Effects of the administration of 2,3-butanedione monoxime during conventional cardiopulmonary resuscitation on ischaemic contracture and resuscitability in a pig model of out-of-hospital cardiac arrest.

AIM OF THE STUDY: Ischaemic contracture compromises the haemodynamic effectiveness of cardiopulmonary resuscitation and resuscitability. 2,3-Butanedione monoxime (BDM) reduced ischaemic contracture by inhibiting actin-myosin crossbridge formation in an isolated heart model. We investigated the effects of BDM on ischaemic contracture and resuscitation outcomes in a pig model of out-of-hospital cardiac arrest (OHCA). METHODS: After 15min of untreated ventricular fibrillation, followed by 8min of basic life support, 16 pigs were randomised to receive either 2mlkg(-1) of BDM solution (25gl(-1)) or 2mlkg(-1) of saline during advanced cardiac life support (ACLS). RESULTS: During the ACLS, the control group showed an increase in left ventricular (LV) wall thickness from 10.0mm (10.0-10.8) to 13.0mm (13.0-13.0) and a decrease in LV chamber area from 8.13cm(2) (7.59-9.29) to 7.47cm(2) (5.84-8.43). In contrast, the BDM group showed a decrease in the LV wall thickness from 10mm (9.0-10.8) to 8.5mm (7.0-9.8) and an increase in the LV chamber area from 9.86cm(2) (7.22-12.39) to 12.15 cm(2) (8.02-14.40). Mixed model analyses of the LV wall thickness and LV chamber area revealed significant group effects and group-time interactions. Spontaneous circulation was restored in four (50%) animals in the control group and in eight (100%) animals in the BDM group (p=0.077). All the resuscitated animals survived during an intensive care period of 4h. CONCLUSION: BDM administered during cardiopulmonary resuscitation reversed ischaemic contracture in a pig model of OHCA.

[Transtibial amputation of the lower extremity in patients with ischemic foot contracture].

The results of operative treatment of 8 patients was analyzed, in whom the lower extremity amputation on the upper third of the shin was performed for severe stage of the ischemic foot contacture. Operative interventions is expedient to perform in a specialized stationary, were exists possibility of further prosthesis. It is necessary to perform the extremity amputation in a residual period of the foot ischemic contracture, when operations for restoration of the sole sensitivity are nonperspective as well as in presence of severe trophic disorders on the sole and the shin, but without purulent--necrotic signs. Confirmed data of clinic--instrumental investigations for chronic course of the ischemic process constitutes an absolute indication for operation.

Volkmann's contracture of the forearm owing to an insect bite: a case report and review of the literature.

Compartment syndrome affecting the upper limb is reported rarely in the literature and is usually limited to single case reports. Upper limb compartment syndrome secondary to envenomation is rare, especially in the UK. Worldwide, it has been reported resulting from snake and insect bites, mostly from snakes from the Viperidae family, and from insects such as bees and wasps. Reports from the UK are limited to one case of an adder bite. We present a case of a previously fit and well adult who developed an ischaemic contracture of the forearm after an insect bite. Surgical exploration revealed segmental necrosis and contracture of the superficial and deep flexors of the fingers, requiring fasciotomy and tendon-lengthening procedures. This is the first report of a compartment syndrome, or a late ischaemic contracture from an insect bite in the UK. Owing to the rarity of compartment syndrome of the upper limb secondary to envenomation, a delay in diagnosis and treatment can lead to irreversible changes in the muscular compartments of the forearm.

[Functional diagnosis of the foot ischemic contracture].

Correlation analysis between severity of the foot ischemic contracture (FIC) and the degree of its function disorder was conducted. The 100-point scale of H. B. Kitaoka was applied for investigation of functional disorders, the FIC severity was estimated according to A. P. Lyabakh, S. S. Strafun (1994) classification. The results obtained have witnessed the dependence of the foot functional state in a residual state from the ischemia severity, what is confirmed by Cruscal - Wallice and Dann criteria. Low indices in patients with a mild B and moderate A FIC severity were caused by impact of some factors, which were noncontrolled by the system of the point estimation, including such as the ischemic affection of own foot muscles.

[Functional and morphologic changes in the tendons and multimicrovacuolar collagen absorbing system of the three-phalanx fingers in disorder of arterial inflow].

