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PubMed1996

Paradoxical effect of ischemic preconditioning on ischemic contracture? NMR studies of energy metabolism and intracellular pH in the rat heart.

Using the blood-perfused rat heart, we have previously shown that although ischemic preconditioning (PC) and cardioplegia (CP) afforded similar protection against post-ischemic contractile dysfunction this effect was not additive even though PC accelerated whereas CP delayed ischemic contracture. Using NMR we examined the effects of these interventions on pHi and ATP metabolism during global ischemia. Isolated rat hearts (n = 6/group) with an intraventricular balloon were aerobically perfused with buffer, subjected to zero flow ischemia (37 degrees C) for 35 min and reperfused for 40 min. The groups were: (1) controls without protection, (2) PC (2 cycles), and (3) St Thomas' cardioplegia, prior to test ischemia. PC accelerated whereas CP delayed ischemic contracture (P < 0.05 v controls). Yet, after 40 min reperfusion, both interventions produced substantial improvements in the recovery of LVDP (P < 0.05 v controls). During 35 min ischemia, the decline of ATP was delayed by CP but accelerated by PC (P < 0.05 v controls). The pHi fell steeply in controls to a plateau of 5.9 after 14 min ischemia. PC had no effect on the rate of fall of pHi but reduced its extent (P < 0.05). CP delayed the onset of the decline in pHi (P < 0.05) but, once initiated, there was no effect on the rate of decline to a plateau. Thus, despite protecting post-ischemic contractile function, PC accelerated ischemic contracture and the depletion of ATP, but substantially reduced intracellular acidosis. In contrast, CP slowed ischemic contracture and the depletion of ATP; it also delayed the onset of acidosis.

Animals↗
PubMed1998

Congenital cutaneous defects as complications in surviving co-twins. Aplasia cutis congenita and neonatal volkmann ischemic contracture of the forearm.

BACKGROUND: During twin pregnancies, several complications may result in the death of a co-twin depending on the date of death. We describe herein 2 infant survivors of monozygotic twin pairs with 2 distinct possible complications: a aplasia cutis congenita and Volkmann ischemic contracture. OBSERVATIONS: One infant had extensive aplasia cutis congenita with an associated monozygotic co-twin who died at 3 months of gestation, and the other child had a localized arm defect due to Volkmann ischemic contracture and brain damage, with a co-twin who died at approximately 6 weeks of gestation. CONCLUSIONS: Congenital cutaneous defects may result in the death of a co-twin. The most common of these defects is aplasia cutis congenita associated with a fetus papyraceus or a dead fetus related to ischemic/thrombotic events in the placenta and fetus. Volkmann ischemic contracture is rare in the newborn but can cause neonatal cutaneous defects. The cause of Volkmann ischemic contracture in newborns is unknown; however, our second observation suggests the possible role of a dead fetus.

Compartment Syndromes↗
PubMed1987

Transmural progression of morphologic changes during ischemic contracture and reperfusion in the normal and hypertrophied rat heart.

The purpose of this study was to compare the functional and morphologic changes that occur during ischemic contracture and reperfusion in the normal and hypertrophied heart. Hearts from Sprague-Dawley, spontaneously hypertensive (SHR), and normotensive Wistar-Kyoto rats were evaluated using a modified Langendorff perfusion apparatus. After obtaining control data, hearts were potassium-arrested, made ischemic, and studied at various time points. Regional coronary flow was assessed with the use of radiolabeled microspheres or Microfil dye infusion, and morphologic changes were evaluated by means of light and electron microscopy. Sarcomere length changes and qualitative morphologic changes during global ischemia demonstrate a transmural progression of ischemic damage starting at the endocardium and extending, with time, epicardially. The progression of ischemic changes in hypertrophied hearts of SHRs was similar to that of normal hearts; however, hypertrophied hearts developed ischemic contracture sooner than normal hearts. In addition, the development of contraction band change after ischemic contracture occurred only when hearts were reperfused and was related to the development of no-reflow.

Animals↗
PubMed1987

Volkmann's ischemic contractures and blowout fractures.

