Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Isotonic Contraction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMed1990

Myofilament spacing and force generation in intact frog muscle fibres.

1. The relation between sarcomere length and steady tetanic tension was determined at 10-12 degrees C for 70-80 microns long length-clamped segments of single fibres isolated from the tibialis anterior muscle of the frog, in normal and hypertonic or hypotonic Ringer solutions. 2. The tension depression and potentiation observed in hypertonic and hypotonic Ringers solutions varied with sarcomere length, so that, as opposed to myofilament overlap predictions, the optimum length for tension development was shorter in hypertonic Ringer solution and longer in hypotonic Ringer solution than in normal Ringer solution. As the fibres were stretched from 1.96 to 2.24 microns sarcomere length, both tension depression in hypertonic Ringer solution and tension potentiation in hypotonic Ringer solution increased by 9 and 5%, respectively. 3. Within this range of sarcomere lengths the length-stiffness relation in hypotonic and in hypertonic Ringer solutions exhibit little or no change relative to that in normal Ringer solution. 4. The results indicate that separation between the thick and the thin myofilaments influences the mechanism of force generation. There is an optimum interfilament distance (10-12 nm surface to surface between the thick and the thin filaments) for tension production. In isotonic Ringer solution, this corresponds to the interfilament distance at sarcomere lengths around 2.10 microns. The force per attached cross-bridge, rather than their number, appears to decrease as the interfilament distance is brought above or below the optimum length. Even if this effect is moderate in isotonic Ringer solution, it should be taken into account in models of the force-generation mechanism.

Actin Cytoskeleton↗
PubMed2006

Force-length relations in isolated intact cardiomyocytes subjected to dynamic changes in mechanical load.

We developed a dynamic force-length (FL) control system for single intact cardiomyocytes that uses a pair of compliant, computer-controlled, and piezo translator (PZT)-positioned carbon fibers (CF). CF are attached to opposite cell ends to afford dynamic and bidirectional control of the cell's mechanical environment. PZT and CF tip positions, as well as sarcomere length (SL), are simultaneously monitored in real time, and passive/active forces are calculated from CF bending. Cell force and length were dynamically adjusted by corresponding changes in PZT position, to achieve isometric, isotonic, or work-loop style contractions. Functionality of the technique was assessed by studying FL behavior of guinea pig intact cardiomyocytes. End-diastolic and end-systolic FL relations, obtained with varying preload and/or afterloads, were near linear, independent of the mode of contraction, and overlapping for the range of end-diastolic SLs tested (1.85-2.05 micro m). Instantaneous elastance curves, obtained from FL relation curves, showed an afterload-dependent decrease in time to peak elastance and slowed relaxation with both increased preload and afterload. The ability of the present system to independently and dynamically control preload, afterload, and transition between end-diastolic and end-systolic FL coordinates provides a valuable extension to the range of tools available for the study of single cardiomyocyte mechanics, to foster its interrelation with whole heart pathophysiology.

Animals↗
PubMed1995

Effects of hypertonic saline and dextran 70 on cardiac functions after burns.

The effects of hypertonic saline-dextran (HSD) on cardiac contractility and hemodynamics after burns were studied in anesthetized animals with full-thickness 50% total body surface area burns that were resuscitated with HSD or lactated Ringer solution (LR) alone. No significant difference in cardiac contractility during 6 h postburn was observed between the two groups, as assessed by the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relationship. An additional bolus of HSD at 6 h postburn caused no significant changes in the end-systolic pressure-volume relationship and stroke work-end-diastolic volume relationship in the burned and sham-burned animals, both of which were resuscitated with HSD. Ten minutes of hemodynamic changes following HSD infusion at 30 min postburn revealed a sudden increase in stroke volume with biphasic responses in left ventricular systolic pressure, which first decreased, then increased, and finally returned to the pre-HSD value. End-diastolic volume was maintained at approximately 110% of the pre-HSD value during this period. We concluded that HSD does not enhance cardiac contractility after severe burns but does produce direct effects on postburn circulation to reduce afterload and augment preload, resulting in a short-lived increase in cardiac output.

Animals↗
PubMed1999

Contribution of the Na(+) channel and Na(+)/H(+) exchanger to the anoxic rise of [Na(+)] in ventricular myocytes.

