Depression Of Tension Research Articles

Adenosine and amrinone reverse felypressin-induced depression of myocardial tissue oxygen tension in dogs.

To determine whether continuous infusion of adenosine triphosphate (ATP), nitroglycerin (NTG) or amrinone (AM) would ameliorate the reductions in coronary blood flow (CBF) and myocardial oxygen tension (PmO2) induced by felypressin. Seven open-chest dogs were studied under urethane and alpha-chloralose anesthesia. Hemodynamic variables including heart rate (HR), systolic blood pressure, diastolic blood pressure (DBP), mean pulmonary artery pressure, pulmonary capillary wedge pressure, CBF (ultrasound flowmetry), PmO2(polarography) and cardiac output (thermodilution method) were recorded. Felypressin was infused in a loading dose of 6 mIU x kg(-1) for five minutes and then continued at 0.2 mIU x kg(-1) x min(-1). After 30 min felypressin infusion, each agent was administered for 15 min to evaluate hemodynamic changes. Infusions were 100 and 200 microg x kg(-1) x min(-1) for ATP, 2.5 and 5 microg x kg(-1) x min(-1) for NTG, and 10 and 20 microg x kg(-1) x min(-1) for AM. After felypressin DBP increased by 17 +/- 5 (mean +/- SD) %; CBF decreased by 49 +/- 9%; CI decreased by 40 +/- 13%; HR decreased by 29 +/- 11%; PmO2 in the inner layer decreased by 21 +/- 7%. The Cl and CBF returned to baseline afterATP 100 and 200 microg x kg(-1) x min(-1), AM 10 and 20 microg x kg(-1) x min(-1), but not after NTG. The PmO2 in the inner layer returned to the baseline value by any infusion except for NTG 5 microg x kg(-1) min(-1) Adenosine and amrinone, but not nitroglycerin reverses the adverse cardiovascular effects of felypressin.

WATER MOVEMENT CAUSED BY SPREADING SURFACTANTS IN UNSATURATED SYSTEMS OF PARTICLES OF NONUNIFORM SIZE

The movement of water originated by the spreading of two surfactants was analyzed in glass beads as well as on soil systems, both of particles of nonuniform size The higher difference of surface tension produced in the system by 1 -hexadecanol compared to that of 1-tetradecanol led therefore to a higher amount of water moved. Decreased proportion of the smaller sized particles in glass beads system produced a decrease in the total water moved by both surfactants. Organic matter acted in soil as a second surfactant in glass beads. This effect was compared in glass beads systems once 1-hexadecanol was evenly distributed among the particles as continuous film, which played a role alike that of organic matter in soil and then a second surfactant 1-tetradecanol was added. These additional surfactant effect diminished the difference between initial and final surface tension (surface tension depression) of the system and so the total water moved. The soil organic matter (1.7%) modified the water movement curve in the presence of low (0.2g) content of 1-hexadecanol, whereas for high content of either alcohol (0.4g) or low content of 1-tetradecanol content (0.2g) the water movement curves were the same

Mechanism of action of sodium cyanide on rat diaphragm muscle.

The effects of sodium cyanide (NaCN) were investigated on the contractile and electrophysiological properties of rat diaphragm muscles in vitro. Sodium cyanide (0.1-1.0 mM) produced an initial potentiation of directly elicited twitch tensions, followed by a slow progressive depression. The potentiation and depression were both dependent on the NaCN concentration and stimulation frequency. Muscles exposed to NaCN exhibited marked reductions of creatine phosphate concentration, but ATP levels were not significantly lowered. Sodium cyanide had no effect on the resting potential, input resistance or action potential, indicating that the toxicity of the metabolic inhibitor is not mediated by alterations of membrane excitability or passive electrical properties. Sodium cyanide reduced the amplitude of contractures elicited by 70 mM K(2)SO(4), suggesting that the actions of NaCN cannot be explained by a failure of action potentials to propagate across the muscle surface or within t-tubular membranes. Sodium cyanide suppressed the first phase of the caffeine contracture, an observation consistent with an impaired release of, or reduced sensitivity to, sarcoplasmic reticular Ca(2+), but did not alter the amplitude of the second phase, which represents rigor following ATP depletion. These results, in conjunction with those of previous studies, suggest that the depression in muscle tension following exposure to NaCN may result from alterations in Ca(2+) homeostasis, intracellular acidosis or from accumulation of one or more products of phosphocreatine breakdown.