Volkmann's ischemic contractures have long been recognized by orthopedic surgeons as a sequela of increased pressure within osseofascial muscle compartments. We present evidence that the same mechanism is a cause of fibrosis and contracture of extraocular muscles following orbital blowout fractures. Surgical treatment of a specific, recognizable type of blowout fracture is proposed.

Adolescent↗
PubMed2006

[Mini-invasive distraction technique for treatment of severe ankle and foot deformities secondary to ischemic contracture of the leg].

OBJECTIVE: To explore the Ilizarov mini-invasive distraction technique for the treatment of severer ankle and foot deformities secondary to ischemic contracture of the leg. METHODS: Based on the tension-stress low of Ilizarov, a serial of adjustable three dimensions external distractive instrument was developed in our department. From April 2002 to March 2004, 8 patients with ankle and foot deformities secondary to ischemic contracture of the leg induced by trauma and fracture were treated with the distractive instrument. Of them, 4 patient were male and 4 female, aged from 13 to 31 years with an average of 23 years. Five affected legs were in the left and 3 in the right. Preoperative abnormal style included talipes equines in 6 feet and equinovarus in 2 feet, with extensive scar contracture in the legs. Five patients suffered from failure of soft tissue release before, two patients with severe bony deformity of the feet were underwent limited foot triple osteotomy in this department before the distractive correction. The distraction was begun from 7 d after operation and distractive time from 29 to 60 d with an average 46 d. RESULTS: All of the 8 patients were followed up from 10 months to 29 months, with an average of 13 months. All of deformities in the feet were corrected satisfactorily, full feet contacted with the ground in stand or walking and achieved with good function. No complication, such as pin tract infection, skin necrosis and neurovascular injury was occurred in this group. CONCLUSIONS: Mini-invasive distraction technique for treatment of severe ankle and foot deformity secondary to ischemic contracture of the leg is safe and mini-injury, it is also an effective approach for the treatment of various kinds of rigid foot anomaly.

Adolescent↗
PubMed1990

Effects of low extracellular calcium on cytosolic calcium and ischemic contracture.

We have shown that myocardial cytosolic calcium [Cai] rises during ischemia. Simultaneously membrane bound stores are depleted. The [Cai] rise precedes the onset of irreversible ischemic contracture. We found that a low extracellular calcium [Cao] (100 microM) perfusate decreased peak contracture pressure and delayed the time to onset and to peak of ischemic contracture in the isolated retroperfused rabbit heart subjected to 37 degrees C ischemia. [Cai] was measured with the intracellular [Cai] fluorescent indicator Fura-2 AM (10 microM) in a separate group. In the group exposed to 2.45 mM Ca2+ there was a significant rise (P less than 0.05) in [Cai] to above 50% of preischemic value after 30 min of ischemia. The [Cai] in the low [Cao] perfused group at 30 min of ischemia was 30% below the preischemic value. The peak of the [Cai] rise in the low [Cao] perfusate group was markedly attenuated and delayed to 40 min. Taken together it appears that low calcium perfusate (100 microM) prior to ischemia attenuates the ischemia-induced [Cai] rise, delays the onset, and decreases the force of contracture with irreversible ischemic injury.

Adenosine Triphosphate↗
PubMed1994

Myocardial ischemic contracture. Metabolites affect rigor tension development and stiffness.

