-induced transmitter release at a frog neuromuscular junction.

1. The influence of barbiturates on neuromuscular transmission at end-plates of frog sartorius muscles was investigated electrophysiologically on preparations bathed in Ringer solution containing a low concentration of calcium and a high concentration of magnesium.2. Effects of a convulsant barbiturate, 5-(2-cyclohexylideneëthyl)-5-ethyl barbituric acid (CHEB), were compared with those of phenobarbitone.3. CHEB and phenobarbitone increased the mean quantum content of the end-plate potentials and decreased the mean amplitude of the miniature end-plate potentials.4. Both barbiturates enhanced the duration of the nerve-terminal action potential and had little or no effect on the effective resistance of the skeletal muscle membrane.

Action Potentials↗

Interaction of competitive antagonists: the anti-curare action of hexamethonium and other antagonists at the skeletal neuromuscular junction.

1. In the rat isolated diaphragm preparation hexamethonium and other low potency competitive antagonists of acetylcholine (ACh), including gallamine and hyoscine butylbromide, reverse block by the potent antagonists tubocurarine, pancuronium and alcuronium. 2. In the presence of tubocurarine, hexamethonium increases the amplitude of the end-plate potential without increasing the quantal content. It enhances the response to ACh applied iontophoretically to the end-plate but does not enhance the response to ACh applied in the bath. 3. The anti-curare effect of hexamethonium is abolished in the diaphragm of the rat, guinea-pig and mouse by inhibitors of acetylcholinesterase. The effect is not observed in the indirectly stimulated toad sartorius muscle. 4. The effect is explained if tubocurarine does not dissociate appreciably in the time taken for ACh to achieve high occupancy of receptors, so that a fraction of receptors is completely excluded from occupation by ACh. Equilibration with hexamethonium reduces the fraction excluded by tubocurarine and the transmitter now competes with hexamethonium for more receptors and produces a larger response. 5. On the basis of this explanation the half-time for dissociation of tubocurarine must be about 1 millisecond. It follows that tubocurarine does not act competitively with ACh at synapses when transmitter action is sufficiently brief, and that its binding to the receptor is probably diffusion-limited.

Acetylcholine↗

The effects of tetraphenylboron on neuromuscular transmission in the frog.

1 The effect of tetraphenylboron (TPB) were studied on the frog sciatic nerve-sartorius muscle preparation. 2 TPB (0.01-1 mM) blocked indirectly elicited twitches of the preparation. 3 TPB (0.01-0.1 mM) produced no depolarization but lowered membrane resistance. TPB increased miniature endplate potential (m.e.p.p.) frequency, the rate of rise of the endplate potential (e.p.p.), and slowed the rate of rise and rate of fall of the muscle action potential. 4 In Mg2+ solutions the quantal content of e.p.ps was initially increased by TPB (0.01 mM). This was followed by a decrease of e.p.p. and m.e.p.p. amplitudes, accompanied by a lack of e.p.p. failures. 5 Larger concentrations of TPB (0.1 mM) produced an increase in e.p.p. amplitude followed by the sudden abolition of e.p.ps. This effect was associated with abolition of the nerve terminal spike. 6 TPB (0.1 mM) exhibited no postjunctional blocking action. 7 The results indicate that TPB acts prejunctionally, initially causing an increased release of acetylcholine. Subsequently, transmitter output is reduced by a reduction of quantal size.

Action Potentials↗

The effects of tetraphenylboron on spontaneous transmitter release at the frog neuromuscular junction.

1 The effects of tetraphenylboron (TPB) on spontaneous transmitter release were studied in the frog sartorius muscle preparation. 2 TPB (0.001-1 mM) produced a time-dependent increase in miniature endplate potential (m.e.p.p.) activity that was not sustained. TPB (0.1 mM) produced similar effects on m.e.p.p. frequency in normal Ringer solutions, in the absence of Ca2+ or Cl- and in the presence of excess Ca2+ and of tetrodotoxin. The effect of TPB (0.01 mM) was reduced but not abolished in the absence of Ca2+. 3 As m.e.p.p. frequency fell from its peak level in TPB (0.04 mM) m.e.p.p. amplitude was reduced. The reduction of m.e.p.p. amplitude was not prevented by choline (30-300 muM). 4 When m.e.p.p. activity fell below the noise level in the presence of TPB (0.1 mM), lanthanum (0.5 mM) was ineffective in promoting measurable m.e.p.p. activity. 5 The effects of TPB were slowly reversible by washing. 6 The results indicate that TPB acts to reduce the nerve terminal stores of acetylcholine, probably by a combination of rapid release and concomitant inhibition of transmitter storage.

Action Potentials↗

Central respiratory and circulatory depression caused by intravascular saxitoxin.

1 In cats anaesthetized with pentobarbitone and vagotomized, observations were made on the phrenic nerve action potential and the diaphragm electromyogram (EMG) at constant end-tidal Pco(2). Arterial blood pressure was stabilized by intravenous infusions of noradrenaline.2 Intravenous administration of saxitoxin (STX) initially abolished respiratory activity in the EMG and caused a slowing of oscillation in the central phrenic neurogram. Additional STX produced apneustic phrenic discharges followed by a progressive loss of nerve action potentials.3 The inspiratory centre in the medulla oblongata was stimulated electrically to evoke a sustained phrenic nerve discharge. STX, given intravenously, resulted in the elimination of spontaneous nerve activity without interfering with the evoked response.4 The cephalic intravascular infusion of STX into a carotid or vertebral artery depressed spontaneous respiratory activity while sparing EMG activity evoked by electrical stimulation of the intact phrenic nerve.5 Spontaneous respiratory discharge in the phrenic nerve was eliminated by smaller doses of STX administered intra-arterially than were required intravenously. In addition, onset of and recovery from neural silence occurred faster following intra-arterial injection of STX.6 Depressant effects on arterial blood pressure coincided with those on respiration when STX was given intra-arterially.7 An electrophysiological assay on frog sartorius muscle was used to measure STX in the cerebrospinal fluid. Levels of STX detected were proportional to amounts of the toxin infused intra-arterially.8 It is concluded that STX exchanges rapidly between blood and brain to bring about central depression and this adds to its peripheral paralytic actions.

Animals↗