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Ultrasound-mediated microbubble cavitation improves perfusion in chronic limb and myocardial ischemia. The purpose of this study was to determine the effects of ultrasound-mediated microbubble cavitation in acute limb ischemia and investigate the mechanism of action. The animal with acute hindlimb ischemia was established using male Sprague-Dawley rats. The rats were randomly divided into three groups: intermittent high-mechanical-index ultrasound pulses combined with microbubbles (ultrasound [US] + MB group), US alone (US group) and MB alone (MB group). Both hindlimbs were treated for 10 min. Contrast ultrasound perfusion imaging of both hindlimbs was performed immediately and 5, 10, 15, 20 and 25 min after treatment. The role of the nitric oxide (NO) pathway in increasing blood flow in acutely ischemic tissue was evaluated by inhibiting endothelial nitric oxide synthase (eNOS) with N ω -nitro-L-arginine methyl ester hydrochloride (L-NAME). In the US + MB group, microvascular blood volume and microvascular blood flow of the ischemic hindlimb were significantly increased after treatment (both p values <0.05), while the microvascular flux rate (β) increased, but not significantly (p > 0.05). The increases were observed immediately after treatment, and had dissipated by 25 min. Changes in the US and MB groups were minimal. Inhibitory studies indicated cavitation increased phospho-eNOS concentration in ischemic hindlimb muscle tissue, and the increase was significantly inhibited by L-NAME (p < 0.05). Ultrasound-mediated microbubble cavitation transiently increases local perfusion in acutely ischemic tissue, mainly by improving microcirculatory perfusion. The eNOS/NO signaling pathway appears to be an important mediator of the effect., (Copyright © 2021 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.)

The floating mural thrombus of abdominal aorta is a rare and serious pathology detected as cause of peripheral and visceral embolism. Isolated aortic mural thrombosis is an unusual pathology occurring in an apparently normal aorta. A thorough search of embolic source must be initiated. Therapeutic management is based on systemic anticoagulation with the use of surgical approach in some cases., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Introduction: Acute upper limb ischemia is a medical and surgical emergency. Studies that have reported revascularization results in acute upper limb ischemia are rare. For this reason, the revascularization delay has remained poorly defined. The purpose of this study was to evaluate surgery results of acute upper limb ischemia related to revascularization delay., Methods: We report a retrospective study of patients operated for acute upper limb ischemia between 2008 and 2016. Patients with thrombotic, traumatic or iatrogenic ischemia were excluded from this study. Patients were divided into two groups (those operated before 12hours and those operated after 12hours). A statistical analysis was performed to compare surgery results between the two groups in terms of limb salvage rate and neurological sequelae rate., Results: Our population consisted of 138 patients. The average age was 69 [31,92]. There were 90 women and 48 men. The mean revascularization delay was 20hours [2,240]. Seventy-six patients were operated on before 12hours and 62 patients after 12hours. At one month, the mortality was 1.4% and the morbidity was 5.7%. The overall limb salvage rate was 86.9% and the overall neurologic sequelae rate was 31.8%. Statistical analysis showed that there was no significant difference between patients operated before or after 12hours in terms of limb salvage (86.8% versus 87%, P=0.258). However, there was a statistically significant difference in terms of neurological sequelae in favor of patients operated after 12hours (15.7% versus 51.6%, P=0.012)., Conclusion: Revascularization of acute embolic upper limb ischemia is often associated with good results even if performed late. Beyond 12hours of ischemia, amputation rate is not significantly higher, however, the rate of neurological sequelae can be high., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)

Purpose: To analyze the immediate outcome of percutaneous mechanical thromboembolectomy in acute infrainguinal leg ischemia in a consecutive cohort of patients with acute lower limb ischemia., Material and Method: We retrospectively analyzed the data of 156 acute infrainguinal ischemic events in 148 patients. Patients presented with acute limb ischemia Rutherford category I in 68 cases (44%), Rutherford category II A in 64 instances (41%) and Rutherford II B in 24 instances (15%). In 62 cases (39.7%), the occlusion site started below the knee joint level, in 94 (60.3%) cases above. As a basic technique, an intervention was started by manual aspiration but if aspiration failed, an additional device was added. Most frequently, a rotational thrombectomy device (Rotarex, Straub Medical, Wangs, Switzerland) was used. An antegrade access to the femoral artery was the preferred access to the limb (154/156)., Results: In 145 of 156 incidents, a technical success was achieved (93%). Aspiration was used in 153 cases (98%). Rotational thrombectomy by use of the Rotarex catheter was added in 60 cases (38%). Directional atherectomy was applied in a total of five patients. As main technical complications, a downward embolization occurred (n = 11). There were four surgical groin revisions. Five patients died during the early follow-up with four not related to the intervention. Clinically, 135 patients (86.5%) showed an improvement in their clinical situation., Conclusion: Acute lower limb ischemia can be successfully treated by mechanical thromboembolectomy only by combining aspiration embolectomy with rotational thrombectomy in most cases but manual aspiration alone will frequently fail especially above the knee joint level.

