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PubMed1983

Potentiation of nerve block in vivo by physiological adjuvants in the solution.

One hundred and seventy-four rats received a standardized 0.4-ml injection into the left infraorbital nerve and all solutions contained lignocaine 0.25 g dl-1. In groups 1-4, the solutions were isoosmotic and contained, besides sodium chloride, potassium chloride 0 or 4 mmol litre-1 and glucose 0 or 20 mmol litre-1 (0 or 360 g dl-1). For groups 5-8, the solutions were hypoosmotic, containing sodium chloride to 0.6 of normal tonicity but were otherwise identical to solutions 1-4. Presence and duration of sensory block were determined from the reflex sublingual electromyographic response to periodic homolateral and contralateral electrical stimulation of the upper lip. In groups 1-4, the presence of potassium chloride 4 mmol litre-1 approximately doubled the duration of blockade (P less than 0.001). Groups 5-8 showed that hypoosmolarity also doubled the duration of block (P less than 0.001), but hypoosmolarity and potassium chloride did not have additive effects. It is concluded that addition of potassium- chloride 4 mmol litre-1 to isotonic solutions of lignocaine is likely to enhance their clinical effectiveness.

Adjuvants, Anesthesia↗
PubMed1996

The effects of sevoflurane on contractile and electrophysiologic properties in isolated guinea pig papillary muscles.

We examined, in guinea pig papillary muscles, whether the negative inotropic effect of sevoflurane is due to the depression of the influx of extracellular Ca2+ or to inhibition of the availability of intracellularly stored Ca2+. Sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normally polarized guinea pig papillary muscles. Sevoflurane produced a depression of contractile force with different rates or patterns of stimulation in the rested state and at low stimulation frequencies. In a potentiated state, sevoflurane did not depress contractile forces. Although sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normal Tyrode's solution, in high K+ Tyrode's solution, it caused a depression of contractile force without a shortening of action potential duration. Sevoflurane also depressed contractile force in normal and high K+ Tyrode's solution with ryanodine 1 microM. Our results suggest that in myocardial contractile force the negative inotropic effect of sevoflurane might be caused by depression of transsarcolemmal Ca2+ influx, accompanied by shortening of the action potential duration.

Action Potentials↗
PubMed1996

The direct effects of propofol on myocyte contractile function after hypothermic cardioplegic arrest.

Propofol is being used more often in cardiac surgery, particularly after hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose of this study was to examine the effects of propofol on isolated myocyte contractile function under both normothermic conditions and after simulated HHCA and rewarming. Myocytes were isolated from the left ventricle of eight pigs. Myocyte contractile function was measured under both normothermic conditions and after simulated HHCA (incubation at 4 degrees C for 2 h in crystalloid cardioplegia; K+ = 24 mEq/L) using computer-assisted videomicroscopy in the presence of 2, 4, and 6 micrograms/mL propofol (11.2, 22.4, and 33.6 microM/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Propofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline = 67 +/- 2 microns/s; propofol = 2 micrograms/mL, 45 +/- 4 microns/s; and propofol = 6 micrograms/mL, 27 +/- 3 microns/s; P < 0.05). HHCA and rewarming caused a significant reduction in myocyte velocity of shortening (29 +/- 0.9 microns/s, P < 0.05), with further significant dose-dependent reductions in contractile function after the addition of propofol. Propofol caused a decrease in beta-adrenergic responsiveness under normothermic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated myocyte contractile function after simulated HHCA is further decreased by propofol administration.

Adrenergic beta-Agonists↗
PubMed1991

Effects of calcium-free solution, calcium antagonists, and the calcium agonist BAY K 8644 on mechanical responses of skeletal muscle from patients susceptible to malignant hyperthermia.