Taking into account the fact, that unsatisfactory results of treatment of the thumbs traumatic damage are significantly caused by presence of anatomic disruption of the thumbs palm's own arteries with chronic tissue ischemia occurrence. One of consequences of damage of the three-phalanx thumbs interphalanx joints and the thumbs palm's own arteries is a formation of quickly progressing secondary flexing contracture of proximal interphalanx joints (PIPHJ). In the investigations accomplished there was established, that the changed tissues of the flexors tendons and their sheaths, forming cicatricial blockade distally to the primary trauma site, are taking part in a PIPHJ contracture development while arterial perfusion presence.The tissues damage severity, as well as a severity of clinical features of the tendons and their sheaths damage, depends on a degree of an arterial perfusion disorder present,

[Neonatal Volkmann's syndrome]. / Syndrome de Volkmann néonatal.

BACKGROUND: Acute limb compartment syndrome or Volkmann's ischaemic contracture is an acquired ischaemia of nerve and muscle causes by raised pressure within a closed fascial space. Congenital Volkmann's ischaemic contracture (CVIC) is a rare entity. PATIENTS AND METHODS: A 2-day-old girl was referred with a problem of the left forearm and arm, which exhibited cold oedema with decreased mobility. Lesions were present at birth and were rapidly complicated by skin necrosis. The mother was taking olazanpine, prazepam and valpromide throughout the entire pregnancy. Delivery was complicated by shoulder dystocia requiring obstetric procedures such as suprapubic pressure, Couder's maneuver and episiotomy. On physical examination her left hemi-thorax, left arm, forearm and hand exhibited marked oedema. A large and well-demarcated bullous, fibrous and ulcerated area of skin necrosis was observed on the elbow fold and on the inner anterior part of the arm. Digital flexion with cyanosis was present. MR angiography revealed extensive oedema of the soft tissue and muscle with fascial effusion, associated with compression of the arm arteries and reduced blood flow in the forearm. A fasciotomy was performed at Day 3 of life. The postsurgical arterial MRI was normal. At Day 10 of life, the patient developed opisthotonos involving spasms and tremors associated with numerous intercritical abnormalities evoking benzodiazepine weaning syndrome. The child's neurological status was stabilized by treatment with phenobarbital and clonazepam. She was subsequently lost to follow-up. DISCUSSION: CVIC has been ascribed to multiples causes. Mechanical compression is the main recognized factor: amniotic band constriction, umbilical cord loops, compression in utero by a deceased co-twin, malposition of the hand, arm or forearm, local or general factors that can add to extraction problems: brachypelvic disproportion, extraction with forceps, oligo/polyhydramnios, pre-term delivery, pre-eclampsia, caesarean section, premature labour, excessive maternal weight gain or diabetes. Our case emphasized three main points. First, the diagnostic value of early MR angiography in the event of associated extensive tissue oedema, multiple arterial compression and decreased vascular perfusion. Second, the role of shoulder dystocia in triggering the traumatic factor reported for the first time. Third, the role of neuroleptic and anxiolytic treatments taken by the mother during pregnancy. Prazepam is a long-acting benzodiazepine that can cause impregnation and withdraw syndromes in neonates. Impregnation "floppy infant syndrome" is an early event characterized by hypotonia, hypoventilation and lethargy. Hypotonia and decreased foetal movements may favour prolonged pressures and malposition with secondary crush injury during delivery. Maternal medication has not been cited hitherto as an aetiological factor in neonatal compartment syndrome.

Role of sarcoplasmic reticulum in mitochondrial permeability transition and cardiomyocyte death during reperfusion.

There is solid evidence that a sudden change in mitochondrial membrane permeability (mitochondrial permeability transition, MPT) plays a critical role in reperfusion-induced myocardial necrosis. We hypothesized that sarcoplasmic reticulum (SR) Ca(2+) cycling may induce partial MPT in microdomains of close anatomic proximity between mitochondria and SR, resulting in hypercontracture and cell death. MPT (mitochondrial calcein release), cell length, and sarcolemmal rupture (Trypan blue and lactate dehydrogenase release) were measured in adult rat cardiomyocytes submitted to simulated ischemia (NaCN/2-deoxyglucose, pH 6.4) and reperfusion. On simulated reperfusion, 83 +/- 2% of myocytes developed hypercontracture. In 22 +/- 6% of cases, hypercontracture was associated with sarcolemmal disruption [Trypan blue(+)]. During simulated reperfusion there was a 25% release of cyclosporin A-sensitive mitochondrial calcein (with respect to total mitochondrial calcein content). Simultaneous blockade of SR Ca(2+) uptake and release with thapsigargin and ryanodine, respectively, significantly reduced mitochondrial calcein release, hypercontracture, and cell death during simulated reperfusion. SR Ca(2+) blockers delayed mitochondrial Ca(2+) uptake in digitonin-permeabilized cardiomyocytes but did not have any effect on isolated mitochondria. Pretreatment with colchicine to disrupt microtubule network reduced the degree of fluorescent overlap between SR and mitochondria and abolished the protective effect of SR Ca(2+) blockers on MPT, hypercontracture, and cell death during reperfusion. We conclude that SR Ca(2+) cycling during reperfusion facilitates partial mitochondrial permeabilization due to the close anatomic proximity between both organelles, favoring hypercontracture and cell death.