More blast injuries are encountered in the civilian setting in recent years as terrorist attacks have increased globally. A 17-year-old male patient with severe blast injury of the right lower extremity was admitted to our department on the fifth day after a terrorist bombing attack. Initially he had been admitted to an emergency department with segmental tibia fracture and arterial injury (Gustilo IIIC). An amputation had been foreseen due to ischemia that persisted even after orthopedic fixation and revascularization interventions, followed by fasciotomy incisions. After consultation with our department hyperbaric oxygen (HBO2) therapy was administered twice daily for the first week. Ischemia improved prominently after 10 HBO2 sessions. HBO2 therapy was continued together with antibiotherapy and wound care. The patient underwent a total of 40 HBO2 sessions and two reconstructive operations and healed without amputation. Vascular injuries with concomitant orthopedic trauma cause most of the delayed amputations in bombing attacks since ischemia can persist at the microvascular level even though adequate treatments are applied. HBO2 corrects hypoxia at tissue level and so provides oxygen for the critically ischemic cells in the injured area. HBO2 also enhances host defense and decreases the ischemia reperfusion injury. In this case, HBO2 was effective in survival and functional recovery (salvage) of the extremity together with regular wound care, antibiotherapy and surgical repair., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright © Undersea and Hyperbaric Medical Society.)

Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia., Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68., Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups., Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease.

Purpose: To illustrate the use of a mechanical thromboaspiration device originally designed for clot retrieval in acute stroke in the treatment of acute distal embolism occurring during percutaneous revascularization of the femoropopliteal and below-the-knee arterial segments., Technique: The Penumbra system was adapted for aspiration of thrombus in the distal foot arteries as a standalone device. The 2 over-the-wire, tapered lumen catheters have long working lengths (139 cm for the 4MAX to 153 cm for the 3MAX) that allow advancement below the ankle even with a retrograde contralateral approach. Once the occluded arterial segment is reached, the catheters are connected to the dedicated pump for continuous vacuum aspiration. The use of the device is illustrated in 3 diabetic patients (1 woman and 2 men; ages 88, 70, and 73 years, respectively) undergoing limb salvage procedures who experienced distal embolization that would have seriously jeopardized the foot circulation. The lumens of the occluded arteries were restored without complication., Conclusion: While further evaluation in a larger cohort of patients is needed, this initial experience using the Penumbra system in the peripheral vasculature suggests that this is a rapid, effective approach to address intraprocedural foot embolization and avoid possible grave clinical sequelae., (© The Author(s) 2015.)

Background: Acute ischemia of the upper limbs is rare in comparison with ischemia of the lower limbs. The origins of this condition are varied., Goals: We retrospectively analyzed cases of acute finger ischemia (Raynaud's phenomena was excluded) in a dermatology department between 2008 and 2013 in order to evaluate the etiology and management of this phenomenon., Results: Thirteen cases of finger ischemia were reported. The mean age was 54 years. Active smoking was noted in 11 cases. Ischemia was acute in 9 cases and subacute in 4 cases. The location was unilateral in 10 cases and bilateral in 2. Etiologies were: dysplasia of the palmar arch, antiphospholipid antibody syndrome, frostbite, distal arteritis linked to smoking, paraneoplastic arteritis, Buerger's disease, polyarteritis nodosa, stenosis of the subclavian artery, and 3 cases of embolic origin (ulnar, cardiac, and paraneoplastic aneurysm). In the acute phase, antiplatelets were given in 6 cases, anticoagulants in 10 cases and ilomedin in 6 cases. Sympathectomy was performed in 1 case and amputation in 2 cases., Discussion: This study illustrates the diversity of etiologies of finger ischemia. The etiological test battery should be broad and include immunological and thrombophilia tests, arterial and cardiac investigations, cervical radiography and CT scan (screening for cancer). Close collaboration between dermatologists, hematologists, vascular surgeons and radiologists is essential for the management of these patients., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)