The purpose of this investigation was to determine if alteration in the function of the dihydropyridine receptor may in turn modify halothane-induced contractures in muscle bundles from patients susceptible to malignant hyperthermia (MH). The effects of Ca(2+)-free Krebs Ringer (KR) solution, 5 microM verapamil, 5 microM nifedipine, and 10 microM of the Ca2+ agonist BAY K 8644 on halothane-induced contracture were therefore investigated. The halothane-induced contracture was prevented in the absence of extracellular Ca2+ and significantly reduced in the presence of verapamil or nifedipine. BAY K 8644 significantly enhanced the 0.5-, 1.0-, and 1.5-vol % halothane-induced contracture in MH-susceptible muscle bundles. When BAY K 8644 was dissolved in Ca(2+)-free KR solution, no contracture was observed in MH-susceptible muscle bundles. These results on cut MH-susceptible human muscle bundles support the hypothesis that halothane-induced contracture in MH can be modified by the binding of Ca2+ agonists or antagonists to the dihydropyridine receptor. The role of Ca2+ entry phenomena remains unclear, but the results suggest that extracellular Ca2+ is required to reprime or to bind to some sites of the dihydropyridine receptors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1980

Preliminary pharmacological characterization of the bovine isolated bronchial artery strip: a new preparation.

1 This paper describes a preliminary pharmacological study of the isolated helical strip of bovine bronchial artery under isotonic conditions in Krebs-Henseleit solution. 2 The tissue contracted to histamine and 5-hydroxytryptamine (5-HT), actions which were selectively antagonized by mepyramine and methysergide respectively. Histamine was not inhibited by metiamide and 5-HT was not affected by morphine. 3 Slow reacting substance of anaphylaxis (SRS-A), prostaglandin F2 alpha (PGF2 alpha) and PGE2 were spasmogenic, whereas PGE1 caused relaxation. No potential antagonists of these agents were tested. 4 Carbachol, at all concentrations, caused contractions of the bronchial artery which were completely, irreversibly blocked by atropine. 5 The spasmogenic action of phenylephrine was selectively blocked by dibenamine. Vessel strips which were partially contracted to histamine, relaxed to isoprenaline and salbutamol. The action of isoprenaline was inhibited similarly by either propranolol or practolol. The evidence therefore suggests the presence of functional alpha, beta 1 and beta 2-adrenoceptors.

Animals↗
PubMed1982

Contractile properties of two varieties of twitch muscle fibres in Xenopus laevis.

The contractile properties of twitch muscle fibres in the iliofibularis muscle of Xenopus laevis with characteristic differences in light-microscopical appearance have been studied under isometric and isotonic conditions. Type 1 fibres (large, pale) have a short contraction time (tc), a shoulder in the relaxation phase, and a high twitch-tetanus ratio. In type 2 fibres (medium-to-large with abundant mitochondria and lipid droplets) tc is longer, half-relaxation time equals tc, and the twitch-tetanus is lower. The capillary density is about 4 times higher for type 2 than for type 1. Computer-fitted hyperbolic force-velocity curves gave the following Hill constants (20 degrees C) for type 1 (2) fibres: P0*/P0 1.03 (1.15), a/P0* 0.48 (0.26), b 3.51 (1.53) 10/s; extrapolated Vmax (0-0.8P0) was 7.60 (6.27) 10/s. Lowered temperature (10 degrees C) increases the curvature of the P-V relation in type 1 fibres, little effect was seen in type 2. Increased PCO2 depressed the isometric tension in both types; in type 1 fibres the P-V relation became less curved, in type 2 fibres no change in curvature was observed. The results suggest that type 1 and type 2 fibres might contain myosin isozymes with slightly different temperature- and pH-sensitivities.

Animals↗
PubMed1968

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog.

