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 1,261 records · Page 70Linked to original sources

Increased myocardial tumor necrosis factor-alpha in a crystalloid-perfused model of cardiac ischemia-reperfusion injury.

BACKGROUND: The heart is a tumor necrosis factor-alpha (TNF-alpha)-producing organ. Recent basic experimental and clinical evidence suggests that TNF-alpha is an important mediator of myocardial injury during acute myocardial infarction, chronic heart failure, cardiac allograft rejection, and cardiopulmonary bypass operations. Although it is known that the myocardium itself is capable of producing TNF-alpha in response to endotoxin, it is unknown whether there is an increase in myocardial tissue TNF-alpha levels after ischemia-reperfusion injury. We hypothesized that ischemia-reperfusion induces the production of TNF-alpha by the heart. METHODS: To avoid blood-borne TNF-alpha as a potentially confounding variable, we examined myocardial TNF-alpha production in a crystalloid-perfused model of cardiac ischemia-reperfusion injury. Isolated rat hearts were perfused with crystalloid solution and subjected to ischemia-reperfusion. Postischemic myocardial TNF-alpha was measured using an enzyme-linked immunosorbent assay and correlated with developed pressure, coronary flow, end-diastolic pressure, and creatine kinase loss (assay of activity in coronary effluent). RESULTS: Ischemia-reperfusion induced a marked increase in myocardial TNF-alpha that was associated with decreased myocardial contractility and coronary flow and with increased end-diastolic pressure and postischemic creatine kinase loss. CONCLUSIONS: The heart produces TNF-alpha in response to ischemia-reperfusion. Ischemia-induced TNF-alpha production may contribute to postischemic myocardial stunning, necrosis, or both. Strategies designed to limit ischemia-induced myocardial TNF-alpha production may have therapeutic utility in the settings of planned myocardial ischemic events.

Animals↗

Experimental deep tissue pain in wrist extensors--a model of lateral epicondylalgia.

The aim of this experimental study was to develop an in vivo model demonstrating sensory and motor interactions comparable to those seen in patients presenting with lateral epicondylalgia (i.e., deep tissue pain and hyperalgesia localised to specific sites in the wrist extensors, attenuation of wrist extension force). The effect of saline-induced deep pain combined with delayed onset muscle soreness (DOMS) on deep tissue sensitivity and motor function in wrist extensors was examined. Muscle pain intensity (visual analogue scale: VAS), distribution, and quality were assessed in 12 subjects. Pressure pain thresholds (PPTs) were recorded at five different sites around the elbow. Maximal wrist extension force was recorded. In the absence of DOMS, hypertonic saline administrated into different parts of the wrist extensors (extensor carpi radialis brevis, supinator, common extensor origin) induced significantly (P<0.05) higher VAS scores and larger pain areas compared with a control injection of isotonic saline. The typical quality of saline-induced pain was described as "drilling", "taut", "nagging" and "intense". In non-exercised wrist extensors, hyperalgesia to pressure was not detected during saline-induced pain but maximal wrist extensor force decreased significantly (P<0.05) compared with pre-pain recordings and recordings post isotonic saline. DOMS induced by eccentric wrist extension contractions generated moderate levels of soreness but no resting pain up to 24h post exercise. PPTs and maximal wrist extension force were significantly decreased (P<0.05) during DOMS compared with baseline and 7 days post exercise (P<0.05). VAS scores to injection of hypertonic saline into the DOMS arm were significantly increased (P<0.05) compared with injections into the unexercised arm. This is another manifestation of muscle hyperalgesia. Saline-induced pain combined with DOMS further decreased maximal wrist extension force (P<0.05). The simultaneous deep tissue pain and hyperalgesia linked with force attenuation support the use of the saline-induced deep tissue pain combined with DOMS as an experimental model simulating the clinical sensorimotor correlates of lateral epicondylalgia.

Adult↗

The dynamic properties of mammalian skeletal muscle.

