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PubMed1980

Myocardial stiffness during hypoxic and reoxygenation contracture.

Isolated rat papillary muscle preparations were used to study hypoxic contracture, and cat papillary muscle preparations with ouabain to study reoxygenation contracture. Electronic analysis of the response to rapid small sinusoidal perturbations gave a continuous measurement of the elastic and viscous components of total stiffness. Increased resting force during hypoxic contracture was characterised by an increase in resting elastic and viscous stiffness relative to the control stiffness-active force relationships. During reoxygenation contracture the stiffness-force relationships followed those of active force development. The linear active force-elastic stiffness relationship (dt/dl=kT+c) was also reversibly altered during hypoxic contracture, predominantly by an increase in intercept c. These data imply that hypoxic contracture unlike reoxygenation contracture is not due solely to a rise in intracellular calcium, but is associated with a component of stiffness not participating an active force development, for example rigor.

Animals↗
PubMed1996

In vitro diagnosis of malignant hyperthermia susceptibility with ryanodine-induced contractures in human skeletal muscles.

The in vitro contracture test with ryanodine is a new method to distinguish malignant hyperthermia (MH) susceptible (MHS) from normal (MHN) patients. The purpose of our investigation was to determine whether smaller concentrations of ryanodine than those used previously may result in a better differentiation. We performed a ryanodine contracture test (RCT) using concentrations of 1 and 2 microM in muscle specimens of 41 MHS, 58 MHN, and 19 MH-equivocal (MHE) patients. Nine patients were excluded from the study due to neuromuscular diseases. All contracture levels (i.e., start of contractures, contractures of 0.2 g and 1.0 g) were attained significantly earlier in MHS than in MHN muscles at both concentrations of ryanodine. Using a ryanodine concentration of 2 microM, all contracture levels were reached significantly faster than with 1 microM. There was no overlap in the range of times between groups at all contracture levels with ryanodine 1 and 2 microM. The median threshold times for all MHE patients were always between those of MHS and MHN. Defining arbitrarily threshold times for MHS and MHN, an assignment of MHE patients to either MHS or MHN using 1 or 2 microM ryanodine was possible in most cases. Ryanodine administration at a concentration of 1 microM led to a better distinction of MHS from MHN patients than 2 microM. The RCT with ryanodine 1 microM should therefore be added to the current diagnostic methods.

Adolescent↗
PubMed1994

Genetic effects on the variability of the halothane and caffeine muscle contracture tests.

BACKGROUND: The spectrum of the clinical presentation of malignant hyperthermia (MH) and the results of recent linkage studies suggest that there is a degree of heterogeneity in MH susceptibility. In the current study, we analyzed in vitro muscle contracture tests from members of large families with MH to evaluate if the results of these tests could be related to genetic influences. METHODS: Forty-seven subjects from four families with an MH-related death and with at least five clinically MH-susceptible individuals per family, as diagnosed by an in vitro muscle contracture test according to the protocol of the European MH Group, were included in the current analysis. We compared the strength of muscle contractures to challenges of halothane, caffeine, or both and the effect of these two drugs on twitch potentiation in response to supramaximal electrical stimulation among the families. RESULTS: Clinical MH susceptibility was confirmed in 36 individuals, and 11 individuals were diagnosed as MH-negative. In MH-susceptible individuals, muscle contractures to the 2% halothane challenge were significantly higher in family 1 (n = 15; 16.2 +/- 2.9 mN, mean +/- standard error of the mean) and in family 4 (n = 5; 16.4 +/- 5 mN) than in family 2 (n = 9; 5.8 +/- 1.5 mN) or family 3 (n = 7; 6.0 +/- 1.1 mN). Muscle contractures to the caffeine challenge (2 mM) were significantly increased in family 1 (7.3 +/- 1.4 mN) compared with those in family 3 (1.3 +/- 1.0 mN). In addition, we found a dose-dependent twitch potentiation to the halothane challenge in family 2 (P < 0.01) and to the caffeine challenge in families 2 (P < 0.001) and 3 (P < 0.01), whereas there was no twitch potentiation in families 1 and 4. CONCLUSIONS: The differences of in vitro muscle contracture tests among several families with MH provide evidence for genetic influences on the variability of this test procedure. However, it is not known if the observed differences are caused by heterogeneity of the MH gene mutation(s) or by other genetic factors that might modify muscle contractures in vitro.