The aim of this study was to quantify the contribution of the Na(+)/H(+) exchanger (NHE) and the Na(+) channel to the rise in cytosolic Na(+) concentration ([Na(+)]) that is seen in anoxic guinea pig ventricular myocytes. [Na(+)] was measured with the use of microfluorometry and was found to rise to 44 mM after prolonged anoxia. This rise was partially sensitive to either TTX or HOE-642, selective inhibitors of the Na(+) channel and NHE1, respectively. [Na(+)] did not significantly rise when both drugs were present, suggesting that other routes of Na(+) entry were insignificant. However, the relative contributions of the NHE and the Na(+) channel were found to be remarkably sensitive to ionic conditions expected to occur during ischemia. The Na(+) channel was the dominant Na(+) source during acidic anoxia. However, the NHE was the dominant Na(+) source during both hyperkalemic anoxia and simulated ischemia (hyperkalemia, low pH, and anoxia). The data suggest that the NHE may prove to be the best pharmacological target to reduce Na(+) entry during true ischemia and that inhibition of Na(+) influx could contribute strongly to the cardioprotective effects of NHE inhibitors.

Animals↗
PubMed1975

Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions.

Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.

Animals↗
PubMedDate not supplied

Experimental cerebral vasospasm. Part 2. Contractility of spastic arterial wall.

We studied the mechanical properties of canine basilar arteries subjected to experimental subarachnoid hemorrhage (SAH). Smooth muscle contractility was determined from pressure-diameter curves obtained after subjecting the basilar arteries to three different conditions: Krebs-Ringer solution (KRS), Krebs-Ringer solution containing serotonin (5HT), and saline solution. Pressure-diameter curves obtained in KRS and 5HT are biphasic and have sharp flexions that yield flexion points. The pressure level at the flexion point increases as vasospasm increases. Strong constriction is retained up to that pressure above which the constriction is released abruptly. These data suggest that increasing the intraluminal pressure dilates the spastic artery nonlinearly and that induced hypertension could relieve the cerebral ischemia caused by vasospasm if blood pressure were maintained above the flexion point. The contractile response of spastic arterial wall to serotonin remains unchanged after SAH although the spastic constriction increases progressively and becomes maximal seven days after SAH. The lesser the arterial wall stiffness, the more efficiently it constricts. This means that the diminution of arterial stiffness observed after SAH might be one of the factors promoting the development of vasospasm.

Animals↗
PubMed1994

Tumor necrosis factor alpha decreases in vivo diaphragm contractility in dogs.

In this study, we hypothesized that tumor necrosis factor alpha (TNF alpha) is an important mediator of sepsis-related impairment in diaphragm contractility (1-2). In 12 anesthetized, ventilated dogs, bipolar stimulating electrodes were placed on the phrenic nerves and diaphragm electromyographic activity (EMG) and shortening were recorded with needle electrodes and piezoelectric crystals, respectively. Transdiaphragmatic pressure (Pdi) was also recorded using esophageal (Pes) and abdominal balloon catheters (Pdi = Pab-Pes). Dogs were randomized to receive saline injection (n = 6), or TNF alpha 60 micrograms/kg (n = 6). All parameters were recorded hourly for 6 h. Mean arterial blood pressure decreased 1 h after infusion in TNF alpha animals (p < 0.05) with no significant change thereafter. Cardiac output increased early after TNF alpha infusion (p < 0.05) and remained at greater than baseline values at study termination. Diaphragm pressure generation and costal shortening decreased progressively from 3 to 6 h post TNF alpha infusion (p < 0.05) with no significant change in control animals. Compound diaphragm action potential in response to supramaximal phrenic stimulation decreased in TNF alpha animals (p < 0.01) with no significant change in control animals 3 and 6 h postinfusion. We conclude that TNF alpha infusion was associated with significant declines in isotonic and quasi-isometric diaphragm contraction and that this could be explained, at least in part, by impaired neuromuscular transmission.

Action Potentials↗
PubMed1976

"Calcium-induced release of calcium" in rectal smooth muscle of mice.

Contractile responses to K, ACh, Ba and exogenous Ca of rectal strips from mice were recorded isotonically. These responses consisted of phasic contraction and subsequent tonic contraction. In Ca-depleted preparations exposed to Ca-free bath medium, the contractions by K and ACh disappeared but the contraction by Ba remained constant. This residual contraction by Ba is presumably due to a direct stimulation of Ba to contractile elements of muscle. Metabolic inhibitors (anoxia and DNP) abolished tonic contraction without affecting phasic contraction by exogenous Ca. In Ca-free bath medium, tonic contraction by exogenous Ca immediately disappeared whereas phasic contraction gradually decreased and about 3 hr later remained constant in parallel with the occurrence of residual contraction by Ba. After pretreatment with the removal of Na from bath medium, which produced Ca-release action, phasic contractions by exogenous Ca in Ca-free bath medium were depressed like those by K, ACh and Ba. These results suggest that the phasic contraction by exogenous Ca is produced mainly by release of Ca and partly by influx of Ca. Thus, it is suggested that the same mechanism of Ca-induced release of Ca from the storage sited as described in skeletal muscle is also operating in rectal smooth muscle of mice.

