Sarcoidosis presenting with large vessel vasculitis and osteosclerosis-related bone and joint pain.

A 34-year-old African-American female diagnosed earlier with idiopathic thrombocytopenic purpura (ITP), lymphadenopathy, splenomegaly, uveitis, and pulmonary nodules, developed a subclavian artery aneurysm, and generalized annular osteosclerotic lesions with disabling arthralgias. Biopsies from bone and lymph node revealed non-caseating granulomas and no evidence of malignancy or infection, confirming the clinical impression of sarcoidosis.

Subclavian artery aneurysm: an unusual manifestation of Takayasu's arteritis.

Complications of Takayasu's arteritis are typically ischemic in nature because of progressive arterial narrowing, with aneurysm formation occurring as a late sequela. A 30-year-old Black woman with Takayasu's arteritis presented with a progressively enlarging and tender pulsatile mass at the base of the right neck. Upper extremity pulses were intact. Chest computed tomography and aortography demonstrated a 6-cm aneurysm of the right subclavian artery, which originated at the takeoff from the innominate artery, which was also ectatic. There was no evidence of occlusive disease. An operation was performed via the median sternotomy with transverse extension into the supraclavicular area. The distal innominate artery, proximal common carotid artery and entire subclavian artery were resected and replaced with a bifurcated stretch ePTFE graft. The aneurysm was without thrombus or atherosclerosis and all vessels were extremely thick-walled. Pathology revealed healed/healing nonspecific arteritis. Aneurysm formation is an unusual complication of Takayasu's arteritis. Previously reported sites of aneurysm formation include the thoracic and abdominal aorta, the innominate, carotid and superior mesenteric arteries, but not the subclavian artery. Of 28 patients enrolled in a recent clinical protocol at the National Institutes of Health with Takayasu's arteritis, none had aneurysm formation. The authors report surgical repair of a large aneurysm of the right subclavian artery in a young Black woman with Takayasu's arteritis.

An aneurysm involving the axillary artery and its branch vessels in a major league baseball pitcher. A case report and review of the literature.

Baseball pitchers appear to be prone to aneurysms of the axillary artery and its branches. The cause is probably related to repetitive compression of or tension on the vessels at the level of the pectoralis minor muscle and the humeral head, which is exacerbated by the pitching motion. The incidence of aneurysms of the axillary artery and its branches among pitchers and other athletes is not known, nor is it clear whether pitchers who are at high risk of vascular injury can be identified before irreversible damage to the vessels has occurred. Perhaps patients who have documented compression or occlusion of the vessel with the arm in the abducted, externally rotated position are at higher risk. Screening pitchers to identify those with axillary artery compression, aneurysm, or thrombosis has also not been shown to be effective. Certainly, many pitchers will have some level of compression of the axillary artery with their arm in the pitching position but will never develop any clinical abnormality requiring treatment. Screening would therefore probably lead to a high false-positive rate. It is clear, however, that pitchers who complain of ischemia-type symptoms such as early fatigue or who have evidence of emboli require a complete evaluation to rule out any abnormality of the axillary artery or one of its branches. Orthopaedic surgeons who see pitchers and other athletes involved in repetitive overhead motions need to be aware of this disorder so that they order the appropriate tests and obtain a vascular consultation--and make a prompt diagnosis. Treatment will vary depending on the type of lesion and on which vessel or vessels are involved, and should be decided on by the team of surgeons treating the patient.

Attenuation of acute lung injury caused by hind-limb ischemia-reperfusion injury by butyrolactone anti-inflammatory agent FL1003.