Acute upper limb ischemia is considered a vascular emergency. These events are mostly thromboembolic and are often detected in patients with atrial fibrillation (AF). Surgical thrombectomy and percutaneous mechanical thrombectomy are the usual methods to treat this medical emergency. In this case, we report the case of a 75-years old woman with a history of AF who initially presented to our center because of syncope resulting from Torsades de pointes due to a known long-QT syndrome. Those episodes were treated adequately from the implanted ICD. In addition to the symptoms of syncope, the patient also noted symptoms of right upper-limb ischemia. Using duplex sonography, we noticed a thrombotic occlusion at the level of the axillary artery. Using femoral access, we performed an antegrade angiography of the axillary artery, which confirmed a fresh thrombotic occlusion. The initially performed thrombus aspiration wasn't successful, and the decision was made to use an ekosonic endovascular system (Ekosonic ™ Endovascular System, Boston Scientific, EKOS) catheter to perform catheter-directed thrombolysis. Locally, 10 mg Actilyse were administrated. Then an EKOS Catheter was delivered to the occlusion area and was placed for 6 h. Symptoms of ischemia were resolved, and the angiographic control showed normal flow in the axillary artery. The patient was discharged without any local deficits of the right hand. [ABSTRACT FROM AUTHOR]

Objectives Acute thrombotic ischemia is a very dangerous limb-threatening and life-threatening disease. It is better treated by catheter-directed thrombolysis. Now, tissue plasminogen activator like alteplase is safer than streptokinase or urokinase. The current study is designed to show its efficacy and safety and to investigate variables that correlate with outcome. Patients and methods This is a prospective cohort study. It included patients with acute thrombotic limb ischemia. Excluded ones were acute ischemia due to embolism, trauma, arterial dissection, complicated aneurysm, bleeding risk, history of recent intracranial bleeding, massive gangrene, or uncontrolled hypertension. The study is approved by ethical committee of Beni-Suef University. Primary end points were technical success, clinical success, and limb salvage. Secondary end points were procedural complications. Results A total of 36 patients were enrolled in the study from March 2019 to February 2020 in Beni-Suef University Hospital. It included 21 (58.33%) male patients. The patients' mean age was 58.42 years and mean BMI was 31.56 kg/m2. Risk factors were smoking in 15 (41.67%) patients, diabetes mellitus in 16 (44.44%) patients, hypertension in 15 (41.67%) patients, ischemic heart disease in nine (25%) patients, and hyperlipidemia in 14 (38.89%) patients. Clinical presentation showed that 16 (44.44%) patients were in Rutherford IIa category and 20 (55.56%) patients were in Rutherford IIb category. Limb salvage was achieved in 14/16 (87.5%) of patients in Rutherford IIa category and 12/20 (60%) of patients in Rutherford IIb category. Statistical analysis showed a correlation of BMI and severity of ischemia with outcome. Moreover, the frequency of risk factors was correlated with outcome. Conclusion Catheter-directed thrombolysis using alteplase is effective and safe to treat acute thrombotic limb ischemia. Its outcome is better with lower BMI, less severe ischemia, and less or no comorbid disease. [ABSTRACT FROM AUTHOR]

We present a case of acute and chronic ischemia in the bilateral cerebellar border zones in a patient with migraine with aura. To our knowledge, this imaging presentation has not been published. The patient presented with 20 years of migraines that had worsened with developing aura prior to MRI, which showed restricted diffusion in the bilateral cerebellar border zones, consistent with acute ischemia. Additional ADC hyperintensities were demonstrated in the border zones, consistent with chronic infarcts. Follow-up CT angiogram showed no occlusion, stenosis, vasospasm, or significant atherosclerosis in the posterior circulation. Additionally, follow-up MRI performed 56 days after initial MRI showed that post-migraine ischemia can be associated with signs of microscopic damage on DWI/ADC map that are not visible with T2 weighted or FLAIR sequences. Cerebellar border zone hypoperfusion from cortical spreading depression and/or transient vasospasm is the most likely etiology due to poor collateral circulation and thus a lower ischemic threshold. Changes in physiologic response to 5-HT during migraine with aura may be responsible for these perfusional abnormalities. Some patients may be more prone due to anatomic variability of the superior cerebellar arteries (SCA) and posterior inferior cerebellar arteries (PICA). Radiologist should be aware of subtle small cerebellar zone infarcts with migraine patients when scrutinizing the posterior fossa. • Migraine may cause borderzone ischemia in the cerebellum • Ischemic lesions due to migraine may be reversible on FLAIR and T2 weighted imaging • ADC map data may show microstructural abnormalities in patients with acute migraine [ABSTRACT FROM AUTHOR]