Solubility effects on surfactant-induced unsaturated flow through porous media

It has been demonstrated that local surface tension depression due to the presence of an insoluble surfactant, myristyl alcohol, can result in capillary pressure gradients that cause significant flow in unsaturated porous media. We hypothesized that the effects of a soluble surfactant, butanol, would differ from those of myristyl alcohol despite the fact that both give a similar reduction in the surface tension of water. We investigated this hypothesis through a series of horizontal column experiments and unsaturated flow modeling. We found that both surfactants induced water flow from regions of high surfactant concentration to regions of low concentration but that the shapes of the resultant moisture content profiles were fundamentally different. Because surface tension depression from myristyl alcohol was confined to the original source zone, we were able to simulate the system using a standard unsaturated flow model by assigning separate sets of hydraulic functions to the initially clean and source zones. Modeling showed that the redistribution of water due to the initial surfactant-induced capillary pressure gradient created moisture content induced capillary pressure gradients which acted to balance the system over time. The moisture content profile within the butanol system indicated a propagation of the zone of reduced surface tension. Because the surface tension of water is a function of solute concentration, surfactant-induced capillary pressure gradients are expected to remain and influence the flow system as long as concentration gradients exist.

Static and dynamic surface tension of dilute polyelectrolyte solutions

The surface tension of aqueous solutions of Polymer JR400, the chloride salt of a trimethylammonium derivative of hydroxyethyl cellulose, has been measured as a function of polymer concentration. Axisymmetric drop shape analysis profile has been employed to record the dynamic surface tension response of the solutions to a sawtooth-shaped variation in the surface area. Dilute solutions of the polymer (concentration <0.05 wt%) exhibited an elevation of the surface tension of water, from 71.9 to 72.7 mJ m −2 (23°C) under both static and dynamic conditions. Under the latter, elevations of as much as 3 mJ m −2 were observed during the surface contraction cycle. Solutions of concentrations higher than 0.05 wt% recovered the more conventional behavior of water surface tension depression and, in the dynamic measurement mode, decreases in the surface tension during the contraction cycle.

Effects of extracts of seed and leaf of Piper guineense on skeletal muscle activity in rat and frog.

The pharmacological effects of leaf and seed extracts of Piper guineense were investigated on phrenic nerve hemidiaphragm activity following electrical stimulation in vitro. The Leaf and seed extracts (10 micrograms-1 mg/mL) and (50-800 micrograms/mL) respectively produced biphasic effects consisting of an initial enhancement followed by secondary transient or prolonged depression of twitch tension in response to electrical stimulation of both muscle and nerve. These effects were similar to that of decamethonium (2-800 mg/mL). An increased concentration of extracellular Ca2+ in vitro reversed the twitch contraction inhibited by the leaf and seed extracts in a dose related pattern following electrical stimulation. It is concluded that the leaf and seed extracts of Piper guineense possess among other pharmacological properties, a depolarizing neuromuscular blocking action.

Physical Model Studies on Slag Foaming.

A physical modelling investigation has been undertaken to determine the relationship between the physico-chemical properties of the liquid phase, the gas bubble size, the gas flux, and the residence times of gas in spherical foams. The testwork was conducted in a 107 mm diameter glass column in a temperature controlled environment. The foams were generated by the injection of compressed air into solutions of distilled water and glycerol. Water glycerol solutions were used to obtain a wide range of liquid viscosities. The strongly adsorbing surfactant, sodium dodecylbenzene sulphonate, was added to the water–glycerol solutions so that the surface tensions of the solutions could also be controlled. The experimental results show that the residence times of gas bubbles in the foam increase with increasing liquid viscosity and increasing surface tension depression, and with decreasing gas bubble size. Furthermore, a transition from a foaming to a non-foaming regime was observed as the mean gas bubble diameter increased above 5 mm.

