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At least 19 recordsLinked to original sources
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↗
PubMed1996

Dichotomy of ischemic preconditioning: improved postischemic contractile function despite intensification of ischemic contracture.

BACKGROUND: Acceleration of ischemic contracture is conventionally accepted as a predictor of poor postischemic function. Hence, protective interventions such as cardioplegia delay ischemic contracture and improve postischemic contractile recovery. We compared the effect of ischemic preconditioning and cardioplegia (alone and in combination) on ischemic contracture and postischemic contractile recovery. METHODS AND RESULTS: Isolated rat hearts were aerobically perfused with blood for 20 minutes before being subjected to zero-flow normothermic global ischemia for 35 minutes and reperfusion for 40 minutes. Hearts were perfused at a constant pressure for 60 mm Hg and were paced at 360 beats per minute. Left ventricular developed pressure and ischemic contracture were assessed with an intraventricular balloon. Four groups (n=8 hearts per group) were studied: control hearts with 35 minutes of unprotected ischemia, hearts preconditioned with one cycle of 3 minutes of ischemia plus 3 minutes of reperfusion before 35 minutes of ischemia, hearts subjected to cardioplegia with St Thomas' solution infused for 1 minute before 35 minutes of ischemia, and hearts subjected to preconditioning plus cardioplegia before 35 minutes of ischemia. After 40 minutes of reperfusion, each intervention produced a similar improvement in postischemic left ventricular development pressure (expressed as a percentage of its preischemic value: preconditioning, 44 +/- 2%; cardioplegia, 53 +/- 3%; preconditioning plus cardioplegia, 54 +/- 4% and control, 26 +/- 6%, P<.05). However, preconditioning accelerated whereas cardioplegia delayed ischemic contracture; preconditioning plus cardioplegia gave an intermediate result. Thus, times to 75% contracture were as follows: control, 14.3 +/- 0.4 minutes; preconditioning, 6.2 +/- 0.3 minutes; cardioplegia 23.9 +/- 0.8 minutes; and preconditioning plus cardioplegia 15.4 +/- 2.4 minutes (P<.05 preconditioning and cardioplegia versus control). In additional experiments, using blood- and crystalloid-perfused hearts, we describe the relationship between the number of preconditioning cycles and ischemic contracture. CONCLUSIONS: Although preconditioning accelerates, cardioplegia delays, and preconditioning plus cardioplegia has little effect on ischemic contracture, each affords similar protection of postischemic contractile function. These results question the utility of ischemic contracture as a predictor of the protective efficacy of anti-ischemic interventions. They also suggest that preconditioning and cardioplegia may act through very different mechanisms.

Animals↗
PubMed1989

Volkmann's ischemic contracture.

Volkmann's ischemic contracture is a complex process that often results in a significant functional disability. Destruction of the forearm musculature can, in certain situations, be reconstructed utilizing muscle transplantation. Proper patient selection, attention to detail at the time of the surgical procedures, and patient compliance during rehabilitation are key factors in a successful outcome. Functional results have been very rewarding, although certain problem areas await resolution.

Compartment Syndromes↗
PubMed1987

[Role of disorders of calcium homeostasis in the development of ischemic contracture of the heart].

The development of ischemic contracture in rat was evaluated in relation to glycolytic production of ATP and Ca2+ homeostasis. When the rate of glycolysis was reduced by glycogen depletion (swimming at 33 degrees C for 2 h, administration of isoprenaline or heart perfusion with it), the rate of ischemic contracture development increased. Isoprenaline increased the development of contracture in a dose-dependent manner, and dexamethasone potentiated the effect of isoprenaline. The decrease in the intensity of ATP/P1 exchange, probably reflecting the intensity of glycolytic phosphorylation of ADP, which, in our conditions, arose from ATP hydrolyzed mostly by Ca2+-ATPase and Na, K-ATPase, correlated with the development of ischemic contracture. Experiments with the rapid equilibration of the extracellular compartment with Ca2+ in various concentrations in the presence or absence of verapamil suggest that the development of ischemic contracture depends on the rate of Ca2+ accumulation in myoplasm. This rate of Ca2+ accumulation correlates with the rate of glycogenolysis and glycolysis which seems to produce ATP for active transport of cations.