Neonatal gangrene is a rare condition during the neonatal period. Its prognosis is generally poor. Acute ischemia of the limbs is most often caused by thromboembolic events. Although there are several predisposing factors, in the majority of cases no causative factor is found. Also the extent of the gangrene is variable; it can affect one or several fingers or toes or even the whole upper or lower limb. We here report a case of congenital gangrene of the hand treated in our Department. [ABSTRACT FROM AUTHOR]

Blockade of the late Na current ( I ) protects from ischemia/reperfusion damage; nevertheless, information on changes in I during acute ischemia and their effect on intracellular milieu is missing. I , cytosolic Na and Ca activities (Na, Ca) were measured in isolated rat ventricular myocytes during 7 min of simulated ischemia (ISC); in all the conditions tested, effects consistently exerted by ranolazine (RAN) and tetrodotoxin (TTX) were interpreted as due to I blockade. The results indicate that I was enhanced during ISC in spite of changes in action potential (AP) contour; I significantly contributed to Na rise, but only marginally to Ca rise. The impact of I on Ca was markedly enhanced by blockade of the sarcolemmal(s) Na/Ca exchanger (NCX) and was due to the presence of (Na-sensitive) Ca efflux through mitochondrial NCX (mNCX). sNCX blockade increased Ca and decreased Na, thus indicating that, throughout ISC, sNCX operated in the forward mode, in spite of the substantial Na increment. Thus, a robust Ca source, other than sNCX and including mitochondria, contributed to Ca during ISC. Most, but not all, of RAN effects were shared by TTX. (1) The paradigm that attributes Ca accumulation during acute ischemia to decrease/reversal of sNCX transport may not be of general applicability; (2) I is enhanced during ISC, when the effect of Na on mitochondrial Ca transport may substantially contribute to I impact on Ca; (3) RAN may act mostly, but not exclusively, through I blockade during ISC. [ABSTRACT FROM AUTHOR]

Background: Hemoglobin tetramers are the major oxygen-carrying molecules within the blood. We hypothesized that a lower hemoglobin level and its reduced oxygen-carrying capacity would associate with larger infarction in acute ischemic stroke patients. Methods: We studied 135 consecutive patients with acute ischemic stroke and perfusion brain MRI. We explored the association of admission hemoglobin with initial infarct volumes on acute images and the volume of infarct expansion on follow-up images. Multivariable linear regression was performed to analyze the independent effect of hemoglobin on imaging outcomes. Results: Bivariate analyses showed a significant inverse correlation between hemoglobin and initial volume in diffusion-weighted imaging (r = –0.20, p = 0.02) and absolute infarct growth (r = –0.20, p = 0.02). Multivariable linear regression modeling revealed that hemoglobin remained independently predictive of larger infarct volumes acutely (p Conclusions: Hemoglobin level at the time of acute ischemic stroke associates with larger infarcts and increased infarct growth. Clarification of the mechanism of this effect may yield novel insights for therapy.

Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia.Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68.Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups.Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the clinical characteristics and treatment outcomes of acute upper extremity thromboembolism. Methods: From April 1997 to July 2012, nineteen patients (10 males, mean age 69.7 years) were treated for acute upper extremity thromboembolism. Iatrogenic or traumatic acute thromboembolisms were excluded. We retrospectively reviewed patient demographics, clinical characteristics (symptom, risk factor, involved artery, and duration from initial symptom onset to primary treatment) and treatment outcomes. Results: Numbness or tingling sense was the most common symptom in patients (84.2%). Twelve patients (63.1%) had cardiac arrhythmia, of which 9 patients had atrial fibrillation (47.3%). Floating thrombus was detected on transesophageal echocardiography in 6 patients. Fourteen patients (73.7%) were treated within 24 hours from the symptom onset. Most thromboembolism was located in the brachial artery bifurcation with or without proximal or distal extension. Fogarty catheter thromboembolectomy was the primary treatment in 17 patients (89.5%), of whom 13 patients (72.2%) were operated under local anesthesia. All patients received anticoagulation or antithrombotic therapy after the procedure. Three patients had recurrent thrombosis on duplex scan; however, their symptoms were improved without further intervention. All other patients were symptom-free without recurrence during the mean follow-up of 17.1±21.3 months. Conclusion: Early diagnosis and Fogarty catheter thromboembolectomy under local anesthesia followed by proper anticoagulation is the most effective and useful treatment in patients with acute upper extremity thromboembolism. [ABSTRACT FROM AUTHOR]

Neuroprotection in retinal experimental work consists primarily of preventing retinal ganglion cell (RGC) loss after exposure to a hostile event. We have studied the neuroprotective effect on RGCs in an ischemia-reperfusion model by activation of the cannabinoid receptor CB1 using topical application of WIN 55212-2. Intraocular pressure (IOP) was increased by continuous infusion of phosphate buffer saline (PBS) into the anterior chamber of the eye. Mean intraocular pressure was increased up to 88.5 ± 0.29 mm Hg (control normal IOP 15.1 ± 0.25 mm Hg), for 35 min. Animals were distributed in 3 groups. Left eyes underwent acute rise in intraocular pressure. First group was treated with topical Tocrisolve™ 100 in both eyes. Second group was treated with 1% solution of CB1 agonist WIN 55212-2 in both eyes. Third group was treated with WIN 55212-2 1% and CB1 antagonist AM 251 1% solutions in both eyes. Subsequently, RGCs were immunolabeled with Brn3a and automated quantification of retinal mosaics of RGCs were performed. The ischemic damage led to a mean loss in RGC density of 12.33%. After topic administration of WIN 55212-2, mean loss of RGCs was of 2.45%. Co-treatment with CB1 antagonist AM 251 abolished almost completely the neuroprotective effect of WIN 55212-2. Topic 1% WIN 55212-2 showed a neuroprotective effect on RGC degeneration after ischemia-reperfusion without pre-activation of CB1 receptors. [ABSTRACT FROM AUTHOR]

Introduction: Civilian and military vascular trauma has evolved dramatically. It is estimated that 80% of all cases of vascular injuries are due to peripheral vascular trauma, most involving the lower extremities. Arterial below-knee injuries by gunshot still remain a challenge, with an associated rate of amputation of 20-54%. Material and Methods: This case reports a 48 year-old male patient who sustained a gunshot below his left knee. At hospital admission, loss of substance and hemorrhage at the medial and lateral faces of the upper third of his left leg were present with signs of distal ischemia. Arteriography revealed infra-popliteal arterial lesions of the three arterial axes. Two reversed great saphenous vein interposition grafts were performed into the anterior and posterior tibial arteries with immediate revascularization of the left leg and foot. Later, soft tissue reconstruction was accomplished by a split-thickness skin graft. Results: At the fifth month of follow-up, the left leg and foot were viable with good healing, without limitations and with controlled pain. Posterior tibial and dorsalis pedis pulses were palpable. Conclusion: This case report shows the importance of an adequate team approach for treatment of a gunshot extremity injury with vascular lesion. The authors want to highlight the scientific background evidence and the value of comparing worldwide civilian trauma center outcomes, mostly reported previously from the military field. [ABSTRACT FROM AUTHOR]

The article presents a study on the capability of ischemia-induced mechanical dysfunction to cause ventricular premature beats (VPBs) during acute regional ischemia in the U.S. The study intends to determine the role of the electromechanical dysfunction on arrhythmogenesis in acute ischemia with the use of the 3D electromechanical model. The findings reveal on the potential of the mechanical induced membrane depolarization to lead to the occurrence for spontaneous arrhythmias.