Acetylcholine↗
PubMed1985

Action of dantrolene sodium on electrical and mechanical activity of guinea-pig ventricular muscles.

Effects of dantrolene sodium on electrical and mechanical activity of guinea-pig ventricular muscles were examined. The application of 2 X 10(-5) M of dantrolene caused a decrease of developed tension by 31% of the control level without noticeable changes in resting membrane potential, amplitude and maximum upstroke velocity (Vmax) of action potentials, and action potential duration. Negative inotropic effects of dantrolene appeared after 10 min application and reached almost a plateau after 15-20 min. Neither amplitude of the slow inward current nor the outward current on depolarization were affected by dantrolene. When muscle preparations were superfused with the low-K+, high-Ca2+ solution, they developed delayed afterdepolarizations and aftercontractions. The application of 2 X 10(-5) M of dantrolene did not reduce amplitudes of both delayed afterdepolarizations and aftercontractions, but depressed twitch tension to 74% of the control level. Dantrolene did not change the amplitude of the transient inward current observed under the low-K+, high-Ca2+ condition. These results suggest that a primary site of action of dantrolene is not the sarcolemma of ventricular myocardium, but possibly the Ca2+ releasing process from the sarcoplasmic reticulum. Its action is further indicated to affect the process of depolarization-induced Ca2+-release, either directly or indirectly rather than to inhibit Ca2+-induced Ca2+-release.

Action Potentials↗
PubMed1992

Superiority of the University of Wisconsin solution over simple crystalloid for extended heart preservation. A study of left ventricular pressure-volume relationship.

To compare the effects of the University of Wisconsin solution with those of an extracellular crystalloid solution, Krebs-Ringer bicarbonate, as cardiac preservation media, we studied 35 adult dogs in an isolated heart preparation. Four groups of seven hearts were preserved in University of Wisconsin solution for 6 or 12 hours or in Krebs-Ringer bicarbonate solution for 6 or 12 hours. An additional group of seven hearts with no ischemia was used for a control group. In the four preservation groups, hearts were arrested by electrolyte solution (Normosol with potassium chloride, 20 mEq/L, added, 4 degrees C), flushed with 200 ml of the preservation solution, and then stored in the same solution at 1 degree to 2 degrees C. The hearts were mounted on an isolated heart preparation equipped with a computer-controlled servo-pump system that used a mock arterial system to modulate the aortic input impedance presented to the left ventricle. Left ventricular pressure-volume loops were measured on-line for 2 hours of reperfusion with autologous warm oxygenated blood. Elastance was derived from the end-systolic pressure-volume relationship, and diastolic compliance was derived from the end-diastolic pressure-volume relationship. The total left ventricular performance was assessed by the preload recruitable stroke work area, the slope, and its x-intercept, all of which derived from the stroke work (pressure-volume area)-end-diastolic volume relationship. Extended global ischemia had more deleterious effects on the end-diastolic than the end-systolic pressure-volume relationship. In confirmation with other studies, elastance did not accurately reflect the level of ventricular contractile dysfunction because of the significant amount of diastolic dysfunction. The preservation of myocardial systolic and diastolic functions, as demonstrated by the preload recruitable stroke work area and diastolic compliance, was better in the University of Wisconsin solution groups than in the Krebs-Ringer bicarbonate solution groups after 6 and 12 hours of preservation. In addition, 6 hours of preservation with University of Wisconsin solution maintained normal systolic and diastolic functions as compared with those of the control group. Preservation with University of Wisconsin solution prevented any myocardial edema formation; by contrast, this was significantly increased after 12 hours in Krebs-Ringer bicarbonate solution. Groups preserved with University of Wisconsin solution had less reperfusion injury as evidenced by the release of coronary sinus creatine kinase during reperfusion; they also had improved oxygen use during reperfusion.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed2005

[Changes of myocardial dynamics in early stage of burn and effect of rapid fluid replacement in delayed resuscitation].