The effects of a soluble surfactant on quadrupole shape oscillations and dissolution of air bubbles in water

Single air bubbles were ultrasonically trapped in aqueous solutions of the soluble surfactant Triton X-100. Quadrupole shape oscillations were induced by modulation of the radiation pressure and the free decay was recorded using an optical extinction technique. The frequency and damping were found to be maximal at a bulk surfactant concentration which only weakly affects the surface tension. At higher concentrations the frequency is reduced due to surface tension depression and the damping approaches a value several times that expected for a clean interface. These results are in qualitative agreement with theoretical predictions based on interfacial viscoelastic considerations. Bubble size and dissolution curves were obtained through the use of digitized bubble images. Dissolution rates are shown to be significantly enhanced by the presence of the surfactant.

Effects of oil and other surface-active organic pollutants on aquatic birds

A variety of organic contaminants can potentially have impact on aquatic birds by their affecting surface tension. Avian plumage constitutes a porous barrier to water and the air trapped between the feathers serves as thermal insulation. When the air is displaced, the birds expend extra energy to maintain a normal body temperature, but this response cannot be sustained for long, especially at low environmental temperatures. When energy stores are depleted, hypothermia and death ensue. Surface tension is the force that resists infiltration of water into the plumage. The critical surface tension for feather wetting is conservatively estimated to be in the range 38–50 mN m-1. The hypothesis that surface-active organic contaminants can have significant detrimental effects on aquatic birds was evaluated. New data obtained in a study of water penetration pressures in Lesser Scaup contour feathers show that the 'wettability safety factor' is reduced by about half during moult. That is, the critical surface tension was raised to approximately 49–58 mN m-1 in moulting Lesser Scaup. The energetic and behavioural effects of oil contamination are reviewed, and it is concluded that even small quantities of organic material may confer significant physiological cost. The available data generally support the hypothesis that waterfowl face a potential risk associated with chronic or periodic mild depression of water surface tension due to organic pollutants, including oils and detergents. However, much of the evidence is indirect and further research, especially long-term assessment of surface tension in marine, estuarine and freshwater habitats, is needed to determine whether a real environmental problem exists.

Priming with rocuronium accelerates the onset of neuromuscular blockade

Study Objective: To investigate the effects of priming rocuronium on the time course of neuromuscular blockade. Design: Prospective, controlled, randomized clinical study. Setting: University teaching hospital. Patients: 42 ASA physical status I and II patients undergoing peripheral surgery with general anesthesia. Interventions: Following a standardized propofol-fentanyl induction, patients in Group 1 (n = 21) received a priming dose of rocuronium 0.06 mg/kg followed two minutes later by an intubating dose of rocuronium 0.54 mg/kg. Patients in Group 2 (n = 21) received a saline placebo injection followed two minutes later by rocuronium 0.6 mg/kg. Anesthesia was maintained with isoflurane and nitrous oxide 60% in oxygen. Measurements and Main Results: Neuromuscular function was assessed at the wrist using mechanomyography with a single-twitch mode of stimulation at a frequency of 1 Hz until tracheal intubation and at 0.1 Hz thereafter. The times from injection of the intubating dose of rocuronium until 95% suppression of the twitch tension (onset time), recovery of twitch tension to 25% of control (clinical duration of action), and the time from 25% to 75% spontaneous recovery of twitch tension (recovery index) were recorded. The trachea was intubated at 95% depression of the twitch tension and the intubating conditions were graded using a 3-point scale. The onset times with priming rocuronium (34 ± 6 s) were significantly shorter ( p < 0.01) than those without priming (59 ± 14 s). The intubation conditions were similar in the two groups; however, the intubating times with priming were significantly shorter. The clinical duration of action and the recovery index did not differ significantly between the two groups. Conclusions: Priming rocuronium decreased the onset times and thus, the intubating times without increasing the clinical duration of action or recovery index.

