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PubMed1975

[Ischemic contractures of muscle and nerve lesions (author's transl)].

Reporting 14 own cases symptomatology and treatment of the common ischemic syndromes of the extremities (Volkmann's contracture, thumb adduction contracture respectively contracture of the intrinsic hand muscles and anterior tibial syndrome) including the regularly concomitant nerve lesions are discussed. Edema and compression beyond the primary ischemia are essential factors in pathogenesis of nerve and muscle lesions. The electromyographic examination is helpful in diagnosis, prognosis and treatment of the severe sequelae of nerve and muscle. Since late diagnosis yields poor therapeutical results, early recognition of ischemic states and prophylaxis are most important.

Adolescent↗
PubMed1983

Reversal of myocardial ischemic contracture and the relationship to functional recovery and tissue calcium.

We subjected isolated rat hearts to normothermic ischemia until contracture developed, then reperfused them for 30 min. Recovery of developed pressure, rate of change in left ventricular pressure (dP/dt), and changes in end-diastolic pressure measured after 30 min of reperfusion were compared with preischemic values for each heart. Values after untreated ischemic arrest were compared with those after potassium arrest, potassium reperfusion (both oxygenated and deoxygenated), and combined potassium arrest and potassium reperfusion. Potassium arrest lengthened the time to the onset of contracture and thus lengthened the total ischemic time. Functional recovery was not improved over that in the untreated hearts, most likely due to this additional ischemic time. The use of buffer with a high potassium content for the first 5 min of reperfusion, however, significantly improved functional recovery if the perfusate was oxygenated, but did not improve functional recovery if the perfusate was deliberately deoxygenated. Combined potassium arrest and reperfusion delayed the onset of contracture and thus increased total ischemic time, yet improved recovery. Tissue calcium was elevated in all hearts undergoing contracture and reperfusion. Our results suggest that contracture can be reversed and that functional recovery can be improved in spite of increased tissue calcium.

Animals↗
PubMed1996

Bioenergetics, ischemic contracture and reperfusion injury.

The mammalian heart is normally well oxygenated and anaerobic glycolysis is extremely rare except for the production of extra ATP during extreme exercise like a marathon race. Anaerobic glycolysis plays a role when there is a serious impairment in coronary blood flow such as during heart attack and open heart surgery. The control of glycolysis in ischemic myocardial tissue appears to be extremely complex. During aerobic glycolysis, phosphofructokinase is the most important regulatory enzyme that controls the energy requirements of the cell. Under anaerobic conditions, however, glyceraldehyde-3-phosphate dehydrogenase becomes the key enzyme because it responds promptly to any changes in the essential supply of co-factors for oxidation. The conversion of pyruvate to acetyl CoA (aerobic metabolism) involves a series of chain reactions primarily catalyzed by pyruvate dehydrogenase complex which is situated at the cross roads between both aerobic and anaerobic glycolysis. It is important to remember that substrate utilization is carefully controlled by substrate availability. During aerobic metabolism, control mechanisms using fatty acids, lactate and glucose as energy substrates regulate the rate of ATP production according to energy demand. This precise mechanism is upset during ischemia and post-ischemic reperfusion for reasons discussed in this review. The demand for ATP can no longer be met by its supply because of severely reduced anaerobic glycolysis and significantly inhibited beta-oxidation of fatty acids. The impairment of bioenergetics is discussed in the context of several diseases such as cardiomyopathy, heart failure, diabetes, arrhythmias, cardiac surgery, heart-lung transplantation, and also in aging and oxidative stress. The regulation of energy metabolism in preconditioned heart is also discussed. Finally, methods used to preserve energy in ischemic myocardium are summarized and quantitation of the high-energy phosphates is discussed. This review challenges scientists to discover drugs which will stimulate energy supply during myocardial ischemia.

Adenosine Triphosphate↗
PubMed1987

Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart.

Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, reduced in a dose-dependent fashion the ischemic contracture due to low perfusion (0.2 ml/min) of isovolumic left heart of rabbit and abolished the irregular rhythm of the heart, thereby restoring the cardiomechanical activity upon reperfusion (20 ml/min). Defibrotide stimulated the release of PG-like material from the heart in a dose-dependent manner without modifying the basal contractility. Both PGE2 and PGI2 (10 ng/ml) have an antiischemic activity on this preparation as shown by the partial reduction of the ischemic contracture and by the improvement of heart contractility upon reperfusion. Indomethacin infusion (1 microgram/ml) completely removed both the antiischemic activity of Defibrotide (400 micrograms/ml) and its ability to increase the generation of prostaglandins in the rabbit heart. These results suggest that Defibrotide has a beneficial influence on ischemic rabbit heart through an increase in prostaglandin synthesis. However other mechanisms not necessarily related to prostaglandin generation, such as a direct effect on membrane function deactivation and mitochondrial Ca2+ overload, should be considered in explaining the antiischemic activity of Defibrotide in the rabbit heart.

Animals↗
PubMed2003

Sodium-hydrogen exchange inhibition during ventricular fibrillation: Beneficial effects on ischemic contracture, action potential duration, reperfusion arrhythmias, myocardial function, and resuscitability.

BACKGROUND: Inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) is emerging as a promising novel strategy for ameliorating myocardial injury associated with ischemia and reperfusion. We investigated whether NHE-1 inhibition (with cariporide) could minimize mechanical and electrical myocardial abnormalities that develop during ventricular fibrillation (VF) and improve outcome using a porcine model of closed-chest resuscitation. METHODS AND RESULTS: Two groups of 8 pigs each were subjected to 8 minutes of untreated VF and randomized to receive either a 3-mg/kg bolus of cariporide or 0.9% NaCl immediately before an 8-minute interval of conventional closed-chest resuscitation. Cariporide prevented progressive increases in left ventricular free-wall thickness (from 1.0+/-0.2 to 1.5+/-0.3 cm with NaCl, P<0.001 versus 0.9+/-0.1 to 1.1+/-0.3 cm with cariporide, P=NS), maintained the coronary perfusion pressure above resuscitability thresholds (10+/-8 versus 19+/-3 mm Hg before attempting defibrillation, P<0.05), and increased resuscitability (2 of 8 versus 8 of 8, P<0.005). In 2 additional groups of 4 pigs each subjected to a briefer interval of untreated VF, cariporide ameliorated postresuscitation shortening of the action potential duration (APD) at 30%, 60%, and 90% repolarization (ie, APD60 at 2 minutes after resuscitation; 75+/-29 versus 226+/-16 ms, P<0.05), minimized postresuscitation ventricular ectopic activity preventing recurrent VF, and lessened postresuscitation myocardial dysfunction. CONCLUSIONS: NHE-1 inhibition may represent a highly potent novel strategy for resuscitation from VF that can ameliorate myocardial manifestations of ischemic injury and improve the effectiveness and outcome of closed-chest resuscitation.

Action Potentials↗
PubMed2004

Isolated ischemic contracture of the mobile wad: a report of two cases.

Two children with isolated ischaemic contractures of the mobile wad (extensor carpi radialis longus, extensor carpi radialis brevis and brachioradialis), which developed after treatment of a supracondylar fracture, are presented. Z-lengthening of the extensor carpi radialis longus and brevis tendons improved wrist flexion.

Child↗
PubMed1982

Pathogenesis of Volkmann's ischemic contracture of the first web space and treatment.

Reporting three cases of sequelae of Volkmann's ischemia of the first web space of the hand, following barbiturate overdose, the authors suggest several pathogenic hypothesis. The major factor is obviously an elective compression of the top of the first commissure on its dorsal aspect but it due to a compartmental syndrome or to a stoppage in the blood flow? The second explanation seems the best; the radial artery compressed at the top of the first commissure over the first dorsal intermetacarpal ligament is not able to vascularize the dorsal digital artery of the thumb and the first dorsal interosseous artery. These arteries being terminal in type, an elective muscle necrosis is takes place in the adductor pollicis and the first dorsal interosseous. This phenomenon being increased in this last muscle by a simultaneous compartmental syndrome. A precocious diagnosis must be made during the acute stage and some logical surgical procedures performed in emergency: fasciectomy, muscle excision and fixation of the trapezometacarpal joint in opposition with a pin.