1. The effect of adrenaline on contracture and twitch tension in frog's ventricle has been examined, using the superfused preparation.2. In 1 mM-Ca Ringer, contractures induced with excess KCl concentrations from 50 to 200 mM, are reduced by 1 x 10(-6) g/ml. adrenaline to an average of 0.62 of control values, in marked contrast to the well known positive inotropic effect of adrenaline on the heart twitch. This effect of adrenaline is directly dose dependent. Increasing [Ca](o) diminishes the effect of adrenaline on contracture tension, and on the twitch tension.3. Adrenaline has a significantly greater effect on the KCl contracture tension than noradrenaline or isoprenaline.4. In 1 mM-Ca Ringer, Na-free contractures are reduced to 0.72 of controls by 1 x 10(-6) g/ml. adrenaline. Adrenaline also significantly reduces tension in contractures induced by 50 c/s alternating current.5. The action of adrenaline on contracture tension is largely complete in 1-2 min at various rates of stimulation and calcium concentrations. A similar time course has been found for the effect of adrenaline on membrane potential.6. Pronethalol blocks the action of adrenaline on both twitch and contracture. The action on the contracture can also be blocked by ouabain (1 x 10(-5)M), and exposure of the tissue to K-free or Na-free Ringer solution.7. Adrenaline hyperpolarizes the membrane potential with a range of [K](o) from 0 to 200 mM. This effect is blocked by pronethalol and ouabain. After exposure to ouabain, adrenaline causes a significant decrease in the membrane potential. This may be due to an increase in the sodium permeability.8. At low values of the [Ca]/[Na](2) ratio, adrenaline takes a relatively constant number of beats for full action, but at high values of the ratio the development of full effect is largely time dependent.9. The time course of the effect on the twitch of changing from 0.5 to 2 mM-Ca Ringer has been studied at various rates of stimulation. The equilibration time has been found to depend on the heart rate.10. The effect on the contracture suggests that adrenaline decreases the calcium permeability. It is further suggested that the development of twitch tension is not due to direct Ca entry but is due to the release of Ca from a local store within or between the cells. The inotropic action of adrenaline is explained in terms of this store.

Animals↗
PubMed1998

Body fluid volume status and the renal response to atrial natriuretic peptide in rats.

The effect of altering the volumes of different body fluid compartments on the renal response to atrial natriuretic peptide (ANP) was studied in anesthetized rats before and during administration of the peptide at 170 ng/min. Four different groups were used. In the first (De), reduction of total body water content was induced by 48 h water deprivation. In the second (De+NaCl), an acute intravenous infusion after the same 48 h dehydration was used to restore the extracellular, but not the intracellular, fluid compartment. In the third (Eu+NaCl), euvolemic rats were infused with isotonic saline at the same rate as in group De+NaCl to expand both intravascular and interstitial components of extracellular fluid. In the fourth group (Eu+BSA) an infusion of hyperoncotic (6%) bovine serum albumin in isotonic saline was used to expand the intravascular volume while contracting the interstitial volume. Excretion of water and salt was predictably reduced in the De group compared with the others. This reduction was associated with increased tubular reabsorption, both upstream from the medullary collecting duct and in the duct itself. Administration of ANP did not significantly affect diuresis and saluresis, or tubular transport. By contrast, there were marked and similar diuretic and natriuretic responses to ANP in groups De+NaCl and Eu+NaCl, associated with transport inhibition primarily in the medullary collecting duct. Surprisingly, the rats infused with hyperoncotic solution (Eu+NaCl) also failed to show marked excretory or duct transport responses to ANP. According to the study design, the two nonresponding groups had, respectively, a decreased or a normal intracellular compartment, and a decreased or increased plasma volume. The common feature of both nonresponding groups was a decreased interstitial fluid compartment, whereas the two responding groups had normal or increased interstitial volume. We suggest, therefore, that a replete interstitial fluid compartment is essential for the renal response to ANP.

Animals↗
PubMed1988

Sr2+ activates cross-bridge phosphorylation and latch state in smooth muscle.