The dynamic characteristics of the rat gracilis anticus muscle at 17.5 degrees C have been determined by isotonic and isometric loading. For a fixed initial length these characteristics were represented either as a family of length-velocity phase trajectories at various isotonic afterloads or as a series of force-velocity curves at different lengths. An alternate method of viewing these data, the length-external load-velocity phase space, was also generated. When the muscle was allowed to shorten from different initial lengths, the velocity of shortening achieved at a given length was lower for longer initial lengths. The amount of departure was also dependent upon the isotonic load, the greater the load the greater the departure. The departures were not caused by changes in the elastic elements of the muscle or fatigue in the ordinary sense. When the behavior of the muscle was investigated at different frequencies of stimulation, the shortening velocity was a function of the number of stimulating pulses received by the muscle at a given frequency. The shortening velocity of the rat gracilis anticus muscle is, therefore, not only a function of load and length, but also of an additional variable related to the time elapsed from onset of stimulation.

Animals↗

Cardiac function after eight hour storage by using polyethylene glycol hemoglobin versus crystalloid perfusion.

Efforts to extend myocardial preservation for transplantation by crystalloid perfusion have been limited by edema and compromised function. We hypothesized that hypothermic perfusion preservation with a polyethylene glycol (PEG) conjugated hemoglobin solution may extend preservation times. The purpose of this study was to compare cardiac function after continuous perfusion by using a hypocalcemic, normokalemic crystalloid perfusate with and without the addition of PEG-hemoglobin (Hb). The hearts of 20 anesthetized and ventilated New Zealand White rabbits were harvested after cold cardioplegic arrest. Group I (n = 10) hearts were continuously perfused with a hypocalcemic, normokalemic 3% bovine PEG-Hb solution at 20 degrees C and 30 mm Hg for 8 hours. Group II (n = 10) hearts were continuously perfused with an identical crystalloid solution without PEG-Hb for 8 hours under the same conditions as group I hearts. Cardiac function was measured with a left ventricular force transducer after transfer to a standard crystalloid Langendorff circuit at 37 degrees C and an aortic root pressure of 59 mm Hg. After 8 hours of perfusion preservation, heart rate was similar for groups I and II (p = not significant [NS]). Coronary blood flow after and during preservation was similar between PEG-Hb and crystalloid preserved hearts (p = NS). Left ventricular developed pressure, peak dP/dt, and peak -dP/dt were superior in hearts preserved with PEG-Hb. Percent water of total ventricular weight was 82.0% for group I and 81.6% for group II (p = NS). Continuous perfusion preservation of rabbit hearts for 8 hours with a hypocalcemic normokalemic PEG-Hb based solution at 30 mm Hg and 20 degrees C yields left ventricular function that is superior to perfusion with a similar crystalloid solution without PEG-Hb, despite similar myocardial edema and coronary flow. Extended cardiac perfusion preservation with this PEG-Hb based solution deserves further study, including comparison with traditional cardioplegic preservation solutions.

Animals↗

Non-cardiogenic pulmonary oedema. A serious complication of transurethral prostatectomy. A case report.

A patient undergoing prostatectomy under epidural analgesia developed clinical signs of a severe TURP syndrome. During resuscitation, it was revealed that serum sodium was only moderately decreased. Plasma oncotic pressure was, however, markedly decreased and the pressure gradient between plasma oncotic pressure and pulmonary capillary wedge pressure (approximately hydrostatic pressure) was 1 mmHg (0.13 kPa) only, allowing almost free filtration of fluid through the pulmonary capillary wall, resulting in a non-cardiogenic pulmonary edema. The patient was successfully resuscitated with albumin and inotropic stimulation with prenalterol.

Aged↗

An evaluation of laparoscopic tissue harvesting for human adult urological smooth muscle physiological experimentation.