Adenosine Triphosphate↗
PubMed1990

Glucose flux rate regulates onset of ischemic contracture in globally underperfused rat hearts.

This study analyzes the importance of the source and rate of ATP production (glucose flux, glycogenolysis, and oxidative phosphorylation) in the prevention of ischemic contracture in isolated rat hearts. Ischemic contracture was initiated at about 10 minutes by buffer perfusion with nonglycolytic substrates whereas the addition of 11 mM glucose prevented contracture for 2 hours. Tissue values of ATP, phosphocreatine, and lactate could be dissociated from onset of ischemic contracture. In hearts perfused with acetate or free fatty acid, with 11 mM glucose, glycolytic ATP production was 2.3-2.8 mumol/g fresh wt/min; as initial rates of glycogenolysis fell, glycolysis was maintained by a steady increase of glucose flux to values in excess of 2 mumol ATP/g fresh wt/min. Decreasing the glucose flux by lowering the perfusate glucose or by the addition of 2-deoxyglucose precipitated ischemic contracture. When oxidative phosphorylation was further reduced by hypoxia, glucose still prevented ischemic contracture; however, when oxidative phosphorylation dropped to near zero (near-anoxic) rates, glycolysis was inhibited, and glucose could only delay ischemic contracture to about 45 minutes. Combined ATP production rates could be dissociated from contracture. The metabolic parameter that correlated best with prevention or delay of ischemic contracture was the rate of glycolytic flux from glucose, which in this model of global low-flow ischemia had to accelerate to provide a rate of ATP production from glucose in excess of 2 mumol/g fresh wt/min within 30 minutes of the start of ischemia to prevent ischemic contracture.

Acetates↗
PubMed1979

Protection of mitochondrial function during ischemia by potassium cardioplegia: correlation with ischemic contracture.

The effect of potassium cardioplegia on mitochondrial function was evaluated in the ischemic isolated rat heart. Mitochondrial function as well as adenosine triphosphate (ATP) levels were determined at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes following contracture completion. Group I received no cardioplegia prior to ischemia, while Group II received potassium cardioplegia prior to the onset of ischemia. The respiratory control index (RCI), which is the primary measure of the intactness of mitochondrial function, was calculated with both a NAD (nicotinamide adenine dinucleotide)-linked substrate and a FAD (flavin adenine dinucleotide)-linked substrate. Potassium cardioplegia significantly delayed ischemic contracture initiation and completion. Although the RCI and ATP levels decreased significantly at successive levels of contracture, there was no difference in the RCI or ATP content between Group I and Group II at contracture initiation or completion. Unlike previous investigations that have used a time-base to examine mitochondrial function and acute cardiac ischemic injury, we correlated mitochondrial function with the measurable physiologic event ischemic contracture. The data indicated that potassium cardioplegia preserved ATP content and mitochondrial function, and that contracture initiation and completion correlate well with specific ATP levels and mitochondrial respiratory control. The relationship between mitochondrial function and ATP content indicates that the beneficial effect of potassium cardioplegia on mitochondrial function may be secondary to the preservation of high-energy phosphate levels which provide energy for mitochondrial maintenance.

Adenosine Triphosphate↗
PubMed1975

Ischemic contracture of the left ventricle. Production and prevention.

Ischemic contracture of the left ventricle ("stone heart") is a recognized complication of prolonged periods of interruption of the coronary circulation during open-heart surgery. We have examined the effects of moderate hypothermia (28 degrees C.) and preoperative beta-adrenergic blockade (propranolol, 0.5 mg. per kilogram; 1.0 mg. per kilogram) on contracture development during ischemic arrest of the heart. Four groups of 8 dogs each were placed on total cardiopulmonary bypass, and ischemic arrest of the heart was produced by cross-clamping the ascending aorta and venting the left ventricle. Intramyocardial carbon dioxide tension was continuously monitored by mass spectrometry. When anaerobic energy production ceased, as indicated by a final plateau in the intramyocardial carbon dioxide accumulation curve, the ischemic arrest was terminated and the contractile state of the heart observed. These results are given in the text. We conclude that beta-adrenergic blockade delays, but does not prevent, the onset of ischemic contracture of the left ventricle under normothermic conditions. Moderate hypothermia appears to prevent this complication completely.