Ischemia enhances translocation of connexin43 and gap junction intercellular communication, thereby propagating contraction band necrosis after reperfusion.

BACKGROUND: In ischemia-reperfusion, contraction band necrosis (CBN) is distributed mainly to the lateral border of the risk area and does not spread into the non-risk area beyond the border. It has been suggested that CBN is propagated through gap junctions (GJs), but it is unclear how GJs transmit CBN exclusively in the risk area. METHODS AND RESULTS: Coronary occlusion for 30 min in rat increased the level of connexin43 (Cx43) protein in the 100,000 x g pellet fraction to 1.5-fold and decreased that in the 1,000 x g pellet to half in the risk area compared with the non-risk area. Immunohistochemical analysis showed an increase of Cx43 at intercalated disks in the risk area. A dye transfer assay demonstrated enhancement of GJ intercellular communication (GJIC) in the risk area compared with the non-risk area in the same section. Administration of a GJ blocker, carbenoxolone, at the onset of reperfusion following 30 min of ischemia reduced the CBN area (1/3 vs PBS) in 5 min of reperfusion and limited the infarct size (2/3 vs PBS) in 6 h of reperfusion. CONCLUSIONS: These data suggest that ischemia enhances translocation of Cx43 to GJs, thereby promoting propagation of CBN exclusively in the risk area through enhanced GJIC after reperfusion.

[Features of ischemic myocardial contracture after asphyxia-induced cardiac arrest in rats].

OBJECTIVE: To investigate the features of ischemic myocardial contracture after asphyxial cardiac arrest in rats. METHOD: Asphyxial cardiac arrest was induced in 8 Wistar rats, and the length and width of the heart were measured at the different time points after cardiac arrest. RESULTS: Obvious ischemic myocardial contracture occurred after the cardiac arrest, reaching the maximal contracture at 4-6 min after the arrest. CONCLUSIONS: Ischemic myocardial contracture induced by asphyxia may be an important factor affecting the outcome of cardiopulmonary resuscitation.

Ischemic contracture of deep posterior compartment of the leg following isolated ankle fracture.

Compartment syndromes and ischemic contractures after ankle fractures are exceedingly rare. We report a case in which a Weber type-C ankle fracture resulted in an unrecognized compartment syndrome and ischemic contracture of deep posterior compartment of the leg. Six weeks after injury, the patient had an obvious deformity and clawing of the toes. The deformities were corrected by lengthening the flexor hallucis longus and the flexor digitorum longus. Full correction of all clawed toes was evident. A deep posterior compartment syndrome may follow an ankle fracture and should be considered in any patient with unrelenting pain in the immediate postoperative period.

Ischemic preconditioning of the whole heart confers protection on subsequently isolated ventricular myocytes.

Current cellular models of ischemic preconditioning (IPC) rely on inducing preconditioning in vitro and may not accurately represent complex pathways triggered by IPC in the intact heart. Here, we show that it is possible to precondition the intact heart and to subsequently isolate individual ventricular myocytes that retain the protection triggered by IPC. Myocytes isolated from Langendorff-perfused hearts preconditioned with three cycles of ischemia-reperfusion were exposed to metabolic inhibition and reenergization. Injury was assessed from induction of hypercontracture and loss of Ca(2+) homeostasis and contractile function. IPC induced an immediate window of protection in isolated myocytes, with 64.3 +/- 7.6% of IPC myocytes recovering Ca(2+) homeostasis compared with 16.9 +/- 2.4% of control myocytes (P < 0.01). Similarly, 64.1 +/- 5.9% of IPC myocytes recovered contractile function compared with 15.3 +/- 2.2% of control myocytes (P < 0.01). Protection was prevented by the presence of 0.5 mM 5-hydroxydecanoate during the preconditioning stimulus. This early protection disappeared after 6 h, but a second window of protection developed 24 h after preconditioning, with 54.9 +/- 4.7% of preconditioned myocytes recovering Ca(2+) homeostasis compared with 12.6 +/- 2.9% of control myocytes (P < 0.01). These data show that "true" IPC of the heart confers both windows of protection in the isolated myocytes, with a similar temporal relationship to in vivo preconditioning of the whole heart. The model should allow future studies in isolated cells of the protective mechanisms induced by true ischemia.