Acute Disease↗
PubMed2000

[Ischemic contractures of the forearm and hand].

This article gives an overview of anatomy, pathophysiology, aetiology, and diagnosis of the compartment syndrome and the resulting ischaemic necrosis of the upper extremity. The relation between compartment syndrome and infection is pointed out. Whereas the therapy of a manifest compartment syndrome is rather uniform consisting in decompression of the involved fascial compartment, the treatment of the ischaemic muscle necrosis is manifold. It depends upon severity and location of the disease. Only the mildest involvement can be treated by nonoperative measures. Surgically, neurolysis, excision of necrotic musculature and scar, muscular slide, elongating tenotomy, tendon transposition and free vascularized muscle transplantation have to be considered. Only the availability of all treatment options gives the surgeon the choice of treatment that fits the demands of the individual patient best.

Compartment Syndromes↗
PubMed1995

Mechanical and metabolic characterization of ischemic contracture in the neonatal pig heart.

Isolated, paced, isovolumetrically beating piglet hearts (n = 37) underwent retrograde aortic perfusion with a crystalloid solution during three periods: 1) baseline (coronary perfusion pressure 60 mm Hg), 2) ischemia (coronary flow 10% of baseline for approximately 80 min), and 3) reperfusion (perfusion pressure returned to baseline). In one group of hearts, glycolysis (using 3H2O formation from [3H]glucose) was assessed. During baseline, peak systolic pressure (PSP) was 101.1 +/- 5.0 mm Hg, end diastolic pressure (EDP) 4.4 +/- 0.5 mm Hg, glycolysis 970.5 +/- 65.3 nmol/min/gwet, and myocardial glycogen 234.8 +/- 12.0 mumol/gdry. During ischemia, PSP decreased to 23.3 +/- 2.7 mm Hg, EDP increased to 12.3 +/- 0.7 mm Hg, myocardial glycogen decreased to 181.5 +/- 30.3 mumol/gdry, and lactate (approximately 154 mumol/gwet) and glycerol (approximately 930 nmol/gwet) were released. Myocardial contracture correlated with a decrease in lactate release. Glycolysis decreased to approximately 400 nmol/min/gwet and remained stable, accounting for approximately 50% of the lactate produced. During reperfusion, PSP recovered to 79.8 +/- 3.5 mm Hg, EDP 6.6 +/- 1.7 mm Hg, and glycolysis 1103.9 +/- 81 nmol/min/gwet. In a second group of hearts, with similar mechanical responses, glucose oxidation (using 14CO2 formation from [14C]glucose) was evaluated. During baseline, glucose oxidation was 165.4 +/- 15.9 nmol/min/gwet and correlated closely (r = 0.957) with mechanical activity. With ischemia, glucose oxidation decreased to approximately 17 nmol/min/gwet, yet accounted for approximately 42% of the ATP produced. Upon reperfusion, glucose oxidation returned to baseline values, but now correlated poorly (r = 0.574) with mechanical activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Ischemic contracture of the foot and ankle: principles of management and prevention.

A variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by: 1) which leg compartments have been affected and to what degree extrinsic flexor or extensor "overpull" is exhibited, 2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles, 3) which foot compartments have been affected and to what degree intrinsic "overpull" is exhibited, and 4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Nonoperative therapy attempts to obtain or preserve joint mobility, increase strength, and provide corrective bracing and accommodative foot wear. Operative management is undertaken for treatment of residual nerve compression or refractory problematic deformities. Established surgical protocols are performed in a stepwise fashion, and include: 1) release of residual or secondary nerve compression; 2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy; 3) tendon transfers or arthrodesis to increase function; and 4) osteotomy or amputation for severe, non-salvageable deformities.

Acute Disease↗