Animals↗
PubMed1999

[Median nerve decompression in ischemic contracture of the forearm].

Ischemic contracture of the forearm known as Volkmann contracture develops from untreated (or treated to late) compartment syndrome within the forearm. Surgery is needed if function of the extremity is to be restored after fully developed Volkmann contracture. The uniform management is accepted in our Department since 1982. Multi-stage surgical treatment is indicated, the first stage consisting of median nerve neurolysis and removal of necrotic tissues to restore physiological excursion of the nerve. A series of 48 patients (16 females, 32 males aged 5-42 years) treated between 1982 and 1995 was included in the study. Complete neurolysis of the median nerve (microsurgical within proximal 1/3 of the forearm) was done in all patients. Long-term assessment of the median nerve function was done at half year to 3 years follow-up. Symptoms of nerve entrapment indicated reoperation. The study confirmed usefulness of an early median nerve decompression for prevention of neurological complications and improvement of the extremity function.

Adolescent↗
PubMed1991

[Ischemic contracture of the forearm and hand. Staging and indications for surgical treatment].

Results of long-term follow up of 66 patients with ischemic contracture of the forearm and hand, all surgically treated in the "Unfallkrankenhaus Hamburg)) between 1961 and 1982, are presented. Whereas ischemic contracture of the forearm flexors resulted mainly from fractures, ischemic contracture of the intrinsic muscles of the hand was most often seen after pressure injuries. All patients in this study presented to us with fully established ischemic contractures. Muscle and nerve damage was retrospectively evaluated according to operative notes, and the degree of damage could be classified into four groups. Most frequently, neurolysis, scar excision and muscle-sliding operations were performed; furthermore, tendon lengthening, tendon transpositions, wrist arthrodesis and nerve grafting were indicated. Results were judged according to twelve separately measured functions, each measurement giving a possible score of three to six points. Muscle-sliding operations result in an improved score regardless of ischemic contracture stage. For a stage 2 contracture, a 20 point improvement can be expected. In stage 1 contracture--presenting with extension deficiency of four or more points--, complete recovery can be expected following a muscle-sliding operation. For isolated muscle injuries, tendon lengthening is recommended. For stage 2 contracture, the transposition of superficial to deep flexor tendons results in the same score as a muscle-sliding operation; however, the transposition procedure should be reserved for special indications. In stage 3 contracture, the muscle-sliding operation is the treatment of choice, with secondary procedures such as tendon transpositions and nerve grafts often being necessary. In stage 4 ischemic contracture, muscle-sliding operations may improve extension deficiency; however, wrist arthrodesis, especially in combination with extensor tendon transpositions, may be beneficial. No experience with free muscle transplantation was made during the study period.

Adolescent↗
PubMed1994

Effects of trimetazidine on ischemic contracture in isolated perfused rat hearts.