Objective. In this study we tested the hypothesis that α-2 adrenergic antagonism could facilitate induction of previously non-inducible ventricular tachycardia (VT) during acute ischemia. Previous reports suggest that VT during ischemia may be modulated by α-2 adrenergic agonists. Design. The left anterior descending artery was occluded after instrumentation of the ischemic risk zone with 21 multipolar plunge needles, each recording 6 bipolar electrograms. Three dimensional mapping characterized the mechanism of VT induced with extrastimuli. Results. Of 16 non-inducible dogs included, eight which were given the α-2 adrenergic antagonist yohimbine all had inducible VT, while all eight in the control group remained non-inducible (p <0.05). Six of the VTs were of focal Purkinje origin. The cycle length of the VT was 119±4 ms. Mean arterial pressure (81±8 to 82±8 mmHg, p =ns), ventricular effective refractory period (146±6 to 144±5 ms, p =ns) and ischemic zone size (55±6% vs. 61±4%, p =0.45) were not altered by yohimbine indicating minimal central or pre-junctional effects of the drug. Conclusions. Yohimbine facilitates induction of VT, especially those with focal Purkinje fiber origin, suggestive of an effect mediated through antagonism of post-junctional α-2 adrenoceptors on Purkinje fibers. [ABSTRACT FROM AUTHOR]

Abstract: The inflammatory cytokine tumor necrosis factor alpha (TNFα) is controversially discussed in ischemia/reperfusion damage of the heart. Purpose of this study was to elucidate cellular sources of TNFα and parameters which possibly influence its release in the heart following ischemia. Isolated hearts of mice were subjected to 15 min of global ischemia and 90 min of reperfusion. We employed hearts of various mice knock-out strains (interleukin-6−/−, matrix metalloprotease-7−/−, mast-cell deficient WBB6F1-KitW/KitW-v, TNF-R1−/−) and wildtype mice, the latter perfused without and with infusion of cycloheximide or TNFα-cleaving-enzyme inhibitor (TAPI-2). Normoxic control hearts showed basal release of TNFα during the whole experiment. Immunohistology identified cardiac mast cells, macrophages and endothelial cells as main sources. TNFα release was stimulated during postischemic reperfusion, occurring in a two-peak pattern: directly after ischemia (0–10 min) and again after 60–90 min. The first peak mainly reflects tissue washout of TNFα accumulated during ischemia. The second, protracted peak arose continuously from the basal level and was abolished by protein synthesis inhibitor cycloheximide. Both properties are characteristic for de novo synthesis of TNFα, e.g., in cardiac muscle cells. However, immunohistological staining for TNFα failed in cardiomyocytes after 90 min of reperfusion. In contrast to hearts of TNF-R1−/− and KitW/W-v-mice, those of IL-6−/− and MMP-7−/− mice lacked the late TNFα peak. TAPI did not suppress release of TNFα. While autostimulation via TNF-R1 also does not seem obligatory and mast cell can be ignored as source of the second peak, IL-6 may support de novo synthesis of TNFα. Additionally, TNFα release may essentially involve cleavage of membrane bound TNFα by MMP-7. [Copyright &y& Elsevier]

The objective of this study was to review a single center's experience of upper limb revascularization over 20 years. All patients undergoing operative or endovascular upper limb revascularization between June 1983 and July 2003 were identified. One hundred eighty-four upper limb revascularization procedures were carried out on 172 patients. Sixty-one patients had a thromboembolic event (35%), 53 patients presented with a traumatic vascular injury (31%), and 29 patients had symptoms of chronic atherosclerotic upper limb ischemia (17%). Fifteen patients had subclavian steal syndrome, eight patients had thoracic outlet compression, and six patients had iatrogenic injuries of the upper limb arteries. Fifty-five thromboembolectomies were performed, 37 under locoregional anesthesia. Ten patients (18.2%) died from cardiopulmonary causes following embolectomy. Fifteen reversed saphenous vein bypass grafts were performed for traumatic damage. Twenty-seven patients had a primary repair, and five required a vein patch. One patient subsequently had an arm amputation, and two patients died. Twelve patients presenting with chronic arm ischemia had a subclavian angioplasty, 12 patients had a proximal bypass, and in 5 patients, stenoses were stented. The mortality in this group was 6.9% (2 of 29). The mortality for upper limb revascularization was 8.7%. Almost all deaths occurred after upper limb embolectomy, and the mortality of this procedure was similar to that of lower limb embolectomy. Deaths were the result of cardiac comorbidity, and this should be actively sought and treated if outcomes are to improve. [ABSTRACT FROM AUTHOR]