OBJECTIVE: To investigate the changes in myocardial dynamics in early phases of burn shock of dogs and the effects of rapid fluid infusion in delayed resuscitation. METHODS: Twelve mongrel dogs were randomly divided into control (n=6) and burn (n=6) groups. The dogs in burn group were subjected to 35% total body surface area (TBSA) III degree burn and were resuscitated with lactate Ringer's solution 6 hours postburn. The volumes and rates of fluid infusion were controlled basically on the urinary output of 1.0 mlxkg(-1)xh(-1) and cardiac output (CO) of 70%-80% of pre-burn values. The mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximum rate of intraventricular pressure rise/down (+/-dp/dt max) and cardiac index (CI) were determined at 0.5, 1,2, 6, 7, 8, 10 and 24 hours postburn. RESULTS: The MAP, LVSP, +/-dp/dt max and CI were significantly lowered from their baseline and those of control group at 0.5 hour postburn, and they kept declining until 6 hours postburn. They showed a tendency of elevation and reached or approached the levels of that in control group within 2 hours of resuscitation, and the differences were not significant between the two groups 4 hours after burn (all P>0.05). The amount of infusion fluid within the first 4 hours of resuscitation was (3.63+/-0.99) ml/kg per 1% TBSA. CONCLUSION: The myocardial dynamics is depressed in the early stage of burn, the effective way to improve it is to infuse a large amount of fluid rapidly when resuscitation is delayed.

Animals↗
PubMed1990

Hypertonic saline dextran resuscitation of thermal injury.

Burn treatment requires large volumes of crystalloid, which may exacerbate burn-induced cardiopulmonary dysfunction. Small-volume hypertonic saline dextran (HSD) resuscitation has been used for effective treatment of several types of shock. In this study isolated coronary perfused guinea pig hearts were used to determine if HSD improved left ventricular contractile response to burn injuries. Parameters measured included left ventricular pressure (LVP) and maximal rate of LVP rise (+dP/dt max) and fall (-dP/dt max) at a constant preload. Third-degree scald burns comprising 45% of total body surface area (burn groups, N = 75), or 0% for controls (group 1, N = 25) were produced using a template device. In group 2, 25 burned guinea pigs were not fluid resuscitated and served as untreated burns; 20 burns were resuscitated with 4 mL lactated Ringer's (LR) solution/kg/% burn for 24 hours (group 3); additional burn groups were treated with an initial bolus of HSD (4 mL/kg, 2400 mOsm, sodium chloride, 6% dextran 70) followed by either 1, 2, or 4 mL LR/kg/% burn over 24 hours (groups 4, 5, and 6, respectively). Untreated burn injury significantly impaired cardiac function, as indicated by a fall in LVP (from 88 +/- 3 to 68 +/- 4 mmHg; p = 0.01) and +/- dP/dt max (from 1352 +/- 50 to 1261 +/- 90 and from 1150 +/- 35 to 993 +/- 59; p = 0.01, respectively) and a downward shift of LV function curves from those obtained from control hearts. Compared to untreated burns, hearts from burned animals treated with LR alone showed no significant improvement in cardiac function. However hearts from burned animals treated with HSD + 1 mL LR/kg/% burn had significantly higher LVP (79 +/- 4 vs. 68 +/- 4 mmHg, p = 0.01) and +/- dP/dt max (+dP/dt: 1387 +/- 60 vs. 1261 +/- 90 mmHg/sc, p = 0.01; -dP/dt: 1079 +/- 50 vs. 993 +/- 59 mmHg/sc, p = 0.01) than hearts from untreated burned animals and generated left ventricular function curves comparable to those calculated for hearts from control animals. Mortality 24 hours after burn was 29% for untreated burns was 0% for control animals, as well as for groups treated with the Parkland formula or HSD plus 1 or 2 mL/kg/% burn lactated Ringer's. The only deaths after treatment occurred in those animals given HSD plus 4 mL/kg/% burn, Parkland formula (17% mortality).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Studies of controlled reperfusion after ischemia. XX. Reperfusate composition: detrimental effects of initial asanguineous cardioplegic washout after acute coronary occlusion.