OBJECTIVE: To evaluate the properties of laparoscopically harvested bladder neck and ureteric smooth muscle, compared with tissue obtained at open surgery. MATERIALS AND METHODS: Bladder neck was harvested from patients undergoing open (eight) or laparoscopic radical prostatectomy (11). Ureter was obtained from patients undergoing nephrectomy (laparoscopic or open) and cystectomy (open only); obtained openly from 16 and laparoscopically from seven. Muscle strips dissected from these samples were perfused in a Brading-Sibley organ bath, and stimulated using standard agonists (100 micromol/L carbachol for bladder neck, 100 mmol/L KCl-enriched Krebs' solution for ureteric muscle). Tensions produced were recorded using strain gauges and analysed using data-acquisition software. Results were compared by a two-tailed Fisher's exact test to determine significance. RESULTS: Openly harvested bladder neck muscle strips from six patients showed a measurable response to the standard agonist. Laparoscopically harvested bladder neck strips from only two patients showed any measurable response. Openly harvested ureteric muscle strips from 12 patients responded to K-enriched solution, while one patient's laparoscopically harvested strips responded to stimulation. This difference was significant in both tissue groups separately (P < 0.025). Histological evaluation identified no specific differences between openly and laparoscopically harvested tissue. CONCLUSION: The yield of smooth muscle available for research is significantly less when the resection is laparoscopic; this might be a result of diathermy damage at a subcellular level. With the increasing use of the laparoscopic approach in urological surgery, the effect on tissue availability for human smooth muscle physiological study is important to researchers in this field.

Adult↗

Isotonic and isometric responses of different tonic muscles to agonists and antagonists.

1 With isotonic recording the percentage of muscle shortening as compared with the maximal possible shortening, and with isometric recording the percentage of developed tension were determined. In relatively 'thick' muscles, such as dorsal leech muscle, frog rectus abdominis or protractor pharynx of holothuria (0.3-0.8 mm thick), the concentrations of a full agonist (carbachol) producing a given percentage of tension, (e.g. 50%) are about 5 times greater than the concentrations, producing the same percentage of shortening. In 'thin' muscles the difference between the percentage of shortening and tension is either small (retractor dentis of the sea urchin, 0.1 mm thick, response to carbachol) or absent (guinea-pig ileum, 0.06 mm thick, responses to methylfurmethide). The possible mechanism underlying this difference is discussed. 2 With partial agonists (dodecamethonium and heptamethonium) the fractional tension of the frog rectus abdominis is always less than the fractional shortening and the correlation between shortening and tension is the same as in the case of full agonists. 3 The blocking activity of (+)-tubocurarine on the frog rectus abdominis is the same in isotonic and in isometric conditions. 4 On the frog rectus abdominis the alkylating agent, decamethonium mustard, does not produce any 'parallel shift' of the dose-response curve for carbachol, the only result of alkylation being a decrease in maximal response, which is more pronounced in isometric than in isotonic conditions. The degree of decrease is in accordance with the correlation between percentage of shortening and percentage of tension in the absence of alkylating agent. Probably this muscle does not possess any 'spare receptors'. 5 On the frog muscle the dose-isometric response curve for acetylcholine (ACh) is shifted toward greater concentration about 33-fold as compared with the dose-isotonic response curve but after the inhibition of cholinesterases the shift is only about 6-fold. The same shift (5-fold) is observed for carbachol, which is not hydrolysed by cholinesterases. The results with ACh are due to the fact, that after cholinesterase inhibition the sensitivity to ACh increases in isotonic conditions only 13-fold, but in isometric conditions it increases 71-fold. Probably under isometric conditions, when the muscle remains in the extended state, the rate of hydrolysis of ACh is much greater than under isotonic conditions when the muscle is shortened during contraction.

Acetylcholine↗

Effect of hyperosmolarity on resting and developed tension in heart muscle.

Simultaneous changes in weight, tension, and electrical activity were studied in the isolated perfused rabbit heart when the Ringer solution perfusion fluid was made hypertonic by the addition of sucrose, urea, glycerol, ethylene glycol, or formamide. The typical responses to each of the molecules was an initial drop in weight and tension followed by a return toward the base-line level. A 0.4 M concentration of sucrose, urea, or glycerol reduced the weight to 40 +/- 4.6, 48 +/- 3, and 52.2 +/- 3% of the initial value, respectively. The tension was simultaneously reduced to 23 +/- 3.5, 31 +/- 2, and 41 +/- 4% of its initial value. The tension drop produced by the solutes tested was linearly related to the amount of water lost by the heart. The falling phases of both tension and weight loss were closely correlated phases of both tension and weight loss were closely correlated in time a magnitude and were both related to the effectiveness of a particular molecule to move water out of the cells. In contrast, the subsequent rising phases of tension and weight were not as well correlated in time and magnitude. Whereas for most of the molecules used, the tension recovery was incomplete; urea, in contrast, caused an overshoot of the control tension level, thus pointing toward a unique inotropic effect of this compound. Resting tension rose for both urea and sucrose but not for the other compounds.