Trimetazidine (1-[2,3,4-trimethoxibenzyl)]-piperazine, TMZ) is a drug with a proposed metabolically based antiischemic action. Because ischemic contracture is a serious complication of ischemia and is considered metabolic in origin, we studied the effect of trimetazidine (TMZ) on development of ischemic contracture in experimental low-flow ischemia. TMZ was either added to the perfusion fluid or given as pretreatment to the donor rats. Langendorff-perfused isolated rat hearts were submitted to 30-min subtotal global ischemia (residual flow = 0.2 ml/min, n = 6 per group) (normal flow = 12.4 +/- 0.8 ml/min, heart fresh weight = 0.9 +/- 0.3 g). Ischemic contracture was measured by a water-filled intraventricular balloon. Thereafter, the hearts were reperfused for 20 min and recovery of intraventricular pressure was monitored. Furthermore, because the mechanisms of action of TMZ may involve cellular energy metabolism, we assessed throughout glycolytic flux by collecting the coronary effluent every 5 min during control perfusion, ischemia, and reperfusion periods. Animals from the pretreated groups received TMZ [3 mg/kg orally (p.o.) twice daily] for 5 days. Animals from the control group received placebo for the same time period. Concentrations of 10(-6) and 10(-4) M were used when the drug was added to the perfusate. In our experimental conditions, TMZ pretreatment alone had no measurable cardioprotective effect, but addition to the perfusate of TMZ 10(-6) M, approximately a therapeutic concentration in humans, reduced ischemic contracture in both pretreated and control groups and improved postischemic recovery of developed pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Metabolic and functional response of neonatal pig hearts to the development of ischemic contracture: is recovery possible?

The potential for functional and metabolic recovery in neonatal hearts after the development of ischemic contracture remains controversial and undefined. This study documents post-ischemic recovery of metabolism and function in the in vivo neonatal heart after the development of onset and peak ischemic contracture. In piglets on cardiopulmonary bypass, hearts were reperfused after the development of either onset (TICo) or peak (TICp) ischemic contracture. Systolic (developed and systolic function, contractility) and diastolic (diastolic function, relaxation) performance was assessed throughout reperfusion. Biopsies were obtained at end-ischemia or end-reperfusion to assess metabolism. By end-ischemia, the metabolic profiles of both TICo and TICp hearts confirmed energy-store depletion and purine degradation that was quantitatively greater in TICp hearts. Hearts reperfused at TICo had consistent moderate impairment of developed function, contractility, diastolic function, and relaxation, whereas hearts reperfused at TICp had much more profound functional impairment. Diastolic function showed the worst functional recovery. In contrast, systolic function was not significantly altered in either study group and, thus, did not reflect the actual extent of injury. In addition, TICo hearts either did not further deplete or partially regenerated energy stores during reperfusion, whereas TICp hearts had further energy-store depletion and lactate accumulation. In summary, neonatal hearts reperfused after TICo maintained or partially restored energy stores and had significant but incomplete functional recovery. In contrast, further metabolic deterioration and profound functional impairment occurred with reperfusion after TICp, potentially indicating ongoing mitochondrial injury and compromised oxidative phosphorylation.

Adenine Nucleotides↗
PubMed2000

Volkmann's ischemic contracture. Prevention and treatment.

It may be concluded that treatment of patients with Volkmann's ischemic contracture is complicated and depends on a number of different variables. Optimal treatment of an established contracture requires a through examination of the extent of damage of the ischemia, followed by conservative therapy or operation. The most important measures concerning Volkmann's ischemic contracture, however, involve measures to prevent the contracture. It is poignant that very simple measures, such as monitoring high-risk injuries and immediate vascular repair or decompression if symptoms of a compartment syndrome are present, can prevent this disabling condition. The following summaries hopefully provide guidelines for prevention and treatment of Volkmann's ischemic contracture.

Arm↗
PubMed1980

Correlation of mitochondrial function and ischemic contracture.

Structural and functional changes in the mitochondrium have been described following timed cardiac ischemia. However, mitochondrial abnormalities associated with acute muscular dysfunction have not been well defined. In the present investigation, the isolated rat heart subjected to global ischemia was used to determine the relationship between the biochemical parameters of high-energy phosphate content and mitochondrial function and the physiological event of ischemic contracture. High-energy phosphate content and mitochondrial structure and function were determined under control conditions, at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes after completion of contracture. Contracture initiation and completion were associated with the anticipated depletion of high-energy phosphate content. Also demonstrated were specific degrees of structural and functional deterioration of the mitochondria associated with specific degrees of contracture. In addition to its prior applications, this model seems well suited for investigation of the interdependence of high-energy phosphate levels, ischemic contracture, and mitochondrial function as affected by specific protective interventions designed to limit ischemic injury.

Adenosine Triphosphate↗