Pharmacokinetic–Pharmacodynamic Modeling of Mivacurium in Rats

The pharmacokinetic (PK) and pharmacodynamic (PD) characteristics of the neuromuscular blocking agent mivacurium were evaluated separately in two groups of rats receiving 0.6mg kg−1 of mivacurium in a 2.5-min intravenous continuous (iv) infusion. The PK parameters for mivacurium were determined in the first group. A two-compartment model describes the kinetics of mivacurium in plasma. The estimates of the apparent volume of distribution at steady-state and plasma clearance [mean(SE)] were 650 (123) mL kg−1 and 9.9 (0.75) mL min−1 kg−1, respectively. In the second group, the evoked tibialis anterior muscle tension was monitored. The PK parameters derived from the first group were used to compute mivacurium plasma concentrations (C) at the times the PD measurements were recorded in the second group. The concentration–neuromuscular effect [% depression of initial twitch tension (E)] relationship was analyzed by two approaches. (1) The relationship of estimated effect site concentrations versus E; a sigmoidal Emax model described the effect compartment concentrations versus E relationship. The estimate [mean(SE)] of Cess50 (steady-state plasma concentration eliciting half of maximum E) was 0.65 (0.01) µg mL-1. The value [mean- (SE)] of keo (rate constant of equilibration between plasma and effect site) was estimated at 0.32 (0.03) min−1. (2) The relationship of descending limb C versus E; a sigmoidal Emax model described such relationship. The estimate [mean(SE)] of C50 (post-infusion Celiciting half of maximum E) was 0.57(0.03) µg mL−1. The PD properties of mivacurium were also evaluated in another two groups of animals receiving either 5- or 10-min continuous iv infusion; PK and PD parameters obtained from the 2.5-min infusion experiments were used to predict the time course of E in the groups receiving 0.6mg kg−1 of mivacurium in 5- and 10-min infusions; simulations using the estimated parameters adequately describe the time course of E in those groups. The effect of mivacurium on the mean arterial blood pressure (MAP) was also investigated; a 10% nonsignificant decrease (p>0.05) in MAP was found in all groups.

Effects of hydrostatic pressure on fatiguing frog muscle fibres.

Effects of increased hydrostatic pressure (range 0.1-10 MPa) on isometric twitch and tetanic contractions of single, intact, frog muscle fibres were examined at 4, 11 and 21 degrees C and at different stages of fatigue. Twitch tension was potentiated by pressure at all temperatures, but the extent of potentiation was more pronounced at higher temperatures (34% MPa-1 at 21 degrees C, compared to 8% MPa-1 at 4 degrees C). Tetanic tension was depressed by pressure at 4 degrees C (approximately 0.7% MPa-1) but was potentiated by pressure at 21 degrees C (approximately 0.4% MPa-1). The effect of hydrostatic pressure on the tetanic tension was dependent on the fatigue status of the muscle fibre: during the early stages of fatigue (when tetanic tension was depressed by < 20%), high pressure produced a tension depression (as in an unfatigued muscle fibre), whilst during the later stages of fatigue high pressure induced a significant potentiation of tetanic. Our results support the suggestion that excitation-contraction coupling and contractile activation are impaired during late fatigue. Pressure-effects were basically similar to caffeine-effects under a variety of conditions, suggesting that an enhancement of Ca2+ release may be contributory to potentiation of twitch tension and, in severely, fatigued muscle, potentiation of tetanic tension. In the rested state and during early fatigue the main effect of pressure is an inhibition of the crossbridge cycle.

Effects of external calcium on contractile responses in rat extensor digitorum longus muscles after sciatic nerve injury at birth

Two types of nerve lesions were performed at birth in rat extensor digitorum longus muscle: sciatic nerve transection (group A) and sciatic nerve crush allowing further reinnervation (group B). Contractile responses were then studied at different times after the denervation (7, 14, 30, and 60 days) and compared with control. Sixty days after the intervention, twitch and tetanic tensions remained dependent upon the extracellular Ca2+ concentration ([Ca]o) both in groups A and B. However, the depression of tensions following Ca2+ withdrawal was more important in group A. Sixty days after birth, in the presence of a Ca2+ channel blocker, Cd2+ (2 mmol L-1), a depression of the twitch tension was observed in group A (similarly to control 1-7 days postnatal muscles), whereas Cd2+ potentiated twitch tension in group B (similarly to control 14-60 days postnatal muscles). After glycerol treatment (detubulating procedure) performed in 60-day-old muscles, twitch tension was abolished in group B and control, whereas twitch tension was potentiated in group A. Thus, in developing muscles, neural control could be involved in the dependence of contractility toward [Ca]o. These results may be relevant for the understanding of the contractile properties of neuromuscular disorders with early onset.