Animals↗

Crystalloid and perfluorochemical perfusates in an isolated working rabbit heart preparation.

Krebs-Henseleit buffer (KH) and a perfluorochemical (FC-43) were compared as perfusates in an isolated working rabbit heart preparation. Both perfusates were oxygenated in an identical manner using an infant bubble oxygenator. After 60 min of perfusion, no difference could be detected in the ratio of wet to dry heart weight between KH- and FC-43-perfused hearts (KH, 6.25 +/- 0.3; FC-43, 5.99 +/- 0.20). Left ventricular systolic pressure, maximal rate of left ventricular pressure rise, mean aortic systolic pressure, cardiac output, aortic flow, left ventricular power, and myocardial O2 consumption (MVO2) were significantly higher in FC-43-perfused hearts throughout the time of perfusion. However, there were no differences in resistance to cardiac output and heart rate. In KH- and FC-43-perfused hearts, MVO2 and left ventricular power were closely correlated (KH, r = 0.793; FC-43, r = 0.831). Significantly higher coronary flow of KH-perfused hearts could be attributed to the lower viscosity of KH (1.05 Pa . s) compared with FC-43 (1.91 Pa . s). Increased O2 extraction during KH perfusion could not compensate for low O2-carrying capacity of KH buffer (345 compared with 705 nmol O2 X ml-1 in FC-43 emulsion). A postischemic increase of coronary flow was observed only in FC-43-perfused hearts (28%). These results demonstrate a different response of perfused heart preparations to FC-43 and KH buffer.

Animals↗

Paradox of enhanced contractility in postischemic rat hearts with depressed function.

Depressed function of postischemic hearts may be related to incomplete recovery of coronary perfusion. To circumvent this factor we studied the properties of papillary muscles under controlled extracellular conditions. First, recovery of function was measured in postischemic rat hearts. Next, a muscle was dissected and superfused in a bath. After 40 min of ischemia, recovery of cardiac output was generally zero. Muscles from this group were relaxed or showed small contractures. After 20-30 min of ischemia recovery of coronary flow and cardiac output was 50-100%, and the isolated muscles showed the following properties (compared with Langendorff-perfused controls): 1) increased force at normal or low [Ca2+]; 2) action potential and postextrasystolic potentiation were unchanged, which indicates that Ca2+ influx per beat was unchanged; 3) the decay of potentiation was slowed, indicating a reduced rate of Ca2+ extrusion via Na(+)-Ca2+ exchange. This implies intracellular Ca2+ accumulation and explains the increased force. Postischemic enhancement of contractility (isovolumic pressure) was demonstrated also in whole heart preparations. We conclude that mild injury by preceding ischemia leads to enhanced contractility (Ca2+ accumulation), advanced injury to local contractures, and finally to a general contracture (Ca2+ overload). Recovery of heart function and coronary flow probably depends on the number and size of local contractures.

Action Potentials↗

Influence of the bathing medium on the contractile responses of the rabbit urinary bladder.

This study examined contractile responses of the in vitro rabbit whole-bladder preparation to field stimulation, bethanechol and KCl in Tyrode's solution and minimum essential medium (MEM). We found frequency-dependent increases in intravesical pressure in bladders incubated in Tyrode's solution and MEM. However, bladders incubated in MEM consistently responded with greater increases in intravesical pressure compared to those incubated in Tyrode's solution. Similarly, there were frequency-dependent increases in the rate of pressure generation in bladders incubated in Tyrode's solution and MEM, and bladders incubated in MEM responded with greater rates of pressure generation than those incubated in Tyrode's solution at frequencies of 1, 2 and 4 Hz. In addition, there were significant increases in intravesical pressure generated in response to administration of 500 mmol/l bethanechol and 186.4 mmol/l KCl in bladders incubated in MEM compared to Tyrode's solution but no changes in the rate of pressure generation. The influence of L-methionine, one of the constituents of MEM, on the responses of whole bladders to nerve stimulation was also investigated. L-methionine at concentrations of 0.1 and 1.0 mmol/l had no effects on the increase in intravesical pressure or rate of pressure generation following nerve stimulation. It is speculated that the increases in contractile responsiveness of bladders incubated in MEM are related to the combination of amino acids, vitamins and other constituents of the cell culture medium.