Adult↗
PubMed2002

Results of contracture tests with halothane, caffeine, and ryanodine depend on different malignant hyperthermia-associated ryanodine receptor gene mutations.

BACKGROUND: More than 20 mutations in the gene encoding for the ryanodine receptor (RYR1), a Ca2+ release channel of the skeletal muscle sarcoplasmic reticulum, have been found to be associated with malignant hyperthermia (MH). This study was designed to investigate the effects of different mutations in the RYR1 gene on contracture development in in vitro contracture tests (IVCT) with halothane, caffeine, and ryanodine. METHODS: Ninety-three MH-susceptible (MHS) patients, diagnosed by the standard IVCT with halothane and caffeine, were included in this prospective study. Surplus muscle specimens were used for an IVCT with 1 microm ryanodine. The contracture course during the ryanodine IVCT was described by the attainment of different time points: onset time of contracture and times when contracture reached 2 mN or 10 mN. In addition, all patients were screened for mutations of the RYR1 gene. RESULTS: In 36 patients, four different mutations of the RYR1 gene (C487-T, G1021-A, C1840-T, G7300-A) were found. The IVCT threshold concentrations of halothane and caffeine were lower in patients with the C487-T mutation compared with patients without a detected mutation in the RYR1 gene. In the IVCT with ryanodine, contracture levels of 2 mN and 10 mN were reached earlier in muscle specimens from patients with C487-T, C1840-T, and G7300-A mutations compared with specimens from patients with the G1021-A mutation and patients without detected mutation in the RYR1 gene. CONCLUSIONS: The differences between the groups in the halothane and caffeine IVCT threshold concentrations and in the time course of contracture development in the ryanodine IVCT underline the hypothesis that certain mutations in the RYR1 gene could make the ryanodine receptor more sensitive to specific ligands. This may be an explanation for varying clinical symptoms of MH crisis in humans.

Adolescent↗
PubMed2001

Capsular contracture after cosmetic breast implant surgery in Denmark.

The authors investigated the association between the occurrence of capsular contracture and implant and patient characteristics. All women with breast implants from 1977 to 1997 were identified from the files of two private plastic surgery clinics in Denmark. Information on implant and patient characteristics, surgical procedure, and complications was obtained through medical records and self-administered questionnaires. Of 754 women (1,572 implants), average age at implantation was 32 years. Implant types were silicone double lumen, textured, 31.2%; silicone single lumen, textured, 27.8%; silicone single lumen, smooth, 24.5%; silicone double lumen, smooth, 0.8%; and other or missing, 15.7%. Placement was submuscular for more than 90% of implants. Capsular contracture occurred in 7.9% of implanted breasts, on an average of 621 days postoperatively, with 51.6% being bilateral. Overall, 66.1% of capsular contractures were recorded within the first 12 months postoperatively, and 79.0% were recorded within 24 months. Double-lumen implants were associated with a significantly (p < 0.01) reduced occurrence of capsular contracture. In summary, capsular contracture typically occurs within the first 2 years of implantation. Host factors may be important because more than half the capsular contractures in the current study were bilateral. Occurrence of capsular contracture did not appear to be associated with implant surface or placement, occurrence of local complications, or patient characteristics, although these findings should be interpreted cautiously.

Adult↗
PubMed2006

Textured surface breast implants in the prevention of capsular contracture among breast augmentation patients: a meta-analysis of randomized controlled trials.

BACKGROUND: Capsular contracture is a common complication associated with the use of breast implants. Numerous randomized controlled trials addressing the efficacy of textured surface breast implants in reducing capsular contracture have yielded nonuniform results. This meta-analysis addresses the use of textured breast implants in the prevention of capsular contracture. METHODS: MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials databases were searched to identify all randomized controlled trials involving the use of textured versus smooth breast implants. The results of these trials were meta-analyzed to obtain a pooled odds ratio of the effect of textured surfacing on capsular contracture rates. In addition, subgroup analyses were performed based on implant type (saline or silicone gel), type of surface texturing (Siltex or Biocell), placement (subglandular or submuscular), and length of follow-up. RESULTS: Eleven trials were reviewed. Four were excluded because they failed to meet a priori inclusion criteria. The remaining seven trials were meta-analyzed. Only three of these studies found significantly lower rates of capsular contracture with the use of textured implants. However, when all seven studies were pooled, the odds ratio was found to be 0.19 (95 percent confidence interval, 0.07 to 0.52), indicating a protective effect for surface texturing on the rate of capsular contracture. Submuscular placement was the only subgroup in which significance was not achieved. However, this subgroup consisted of a single study, which was dramatically underpowered. CONCLUSION: The results of this meta-analysis demonstrate the superiority of textured over smooth breast implants in decreasing the rate of capsular contracture.