Myocardial ischemia is characterized by a decrease in phosphocreatine (PCr) and Mg(2+)-ATP contents as well as an accumulation of myosin ATPase reaction products (inorganic phosphate [P(i)], protons, and Mg(2+)-ADP). The possibility that these metabolites play a role in rigor tension development was checked in rat ventricular Triton X-100-skinned fibers. Rigor tension was induced by stepwise decreasing [Mg(2+)-ATP] in the presence or in the absence of 12 mmol/L PCr. To mimic the diastolic ionic environment of the myofibrils, [free Ca2+] was set at 100 nmol/L (pCa 7); [free Mg2+], at 1 mmol/L; and ionic strength, at 160 mmol/L. In control conditions (pH 7.1, with no added P(i) or Mg(2+)-ADP), the pMg(2+)-ATP for half-maximal rigor tension (pMg(2+)-ATP50) was 5.07 +/- 0.03 in the presence of PCr. After withdrawal of PCr, the pMg2+)-ATP50 value was shifted toward higher Mg(2+)-ATP values (3.57 +/- 0.03). Addition of 20 mmol/L P(i) shifted the pMg(2+)-ATP50 to 3.71 +/- 0.04 (P < .05) in the absence of PCr and in the opposite direction to 4.98 +/- 0.02 (P < .01) in the presence of PCr. Acidic pH (6.6) strongly increased pMg(2+)-ATP50 in both the absence (3.90 +/- 0.03, P < .001) and presence (5.44 +/- 0.02, P < .001) of PCr. Conversely, Mg(2+)-ADP (250 mumol/L) decreased pMg(2+)-ATP50 to 3.26 +/- 0.06 (P < .001) in the absence of PCr; at pMg(2+)-ATP 4, no rigor tension was observed until PCr concentration was decreased to < 2 mmol/L. At acidic pH, maximal rigor tension was lower by 29% compared with control conditions, whereas in the presence of Mg(2+)-ADP, maximal rigor tension developed to 143% of the control value; P(i) had no effect. The tension-to-stiffness (measured by the quick length-change technique) ratio was lower in rigor (no PCr and pMg(2+)-ATP 6) than during Ca2+ activation in the presence of both PCr and ATP. Compared with control rigor conditions, this parameter was unchanged by Mg(2+)-ADP and decreased by acidic pH, suggesting a proton-induced decrease in the amount of force per crossbridge. In addition to their known effects on active tension, Mg(2+)-ADP and protons affect rigor tension and influence ischemic contracture development. It is concluded that ischemic contracture and increased myocardial stiffness may be mediated by a decreased PCr and local Mg(2+)-ADP accumulation. This emphasizes the importance of myofibrillar creatine kinase activity in preventing ischemic contracture.

Adenosine Diphosphate↗
PubMed1978

A comparison between propranolol and hypothermia in preventing ischemic contracture of the left ventricle (stone heart).

Ischemic contracture of the left ventricle ("stone heart") was studied utilizing a previously described stone heart model. Our studies suggest that beta-adrenergic blockade is not quantitatively as important as hypothermia in protecting ischemic myocardium. On the basis of reduced fibrillatory activity and a slight protective effect shown by electron microscopy, it would appear that combining propranolol with hypothermia may be superior to either used singly.

Animals↗
PubMed2000

Congenital Volkmann-Lesser ischemic contracture of the upper limb.

Neonatal vascular compromise to limbs has been associated traditionally with perinatal injury of the brachial plexus, fracture of the clavicle or humerus, or iatrogenic causes. Congenital Volkmann's ischemic contracture is an exceptional etiology of ischemic limb in the newborn. Fewer than 10 cases had been described in the literature. The authors report a newborn presenting at birth with partial bluish discoloration of the right forearm. The clinical picture and laboratory studies lead to the diagnosis of congenital Volkmann-Lesser ischemic contracture.

Arm↗
PubMed1994

Development of ischemic contracture in isolated skeletal muscles: relation to the capacity for anaerobic glycolysis.

In order to evaluate the dependence of the rate of ischemic contracture development in isolated skeletal muscles on the capacity for anaerobic glycolysis, factors affecting ischemic contracture development were examined using rat soleus and quadriceps muscles. The contracture developed faster in slow-twitch oxidative (SO) fibers than in fast-twitch glycolytic (FG) fibers. In both types of fibers, the rate of contracture development was inversely related to the medium pH. Addition of lactate increased the rate of contracture development. In FG fibers, the lactate level during contracture was directly, and the glycogen level inversely, proportional to the medium pH. An increase in muscle lactate level by 4-h swimming accelerated the contracture development, and reduced further lactate accumulation during contracture. Types of exercise training known to influence the capacity for anaerobic glycolysis (interval training and repeated fast climbing and swimming) decreased the velocity of contracture development. Isoprenaline administration in vivo accelerated contracture development in association with reduced lactate level during contracture. Swimming training counterbalanced the action of isoprenaline. Adrenalectomy accelerated contracture development in SO fibers, and decreased lactate accumulation during contracture in FG fibers. In adrenalectomized rats, the effects of exercise were more pronounced in SO fibers than in FG fibers. These results indicate that the rate of contracture development in isolated skeletal muscle is inversely related to the capacity for anaerobic glycolysis.