Sr2+ induced myosin phosphorylation and stress development in both skinned and K+-depolarized, Ca2+-depleted, intact swine carotid media. Although higher concentrations of Sr2+ than Ca2+ were required for phosphorylation and stress development, the dependence of stress on phosphorylation was the same in intact tissues. K+ depolarization in the presence of 5 mM Sr2+ produced a transient in phosphorylation (53.2 +/- 5.1% at 1 min, falling to a steady-state value of 21.7 +/- 2.0%) in Ca2+-depleted tissues in which intracellular stores were refilled with Sr2+. Stress developed without a transient (T1/2 = 0.70 min) to a steady state of 89.7 +/- 2.0% of the stress induced by K+ depolarization in the presence of 1.6 mM Ca2+ (K-PSS). Cross-bridge cycling rate as measured by isotonic shortening velocity was proportional to myosin phosphorylation throughout the contraction. When intracellular stores were not refilled with Sr2+, phosphorylation rose to a sustained value of 28.8 +/- 2.7% and stress developed slowly (T1/2 = 2.9 min) to a steady state of 95.9 +/- 1.5% K-PSS-induced stress. Therefore, an initial phosphorylation transient induced by intracellular Sr2+ release only accelerated stress development without significant effects on steady-state stress or phosphorylation (as was true for Ca2+- induced responses). We concluded that Sr2+ substitutes for Ca2+ in phosphorylation and regulation of the latch state in the swine carotid media.

Animals↗
PubMed1982

After effects of perfusion with glucose-insulin-potassium solution on the membrane current and tension components of frog atrial muscle.

As glucose-insulin-potassium solution (GIK) has been used as clinical cardioplegia during open heart surgery, we studied the fundamental effects of GIK on the electrical and mechanical activities of the bullfrog atrial muscle under voltage clamped and unclamped conditions by the double sucrose-gap method. GIK produced an immediate disappearance of the action potential and twitch tension with pronounced depolarization accompanied by transient contracture. Reperfusion with normal Ringer's solution after GIK perfusion (30-180 min) resulted in recovery of the action potential, with an initial lengthening followed by a sustained shortening in duration. Recovery of twitch tension was incomplete, and perfusion with GIK for a longer period caused stronger suppression. Voltage clamp studies revealed that after removal of GIK, the slow inward current (Is) and Is-dependent tension were markedly depressed, while the delayed outward current (Ix) was augmented. The fast inward current (INaf), background current (Ik1), and Is-independent tension gradually recovered to the control levels. Perfusion with low Ca Ringer's solution or verapamil Ringer's solution for 10 min at the initial reperfusion phase significantly improved the recovery of Is and the Is-dependent tension. These results indicate that the after-effects of GIK are mainly governed by Ca influx at the initial reperfusion phase. Therefore, a lowering of the Ca influx in this period is expected to produce a beneficial effect on cardiac function after GIK treatment.

Action Potentials↗
PubMed2001

A study on the low frequency oscillations in the activation of the muscle under sustained isometric task.

We studied the periodicity of a relatively slow oscillation of the muscle activation, via the surface electromyogram (EMG), recorded from the Biceps and Brachioradialis muscles, under an endurance isometric task. The peaks in the Root Mean Square (RMS) of the EMG were assigned as peaks of the muscle activation; the estimate of their periodicity was checked via correlation. 32 subjects participated in different exercises involving isometric isotonic tasks, at 25%, 50% and 75% MVC (maximal voluntary contraction). The activation of the muscle under such an exercise has an overall low frequency periodicity of between 14.29 s and 16.75 s with standard deviations (sd) between 2.97 s and 5.04 s, independent of the intensity of the task and sex. They are larger for the Brachioradialis (mean 15.08-19.6 s/sd 2.59-6.3 s) than for the Biceps (mean 11.96-16.41 s/sd 1.24-4.86 s).

Adult↗
PubMedDate not supplied

[The role of osmotic factors in the effect of mineral water Naftusia on smooth muscles of the portal vein].

The effect of the Krebs solution tonicity on the electrical and mechanical activity of smooth muscles has been studied while adding 1-5% volume of mineral water Naftusya, its artificial salt analog, and distilled water into the above solution. It is shown that effects observed are induced by the medium tonicity changes rather than by biologically active components of the mineral water. The smooth muscle cells of the rat portal vein are sensitive osmometers which affect hypotonic Krebs solution by 1%.

Animals↗