Breast↗
PubMedDate not supplied

Verapamil-induced contracture in an excised, blood-perfused skeletal muscle preparation from the dog.

The ability of verapamil to induce a contractile response in skeletal muscle was investigated using the canine isolated, blood-perfused diaphragm preparation. Verapamil-induced contracture was characterized by a biphasic increase in muscle tension consisting of an initial phasic and subsequent tonic contracture. The second tonic component of the verapamil-induced contracture was inhibited by procaine, but procaine had no effect on the initial phasic contracture. Verapamil potentiated both KCl- and caffeine-induced contractures during the second tonic stage. This action might be explained by enhancement by the drug of availability, or by an increased sensitivity of the contractile machinery to calcium liberated by membrane depolarization or by the calcium-induced calcium release mechanism. The second tonic component of verapamil-induced contracture was much less than the initial phasic component. It seems, therefore, that the calcium release induced by the procaine-resistant process is the principal action of verapamil in inducing contracture in skeletal muscle.

Animals↗
PubMed1977

Prenylamine-induced contracture of frog skeletal muscle.

1. Experiments were performed to determine the influence of prenylamine on excitation-contraction coupling in frog sartorius muscle. 2. Prenylamine (0.2-1.0 mM) produced a biphasic contracture in skeletal muscle characterized by an initial phasic and subsequent tonic contracture. 3. Neither dantrolene nor procaine blocked the prenylamine-induced contracture. Pretreatment with 100 mM K+ blocked the phasic but not the tonic component of the prenylamine contracture. 4. Prenylamine produced a sustained increase in 45Ca efflux at all concentrations that produce contracture. These concentrations of prenylamine also depressed the action potential, muscle twitch and resting potential. 5. Low concentrations of prenylamine (0.05 mM) which produced neither contracture, 45Ca efflux nor 45Ca influx, depressed the action potential, muscle twitch and K+ contracture. 6. The results suggest that prenylamine not only alters calcium mobility but also membrane permeability to other ions.

Action Potentials↗
PubMed1984

The effects of external potassium, multivalent cations and temperature on caffeine contractures in rat skeletal muscle.

The effects of multivalent cations, membrane potential and temperature on caffeine contractures of rat soleus and extensor digitorus longus (e.d.l.) muscles were investigated. The amplitude of the caffeine contracture was depressed by the removal of calcium and by the addition of a high concentration (1 mM) of lanthanum. Low concentrations of lanthanum (0.1-0.5 mM) augmented the caffeine contracture. Low levels of depolarization by potassium (10-40 mM) augmented the amplitude of the caffeine contracture, while higher concentrations of potassium depressed the contracture. Maximum augmentation of the caffeine contracture occurred with a higher concentration of potassium (20 mM vs 10 mM) in the e.d.l. than in the soleus muscle. The amplitude of contractures was directly related to temperature between 22 and 37 degrees C and inversely related to temperature below 22 degrees C. The effects of caffeine in rat skeletal muscle are suggested to be exerted on the sarcolemma and the mechanisms of action are by modification of the processes of activation and inactivation.

Animals↗
PubMed1998

Comparative studies on the induction of muscle contracture in mouse diaphragm and Ca2+ release from sarcoplasmic reticulum vesicles by organotin compounds.

Effects of organotins, including triethyltin and tributyltin, on skeletal muscle were studied with diaphragm and isolated sarcoplasmic reticulum membrane vesicles. Triethyltin induced muscle contracture in mouse diaphragm while tributyltin had comparatively less potency and efficacy in inducing the muscle contracture. The contracture induced by tributyltin was inhibited when the diaphragm was pretreated with low Ca2+ medium or caffeine while the contracture induced by triethyltin persisted in the Ca2+-free medium but was inhibited by pretreatment of caffeine. Pretreatment of dithiothreitol blocked the contracture induced by tributyltin but not that by triethyltin. Triethyltin dose-dependently induced Ca2+ release from sarcoplasmic reticulum vesicles and inhibited the Ca2+-ATPase activity. These results suggested that triethyltin induced contracture in mouse diaphragm was mainly by induction of Ca2+ release and inhibition of Ca2+ uptake of the internal Ca2+ storage site the sarcoplasmic reticulum, while the tributyltin induced contracture might be due to enhancement of extracellular Ca2+ influx which further induce the release of internal Ca2+ through the Ca2+-induced Ca2+ release mechanism.