Adrenalectomy↗
PubMedDate not supplied

Ischemic contracture in the lower limb.

Twenty cases of ischemic contracture in the lower limb demonstrate that the age distribution may be higher than that of patients with similar lesions in the upper limbs. Non-traumatic and traumatic causes are encountered equally frequently. Pain is one of the most important symptoms associated with long standing lesions. The ischemic lesion develops most frequently and severely in the anterior compartment of the leg. The functional prognosis is poor when both nerves are affected and when the deformity is severe.

Adolescent↗
PubMed2005

Functional results after treatment of Volkmann's ischemic contracture: a long-term followup study.

The main objective of this retrospective study was to evaluate the long-term functional outcome in patients treated for Volkmann's ischemic contracture. In this study, functional outcome (measured as mobility, grip strength, and sensibility) and arm length difference after treatment of Volkmann's ischemic contracture were analyzed and discussed. Twenty-five patients treated between 1969 and 2001 were evaluated. The method of treatment was related to the severity of the infarction, ranging from conservative to free vascularized muscle transplantation. Although the study population was small, we could observe a wide range of functional outcome. Substantial improvement of function was obtained in patients who had free vascularized muscle transplantation. Unfortunately in one patient with an occlusion of the distal brachial artery and an insufficient flow through the collateral circulation of the radial artery, the gracilis muscle was lost. Tendon lengthening had unsatisfactory results because of recurrence of the contracture. Excision of fibrotic muscle tissue, neurolysis and tenolysis sometimes combined with a tendon transfer gave good hand function results in patients with sufficient remaining muscle tissue. In most of the patients in whom the contracture developed during childhood, a difference in forearm length was observed.

Compartment Syndromes↗
PubMed1998

Volkmann's ischemic contracture of the upper extremity.

Upper extremity deformity of ischemic contracture usually includes elbow flexion, forearm pronation, wrist flexion, thumb flexion and adduction, digital metacarpophalangeal joint extension, and interphalangeal joint flexion. Treatment of mild contractures consists of either nonoperative management with a comprehensive rehabilitation program (to increase range of motion and strenght) or operative management consisting of infarct excision or tendon lengthening. Treatment of moderate-to-severe contractures consists of release of secondary nerve compression, treatment of contractures (with tendon lengthening or recession), tendon or free-tissue transfers to restore lost function, and/or salvage procedures for the severely contracted or neglected extremity.

Arm↗
PubMed1991

Ischemic contracture begins when anaerobic glycolysis stops: a 31P-NMR study of isolated rat hearts.

The relationships among myocardial ATP, intracellular pH, and ischemic contracture in Langendorff-perfused rat hearts were investigated by 31P nuclear magnetic resonance spectroscopy during total global normothermic ischemia while the left ventricular pressure was recorded continuously via an intraventricular balloon. Glucose-perfused hearts (n = 63) were divided into five groups based on the time of onset of contracture (TOC), and three other groups of hearts were treated to vary the ischemic glycogen availability. ATP levels, which showed no evidence of accelerated ATP depletion during contracture, were significant and variable at TOC. Intracellular pH initially declined and then leveled off at TOC, with lower final pH in hearts with later TOC. We conclude that contracture began when anaerobic glycolysis (and thus glycolytic ATP synthesis) stopped. These results, though consistent with the concept that ischemic contracture in normal hearts results from rigor bond formation due to low ATP levels at the myofibrils, suggest that TOC is more closely related to glycolytic ATP production than to total cellular ATP content, thus providing evidence of some degree of subcellular compartmentation or metabolite channeling. In glycolytically inhibited hearts, the quite early contracture may have a Ca2+ component.

Anaerobiosis↗