Effect of Oxygen Free Radicals on Cardiac Contractile Activity and Sarcolemmal Na+–Ca2+ Exchange

BACKGROUND: Although oxygen free radicals have been shown to induce myocardial cell damage and cardiac dysfunction, the exact mechanism by which these radicals affect the heart function is not clear. Since the occurrence of intracellular Ca(2+) overload is critical in the genesis of cellular damage and cardiac dysfunction, and since the sarcolemmal Na(+)-Ca(2+) exchange is intimately involved in Ca(2+) movements in myocardium, this study was undertaken to examine the effects of oxygen free radicals on the relationship between changes in cardiac contractile force development and sarcolemmal Na(+)-Ca(2+) exchange activity. METHODS AND RESULTS: Isolated rat hearts were perfused with a medium containing xanthine plus xanthine oxidase for different times, and changes in contractile force as well as sarcolemmal Na(+)-(2+) exchange activity were monitored. Perfusion of the heart with xanthine plus xanthine oxidase resulted in a transient increase followed by a marked decrease in contractile activity; the resting tension was markedly increased. The xanthine plus xanthine oxidase-induced depression in developed tension, rate of contraction, and rate of relaxation, except the transient increase in contractile activity, was prevented by the addition of catalase, but not by superoxide dismutase, in the perfusion medium. A time-dependent depression in sarcolemmal Na(+)-Ca(2+) was also evident upon perfusing the heart with xanthine plus xanthine oxidase. This depression in Na(+)-dependent Ca(2+) uptake was associated with a decrease in the maximal velocity of reaction without any changes in the affinity of Na(+)-Ca(2+) exchanger for Ca(2+). The presence of catalase, unlike superoxide dismutase, prevented the decrease in sarcolemmal Na(+)-Ca(2+) exchange activity in hearts perfused with xanthine plus xanthine oxidase. CONCLUSIONS: The results support the view that a depression in the sarcolemmal Na(+)-Ca(2+) exchange activity may contribute to the occurrence of intracellular Ca(2+) overload and subsequent decrease in contractile activity. Furthermore, these actions of xanthine plus xanthine oxidase in the whole heart appear to be a consequence of H(2)O(2) production rather than the generation of superoxide radicals.

The ageing spontaneously hypertensive rat as a model of the transition from stable compensated hypertrophy to heart failure.

Spontaneously hypertensive rats (SHR) of advanced age exhibit depressed myocardial contractile function and ventricular fibrosis, as stable compensated hypertrophy progresses to heart failure. Transition to heart failure in SHR aged 18-24 months was characterized by impaired left ventricular (LV) function, ventricular dilatation, and reduced ejection fraction without an increase in LV mass. Studies of papillary muscles from SHR with failing hearts (SHR-F), SHR without failure (SHR-NF), and age-matched Wistar Kyoto (WKY) rats allowed examination of changes in the mechanical properties of myocardium during the transition to heart failure. Papillary muscles of SHR-F exhibited increased fibrosis, impaired contraction, and decreased myocyte fractional area. These findings in papillary muscles were correlated with a higher concentration of hydroxyproline and increased histological evidence of fibrosis in the LV free wall. While a depression in active tension accompanied these structural alterations in papillary muscles, it was not evident when active tension was normalized to myocyte fractional area. Together, these data suggest that individual myocyte function may be preserved but that myocyte loss and replacement by extracellular matrix contribute substantially to the decrement in active tension. An absent or negative inotropic response to isoproterenol is observed in SHR-F and SHR-NF papillary muscles and may result in part from age-related alterations in beta-adrenergic receptor dynamics and a shift from alpha- to beta-myosin heavy chain (MHC) protein. During the transition to failure, ventricles of SHR exhibit a marked increase in collagen and fibronectin mRNA levels, suggesting that an increase in the expression of specific extracellular matrix genes may contribute to fibrosis, tissue stiffness, and impaired function. Transforming growth factor-beta 1 (TGF-beta 1) mRNA levels also increase in SHR-F, consistent with the concept that TGF-beta 1 plays a key regulatory role in remodelling of the extracellular matrix gene during the transition to failure. The renin-angiotensin-aldosterone system is also implicated in the transition to failure: SHR treated with the angiotensin converting enzyme inhibitor captopril starting at 12 months of age did not develop heart failure during the 18-24 month observation period. Captopril treatment that was initiated after rats were identified with evidence of failure led to a reappearance of alpha-MHC mRNA but did not improve papillary muscle function. Research opportunities include investigation of apoptosis as a mechanism of cell loss, delineation of the regulatory roles of TGF-beta 1 and the renin-angiotensin-aldosterone system in matrix accumulation, and studies of proteinase cascades that regulate matrix remodelling.