Animals↗
PubMed1966

Potassium contractures in single muscle fibres of the crayfish.

1. Contractures were evoked in isolated muscle fibres of the extensor carpopoditi muscle of the crayfish (Astacus fluviatilis) by increasing [K](o) at constant [Cl](o) or at constant [K](o)[Cl](o) product.2. The relation between tension and log [K](o) is S-shaped with a less steep slope if [K](o) was increased at constant [Cl](o). This is due to a smaller drop in membrane potential for a given change in [K](o) in the latter case.3. The curves relating the tension to the membrane potential overlap in either case. In the linear part of the curve, the slope is around 0.3 kg cm(-2)m V(-1).4. The mechanical threshold of contracture is about -55 mV and mechanical saturation is at -20 mV.5. Fibres exert the greatest tension when stretched to 1.25 l(o) (8 kg/cm(2)), where l(o) is the length at which the fibres are just taut in the solution. Tension falls on either side of this optimal length. Tension vanishes when the fibre is stretched to 1.95 l(o).6. Sarcomere length at optimal fibre length is 10.5 +/- 0.3 mu. The A band is 3.95 +/- 0.8 mu long and does not alter during stretch.7. The crayfish muscle fibres were of the phasic type, since they relaxed spontaneously at maintained high [K](o).8. At [K](o) near saturation point, contractures attain the maximum tension in 5 +/- 1.3 sec and the time to half decay is 8.1 +/- 0.5 sec.9. If the contracture is allowed to relax spontaneously, it is not possible to obtain initial tension until after 20-30 min. When the contracture is terminated by a return to low [K](o) after reaching its maximum, but before spontaneous relaxation appears, the fibre is capable of repeatedly exerting the initial tension.10. The rate of recovery after a spontaneously relaxed contracture depends on [K](o) in the solution, in which the fibre lies before evoking the test contracture. The relation of recovery upon log [K](o) is S-shaped and the tension is the greater, the lower the [K](o) in the solution in which recovery is taking place.

Animals↗
PubMed1986

Effects of external calcium on potassium contractures in tonic muscle fibers of the frog (Rana pipiens).

K+ contractures of tonic bundles from cruralis muscle of the frog were studied with different K+ concentrations (10-120 mM). K+ contractures had an initial transient phase followed by a sustained tension. The amplitude of the sustained tension diminished with high K+ concentration (80-120 mM). However, in all cases, tension was maintained for several minutes. External Ca2+ reduction practically abolished the sustained phase of the K+ contractures. The initial phase was also reduced and tension spontaneously relaxed. The curve relating the peak tension with log [K+]o, showed that the threshold was not affected but the peak tension was reduced to about 70% in low-Ca2+ saline (0 Ca2+ + 3 mM-Mg2+) and 50% in Ca2+-free saline (1 mM-EGTA + 3 mM-Mg2+). The dependence of the sustained tension on external Ca2+ was further confirmed by Ca2+ withdrawal and re-establishment and/or by Ni2+ substitution for Ca2+ before or during K+ contractures. These results indicate that external Ca2+ had to be continuously present to maintain the tension during K+ contractures and that Ni2+ was not able to restore the normal temporal course of K+ contracture. The sustained phase was diminished by blocking agents of Ca2+ channels, such as nifedipine (1 microM) and diltiazem (1-10 microM). The present results can be explained by a direct control of the Ca2+ currents on K+ contracture or by specific interactions between external Ca2+ and Ca2+-binding sites in the membrane.

Animals↗
PubMed1988

Effect of Ca2+ channel blockers on K+ contractures in twitch fibres of the frog (Rana pipiens).