UNLABELLED: This study tests whether initial asanguineous washout of potentially toxic substances that accumulate during ischemia improves recovery produced by blood cardioplegic reperfusion and evaluates the role of plasma versus whole blood cardioplegia. METHODS: Twenty-four dogs underwent 2 hours of occlusion of the left anterior descending coronary artery and 20 minutes of blood cardioplegic reperfusion on total vented bypass. In 13 dogs, a 5-minute infusion of either a crystalloid (n = 7) or plasma (n = 6) cardioplegic solution (containing the same pH, calcium potassium, and osmolarity as blood cardioplegia) was given immediately before reoxygenation with blood cardioplegia. Regional oxygen uptake and coronary vascular resistance were measured during controlled reperfusion, and segmental shortening (ultrasonic crystals), tissue water content, and histochemical damage (triphenyltetrazolium chloride stain) were assessed 1 hour after bypass was discontinued. RESULTS: Asanguineous cardioplegic washout before reoxygenation with blood cardioplegic solution resulted in a progressive (+42%) increase in coronary vascular resistances (from 123 to 176 units, p less than 0.05) and low oxygen utilization during 20 minutes of blood cardioplegic reperfusion (29 ml/100 gm, p less than 0.05); coronary vascular resistance remained low throughout blood cardioplegic reperfusion without washout (from 109 to 98 units), and oxygen utilization was 54 ml/100 gm (p less than 0.05). Neither plasma nor crystalloid washout restored substantial regional systolic shortening (3% systolic shortening versus 73% systolic shortening with blood cardioplegia), and asanguineous washout caused more myocardial edema (81.1% +/- 80.9% versus 79.5% water content, p less than 0.05) and produced extensive transmural triphenyltetrazolium chloride damage (48% +/- 41% versus 8% nonstaining in area at risk, p less than 0.05) than initial blood cardioplegic reperfusion. CONCLUSION: Asanguineous cardioplegic washout before blood cardioplegic reperfusion limits oxygen utilization during subsequent controlled reperfusion, restricts early recovery of systolic shortening, allows more myocardial edema, and produces extensive histochemical damage, which may be avoided by initial reoxygenation with blood cardioplegia. The red blood cells appear more important than the plasma components of blood cardioplegia.

Adenosine Triphosphate↗
PubMed1991

Studies of controlled reperfusion after ischemia. XXI. Reperfusate composition: superiority of blood cardioplegia over crystalloid cardioplegia in limiting reperfusion damage--importance of endogenous oxygen free radical scavengers in red blood cells.

UNLABELLED: Postischemic damage is caused partially by oxygen free radical-mediated injury. This study will show that (1) crystalloid cardioplegia with room air oxygen is deleterious because it is devoid of free radical scavengers and (2) blood cardioplegia limits damage because it contains endogenous free radical scavengers in red blood cells. METHODS: Thirty-two dogs underwent 2 hours of ligation of the left anterior descending coronary artery followed by 20 minutes of regional blood cardioplegic reperfusion on bypass. Ten dogs received only the blood cardioplegic solution (containing its endogenous free radical scavengers); five received initial blood cardioplegia (5 minutes) with endogenous free radical scavengers (catalase and glutathione peroxidase) blocked by aminotriazole and N-ethylmaleimide, respectively; 12 received initial crystalloid cardioplegic solution oxygenated by room air (oxygen tension = 150 mm Hg); seven without and five with exogenous free radical scavengers (superoxide dismutase, catalase, coenzyme Q10); five received initial deoxygenated crystalloid cardioplegic solution (oxygen tension = 6 mm Hg); and five received deoxygenated crystalloid cardioplegic solution. RESULTS: Blood cardioplegia with endogenous free radical scavengers produced the best recovery of systolic shortening (69% systolic shortening) and resulted in the least histochemical damage (11% triphenyltetrazolium chloride nonstaining). The worst recovery and most damage occurred if blood cardioplegia was preceded by oxygenated crystalloid cardioplegia (3% systolic shortening, 48% triphenyltetrazolium chloride nonstaining; p less than 0.05 versus blood cardioplegia) or if free radical scavengers were blocked in the initial period of blood cardioplegia (3% systolic shortening, 41% triphenyltetrazolium chloride nonstaining; p less than 0.05 versus blood cardioplegia). Conversely, deoxygenation or supplementation of oxygenated crystalloid cardioplegic solution with exogenous free radical scavengers restored 60% systolic shortening (p less than 0.05 versus oxygenated crystalloid cardioplegia) and 54% systolic shortening (p less than 0.05 versus oxygenated crystalloid cardioplegia) and reduced damage to 34% and 21% (both p less than 0.05 versus oxygenated crystalloid cardioplegia). CONCLUSION: Blood cardioplegic solutions containing their own endogenous free radical scavengers are superior to crystalloid cardioplegic solutions, because they limit oxygen-mediated perfusion damage and restore contractile function. Initial crystalloid cardioplegic washout negates the salutary effect of blood cardioplegia. Exogenous free radical scavenger supplementation or deoxygenation of the cardioplegic reperfusate is necessary only if crystalloid cardioplegia is used.

Adenosine Triphosphate↗