Resistance to atracurium in rats with experimental inflammation: role of protein binchng

The influence of altered protein binding on the neuromuscular effect of atracurium has been studied in rats with experimental inflammation induced by subcutaneous injection of turpentine oil. Doses of atracurium ranging from 0.45 to 1.5 mg.kg-1 were administered to control (n = 30) and to experimental inflammation induced rats (n = 30). Neuromuscular transmission was monitored by recording the twitch tension of the tibialis-anterior muscle elicited by stimulation of the sciatic nerve. Three effect parameters were recorded: (i) intensity of the effect, measured as percentage depression of baseline twitch tension, (ii) duration of drug action (min) and (iii) recovery time (min). The dose-intensity of the effect relationship was modelled using a sigmoid Emax model. The ED50 (effective dose eliciting 50% of the maximum effect) was significantly increased (P < 0.01) in the inflammation group as compared to the control group (0.94 vs. 0.68 mg.kg-1). This change was reflected in a shift of the dose-response curve to the right in the pretreated rats. For equipotent doses ED95 (defined as the effective dose eliciting 95% of maximum effect), no differences were found in recovery time and duration of action between the two groups of rats. Mucoproteins levels (index of alpha 1-acid glycoprotein (AAG) and protein binding were significantly increased in rats with experimental inflammation as compared to control rats. Based on these results, altered serum protein binding of atracurium appears to be responsible, at least in part, for the resistance to atracurium.

The effect of nickel chloride on the isolated hemidiaphragm of the rat

1. 1. NiCl 2 (cumulative concentrations of 0.56–1.91 mmol 1 −1) produced concentration-dependent depression of tension developed ( Td) and the maximum rate of rise of tension (d T/d t) max) of isometric contraction of the isolated rat hemidiaphragm, during direct subtetanic (DST) electrical stimulation, only. EC 50 values for NiCl 2-induced depression of Td and d T/d t max were 0.88 ± 0.06 and 0.83 ± 0.13 mmol 1 −1, respectively. NiCl 2 did not significantly change either parameter of the isometric contraction during direct single-pulse (DSP) electrical stimulation. 2. 2. Maximal depression of Td and d T/d t max, produced by a single concentration of NiCI 2 (1 mmol 1 −1) during DST electrical stimulation was obtained 20 min after addition of the drug in the bathing medium. 3. 3. In the normal Tyrode solution, addition of CaCl 2 (final concentration of 5.86 mmol 1 −1) almost completely antagonized the depressant effect of NiCl 2 (1 mmol l −1) on Td and d T/d t max during DST electrical stimulation. In the calcium-free solution, the depression both of Td and d T/d t max produced by NiCl 2 (1 mmol 1 −1) was significantly more pronounced in comparison with the effect of NiCl 2 in the normal Tyrode solution. 4. 4. l-calcium channel activator, Bay K 8644 (25 μmol 1 −1), significantly potentiated both Td and d T/d t max during DST electrical stimulation, but NiC1 2 (1 mmol 1 −1) decreased both parameters of the isometric contraction even in the presence of this concentration of Bay K 8644. On the other hand Bay K 8644 (25 μmol 1 −1) did not antagonize NiCl 2-induced depression of Td and d T/d t max. 5. 5. Verapamil (2.5 μmol l −1; 45 min of incubation) and lidocaine (0.10 mmol l −1; 30 min of incubation) significantly potentiated the depression of Td and d T/d t max, produced by NiCl 2 (1 mmol l −1), during DST electrical stimulation. The addition of CaCl 2 (final concentration of 7.20 mmol 1 −1) in the bathing medium only partially antagonized the depressant synergistic action of both verapamil or lidocaine and NiCl 2 on Td and d T/d t max. 6. 6. Forskolin (cumulative concentrations of 2.60–44.20 μmol 1 −1) fully antagonized NiC1 2-induced depression of both Td and d T/d t max; propranolol (1 μmol l −1) did not abolish this antagonizing action of forskolin. Also, NiCl 2 (cumulative concentrations of 0.56–1.54 mmol 1 −1) did not change potentiating effect of forskolin (23.4 μmol 1 −1). 7. 7. In conclusion, NiCl 2-induced depression of both Td and d T/d t max of the isolated rat hemidiaphragm, during DST electrical stimulation could be specific in part, due to the block of calcium influx, and partially non-specific.