1. The effects of Ca2+ channel blockers (nifedipine, nitrendipine and diltiazem) were tested on K+ contractures in single muscle fibres of the frog, Rana pipiens. 2. Nifedipine (1 microM) reduced the area under K+ contractures to 24 +/- 9% (4) (100 mM-K+) and 34 +/- 24% (4) (190 mM-K+). Nitrendipine (0.1 microM) reduced the area to 30 +/- 10% (4) (120 mM-K+). The blockade of the contractures was reversible. 3. Diltiazem (1 microM) shortened the first 190 mM-K+ contracture without affecting the peak amplitude. The first contractures, performed at 15-20 min after the removal of diltiazem, were greatly reduced to 29 +/- 14% (4). This effect was reversed after three to five contractures in the absence of the drug. Similar results were obtained with 60 and 100 mM-K+. 4. The resting potential in control saline and after a brief exposure to 120 mM-K+ was not affected by the dihydropyridines and diltiazem. 5. Slow and fast Ca2+ currents were not modified by 1 microM-diltiazem at any stimulation rate or with pre-pulse depolarizations. Diltiazem (50 microM) did not affect the fast Ca2+ current and reduced the slow one to 48 +/- 10% (4). 7. The reduction of K+ contractures by Ca2+ channel blocking agents was not related to a blockade of Ca2+ currents. This can be tentatively explained by interactions of these compounds on membranes sites which regulate the coupling between membrane depolarization and contraction.

Action Potentials↗
PubMed1996

Elevated intracellular Ca2+ and myofibrillar Ca2+ sensitivity cause iodoacetate-induced muscle contractures.

Ischemic stimulation of iodoacetic acid (IAA)-treated rat extensor digitorum longus (EDL) muscles produced contractures. Similar ischemic stimulation of control EDL muscles did not result in contracture. At the onset of contracture, ATP concentration was not reduced, phosphocreatine concentration was reduced > 75%, ADP concentration was increased 9-fold, Ca2+ concentration ([Ca2+]) was increased approximately 11-fold, and inorganic phosphate concentration increased less in IAA-treated muscles than in stimulated control muscles. To test whether contracture resulted from elevated [Ca2+] and/or increased Ca2+ sensitivity of the contractile proteins, this laboratory made skinned fiber-activating solutions that simulated four different conditions: unstimulated IAA-treated and control muscles, IAA-treated muscles at contracture, and ischemically simulated control muscles. Skinned EDL fibers had lower single-fiber tensions and reduced Ca2+ sensitivities in activating solutions that mimicked the conditions in stimulated control muscles compared with activating solutions that simulated the conditions in unstimulated muscles. In contrast, the maximum tension was maintained and Ca2+ sensitivity was increased in activating solutions that simulated contracture. Tension at contracture resulted from increased intracellular [Ca2+] and increased myofibrillar Ca2+ sensitivity compared with the Ca2+ sensitivity of stimulated control fibers.

Animals↗
PubMed1994

The relative importance of myocardial energy metabolism compared with ischemic contracture in the determination of ischemic injury in isolated perfused rabbit hearts.

The mechanical effects of ischemic contracture may be important in the development of irreversible cellular damage as it increases mechanical stress on sarcolemmal membranes and restricts endocardial perfusion. To assess the relative importance of these mechanical effects compared with decreased energy supply in the development of irreversible injury, the effects of inhibiting ischemic contracture with 2,3-butanedione monoxime (BDM), an agent that disrupts excitation-contraction coupling, were delineated in isovolumically contracting isolated rabbit hearts. Administration of 20 mmol/L BDM in 12 hearts subjected to 60 minutes of low-flow ischemia prevented ischemic contracture (left ventricular end-diastolic pressure [LVEDP], 12 +/- 3 compared with 48 +/- 14 mm Hg in 20 control hearts; P < .001), reduced membrane damage (creatine kinase [CK] release, -54% compared with control hearts; P < .05), and enhanced functional recovery during reperfusion (left ventricular developed pressure [LVDP], 86 +/- 10% of baseline compared with 56 +/- 23% in control hearts; P < .01). These observations were not related to increased intracavitary pressure and its effects on flow distribution, since venting the left ventricle in additional hearts did not result in improved function during reperfusion. Although it would be tempting to conclude that BDM protected ischemic myocardium by preventing ischemic contracture, administration of BDM was also associated with reduced depletion of ATP during ischemia, perhaps related to diminished energy demand. To distinguish between the relative importance of inhibiting contracture from provision of adequate energy, the period of ischemia was extended to 120 minutes. BDM still prevented ischemic contracture (LVEDP, 10 +/- 6 mm Hg) and preserved ATP stores, but it did not prevent membrane damage (CK release, 483 +/- 254 U/g dry weight) or contractile failure during reperfusion (LVDP, 68 +/- 7% of baseline). In contrast, increasing the rate of anaerobic glycolysis during ischemia by doubling glucose and insulin in the presence of BDM markedly decreased membrane damage (CK release, 114 +/- 72 U/g dry weight; P < .05) and contractile failure during reperfusion (LVDP, 88 +/- 7% recovery of baseline; P < .01). These results suggest that insufficient energy production is primarily responsible for myocardial ischemic damage, whereas mechanical effects of ischemic contracture appear to play only a minor role.