Animals↗

Anion manipulation: a new antiarrhythmic approach. Action of substitution of chloride with nitrate on ischemia- and reperfusion-induced ventricular fibrillation and contractile function.

The role of anions in the initiation of ischemia- and reperfusion-induced arrhythmias is unknown. We examined the antiarrhythmic effects of isotonic substitution of extracellular Cl- with NO3- by using the rat Langendorff preparation (n = 12 per group). During 30 minutes of regional ischemia, the incidence of ventricular fibrillation (VF) was reduced from 50% in hearts perfused with control solution (containing a Cl-:NO3- ratio of 100:0) to 25%, 0% (p less than 0.05), 0% (p less than 0.05), and 0% (p less than 0.05) by perfusion with solution containing Cl-:NO3- ratios of 75:25, 50:50, 25:75, and 0:100, respectively. The incidence of reperfusion-induced VF was also reduced from 58% to 25%, 8% (p less than 0.05), 8% (p less than 0.05), and 0% (p less than 0.05), respectively. Similar effects were produced in hearts reperfused after briefer durations of ischemia (10 or 15 minutes). Substitution of NO3- for Cl- also facilitated spontaneous termination of VF. Heart rate and occluded zone size were not affected by anion manipulation. Coronary flow was affected by NO3-, but changes did not correlate with arrhythmias. During ischemia, electrocardiographic changes indicative of class III activity (widening of the ventricular complex) were produced by anion substitution. These changes occurred selectively in the ischemic tissue with no significant influence before ischemia onset. However, the relation between this effect and arrhythmia reduction was not linear and a cause-effect relation is therefore unlikely. In separate groups of hearts (n = 12 per group), switching from 100:0 to 0:100 Cl-:NO3- solution or vice versa 10 seconds after coronary occlusion or just before reperfusion demonstrated that 1) protection against ischemia-induced VF resulted partly from an action in the ischemic zone and partly from an action in the nonischemic zone, and 2) protection against reperfusion-induced VF resulted principally from an action occurring during reperfusion and within the reperfused tissue. To assess whether benefit was offset by deleterious effects on contractile function in nonischemic tissue, we constructed Starling curves in isolated rate hearts. The 0:100 Cl-:NO3- solution had no effect on compliance or contractility at physiological end-diastolic pressures but reduced the slope of the peak systolic pressure-volume relation by approximately 20% as end-diastolic pressure was increased above 10 mm Hg. In conclusion, anions appear to play a hitherto unrecognized role in arrhythmogenesis in ischemia and reperfusion. Manipulation of anion homeostasis may represent a novel target for antiarrhythmic drug development.

Animals↗

The role of Na+ channels in twitch generation during exposure of the frog rectus abdominis to Ca-free Ringer solution with Na2EDTA.

The aim of the study was to investigate whether Na+ channels play a role in the twitch component of the response of the isolated frog rectus abdominis to Ca(2+)-free Ringer solution with 0.2 mM Na2EDTA by using tetrodotoxin and some other well known drugs that exhibit a blocking action on Na+ channels. In the presence of 5 x 10(-7) M tetrodotoxin, the twitch component, measured isotonically, disappeared. Although 10(-7) M d-tubocurarine was found to be ineffective, a complete blockage of twitch amplitude was observed at 5 x 10(-6) M concentration of the drug. The inhibitory action of d-tubocurarine on twitch response was not antagonized by 10(-6) and 10(-5) M carbachol. Propranolol (10(-6) - 10(-5) M), lidocaine (2 x 10(-6) - 10(-5) M), quinine (10(-6) - 2 x 10(-5) M) and quinidine (10(-6) - 2 x 10(-5) M) inhibited maximal twitch amplitude in a concentration dependent manner. These findings strongly suggest that activation of tetrodotoxin sensitive Na+ channel may play a primary role at twitch generation during exposure of the frog rectus abdominis to Ca(2+)-free Ringer solution with Na2 EDTA.

Animals↗