The effect of neostigmine on twitch tension and muscle relaxant concentration during infusion of mivacurium or vecuronium.

An investigation suggested that neostigmine may not effectively antagonize mivacurium, presumably because neostigmine impairs mivacurium's metabolism. However, the effect of neostigmine on mivacurium's metabolism in vivo has not been reported. Therefore, the effect of neostigmine on neuromuscular function and plasma mivacurium concentrations during constant mivacurium infusion was determined. Mivacurium was infused in five patients to maintain 90% depression of adductor pollicis twitch tension, then 50 micrograms/kg intravenous neostigmine was administered without altering the mivacurium infusion. Peak twitch tension after neostigmine, plasma cholinesterase activity, and mivacurium concentrations before and after neostigmine were measured. Five additional patients were given 50 micrograms/kg neostigmine to antagonize block due to continuous infusions of vecuronium. Neostigmine produced less antagonism of mivacurium (39 +/- 11%) than of vecuronium (54 +/- 9%, P < 0.05). Neostigmine decreased plasma cholinesterase activity and increased plasma concentrations of the trans-trans and cis-trans stereoisomers of mivacurium (P < 0.05). Neostigmine is less effective at antagonizing the neuromuscular effect of mivacurium than that of vecuronium during constant infusion. Neostigmine increases plasma mivacurium concentrations, likely explaining its limited efficacy. Our results confirm that neostigmine impairs the metabolism of mivacurium in vivo and may explain the observation that neostigmine may not effectively antagonize mivacurium-induced block.

Induction of giant miniature end-plate potentials during blockade of neuromuscular transmission by textilotoxin.

The present study investigated the action of textilotoxin, isolated from the venom of the Australian common brown snake Pseudonaja textilis, on neuromuscular transmission in isolated toad nerve-muscle preparations. Initial muscle twitch tension experiments revealed a triphasic pattern of changes in muscle tension and a irreversible binding action of textilotoxin (10 micrograms/ml) similar to other snake beta-neurotoxins. This was characterised by an initial depression of twitch tension, followed by a period of enhanced tension, eventually leading to a reduction in tension to complete neuromuscular blockade. These actions on muscle tension were investigated further by assessing the action of textilotoxin on end-plate potential amplitude (EPP). This revealed a similar triphasic alteration of the nerve-evoked release of acetylcholine from the motor nerve terminal. These actions on acetylcholine release were confirmed to be of a presynaptic origin since the modal amplitude of miniature end-plate potentials (MEPPs) was not reduced and in twitch tension experiments the muscle still contracted in response to direct muscle stimulation when nerve-evoked release was completely blocked. Interestingly dramatic effects were observed on the spontaneous release of acetylcholine, including an marked increase in MEPP frequency, a skewing of the MEPP amplitude frequency histogram to the right, and a resultant increase in the number of 'giant' MEPPs. These results indicate that textilotoxin causes a presynaptic blockade of neuromuscular transmission involving a disruption of the regulatory mechanism that controls acetylcholine release.

Enhancement of Nucleate Boiling Heat Transfer and Depression of Surface Tension by Surfactant Additives

Enhancement of Nucleate Boiling Heat Transfer and Depression of Surface Tension by Surfactant Additives