Animals↗
PubMed1991

Myometrial contracture-related increases in plasma adrenocorticotropin in fetal sheep in the last third of gestation are abolished by maintaining fetal normoxemia.

Low amplitude, long-lasting epochs of myometrial activity, contractures, occur throughout the majority of pregnancy in all species studied to date. Contractures are associated with a fall in fetal oxygenation and changes in fetal behavioral state. In the present study we observed that contractures produced by the administration of 70 mU oxytocin iv to the pregnant ewe at 125-139 days gestational age (term 145-150 days) result in a fall in fetal carotid arterial PO2 of approximately 2.5 mm Hg and are followed by a rise in fetal carotid arterial plasma ACTH of 16.3 +/- 9.6 pg.ml-1 (mean +/- SEM). When the contracture-induced fall in fetal arterial PO2 was prevented by administration of oxygen to the ewe, fetal ACTH did not rise after the contracture. In conclusion, these observations demonstrate that the relatively small fall in fetal PO2 that accompanies a contracture can be sensed by the fetus and is an essential part of the stimulus to the increased secretion of fetal ACTH that accompanies a contracture. These findings support the view that myometrial activity is one of the factors that influence fetal ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1977

Time- and Na-dependent effects of Ca depletion on potassium contracture in frog twitch muscle fiber.

The effect of the extracellular Ca depletion on potassium contracture was investigated in single fibers isolated from frog semitendinosus muscle mainly in relation to its time and Na dependency. The shortening of plateau duration and the increase in the rate of relaxation of the potassium contracture appeared within 3--5 sec and 15 sec, respectively, after the fiber was immersed in Ca-free Na Ringer solution containing 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) (EGTA-Na Ringer solution) or Ca-free choline Ringer solution containing 1 mM (EGTA (EGTA-choline Ringer solution). These effects were independent of the presence or absence of extracellular Na. In EGTA-Na Ringer solution, the potassium contracture tension was inhibited only by about 20% after 20--90 min and was abolished after 120 min. The inhibition of the peak tension was accelerated by the depletion of extracellular Na; in EGTA-choline Ringer solution, the tension was gradually inhibited by about 20% during the first 7 min and abolished after 10--12 min. When the peak tension of potassium contracture was abolished in EGTA-choline Ringer solution, the depolarization by Ca depletion was about 10 mV and the caffeine contracture was sufficiently produced. The results suggest that the inhibition of the potassium contracture tension in EGTA-choline Ringer solution is due to the dissociation of excitation-contraction coupling. On the basis of these results, an aspect of the inactivation of the potassium contracture was proposed.

Animals↗
PubMed1978

Selective inhibition of potassium contracture in guinea pig taenia coli by ruthenium red.

Effects of ruthenium red on isotonic KCl induced contracture (K-contracture), cellular 45Ca uptake and 45 Ca binding to surface membranes were examined in the smooth muscle cells of guinea pig taenia coli. These results were compared with those using lanthanum (La3+). The tonic component of the K-contracture was selectively inhibited by 1 mM ruthenium red. In contrast, 1 mM La3+ inhibited the phasic component of the K-contracture to a large extent. Use of 1 mM ruthenium red selectively inhibited the tonic component of K-contracture and caused a marked decrease in cellular 45Ca uptake in that component of K-contracture. In contrast, 1 mM La3+ largely inhibited the phasic component and caused a significant decrease in cellular 45Ca in that component. According to Scatchard plot analysis, there are two kinds of Ca2+ binding sites of high and low affinity, respectively, on the surface membrane of the taenia coli. One mM ruthenium red suppressed those of low affinity more strongly than those of high affinity. In contrast, 1 mM La3+ suppressed high affinity sites more markedly than low affinity sites. Based on these results, it seems possible to conclude that ruthenium red mainly blocks the initial binding sites linked with Ca2+ influx which is related to the production of the tonic component while La3+ blocks those sites related to the phasic component of the K-contracture of guinea pig taenia coli.

Animals↗