OBJECTIVE: Activation of systemic inflammation after reperfusion of ischemic tissue results in severe acute lung injury. Neutrophil activation and oxygen radical generation have been implicated in the pathogenesis. This study tested the hypothesis that treatment with FL1003, a butyrolactone with in vitro antioxidant properties, will down-regulate this response and abrogate acute lung injury. METHODS: Male Sprague-Dawley rats (n = 16) were divided into a surgical sham group (n = 4), a group that received 2 hours of ischemia by infrarenal aortic clip followed by 1 hour of reperfusion (n = 7), and an ischemia-reperfusion (I/R) group that received FL1003 100 mg/kg intravenously before ischemia (n = 5). After reperfusion, the heart and lungs were excised en bloc in an isolated lung perfusion apparatus for 1.5 hours of perfusion, while pulmonary artery pressures were held between 5 and 12 mm Hg and venous effluent was collected. Bronchoalveolar lavage fluid and both lungs were harvested at death for determination of tissue water content, pulmonary microvascular permeability, and indicators of neutrophil activation and tissue oxidation. RESULTS: After I/R, there were significant (p < 0.05) increases in intravenous fluid (IVF) requirements (18 +/- 1.2 mL) to maintain hemodynamic stability, wet weight/dry weight ratio of lung tissue, and isolated-lung lavage Ficoll concentrations (0.58 +/- 0.02 microg/mL) compared with sham animals (IVF, 0 mL; Ficoll concentration, 0.08 +/- 0.03 microg/mL). In addition, lung myeloperoxidase activity (0.60 +/- 0.03 vs. 0.12 +/- 0.02 units/g of tissue) and levels of lipid-conjugated dienes (0.042 +/- 0.012 vs. 0.018 +/- 0.006 optical density of 233 nm (OD233)/mL) were significantly higher (p < 0.05) compared with the sham group. In I/R animals treated with FL1003, the IVF requirement (8.5 +/- 1.0 mL), wet weight/dry weight ratio, lung tissue Ficoll concentration (0.21 +/- 0.02 microg/mL), myeloperoxidase concentration (0.217 +/- 0.02 units/g), and lipid-conjugated diene levels (0.012 +/- 0.005 OD233/ mL) were all significantly lower (p < 0.05) than after untreated I/R. CONCLUSION: A pulmonary microvascular permeability defect with pulmonary edema, neutrophil aggregation, and cell membrane damage resulted from ischemia and reperfusion. Treatment of animals with FL1003 significantly attenuated the inflammatory response associated with acute lung injury.

Ischemia-reperfusion injury in myocutaneous flaps: role of leukocytes and leukotrienes.

Leukotriene B4 is a potent inflammatory mediator that is derived from the 5-lipoxygenase pathway of arachidonic acid metabolism and that has been implicated in the pathophysiology of polymorphonuclear leukocyte-dependent reperfusion injury in a variety of organ systems. The objectives of these investigations were to determine whether inhibition of leukotriene B4 attenuates postischemic polymorphonuclear leukocyte infiltration and subsequent injury in myocutaneous flaps. Anesthetized female Yorkshire pigs were randomized to receive normal saline (n = 8), the 5-lipoxygenase inhibitor diethylcarbamazine (n = 7), or the leukotriene B4 receptor antagonist SC-41930 (n = 7). All animals underwent 6 hours of rectus abdominis myocutaneous flap ischemia followed by 4 hours of reperfusion. In saline-treated controls, flap ischemia was associated with massive polymorphonuclear leukocyte infiltration at 1 and 4 hours of reperfusion (252 +/- 70 and 619 +/- 137 polymorphonuclear leukocytes per 25 high-power fields, respectively). Skeletal muscle neutrophil content was significantly attenuated by pretreatment with diethylcarbamazine (72 +/- 29 and 229 +/- 63 polymorphonuclear leukocytes per 25 high-power fields; p < 0.05) or SC-41930 (25 +/- 3 and 193 +/- 25 polymorphonuclear leukocytes per 25 high-power fields; p < 0.05). Wet-to-dry weight ratios of full-thickness flap biopsies were lower in the diethylcarbamazine and SC-41930 groups (2.98 +/- 0.15 and 2.90 +/- 0.26, respectively) than in the control group (4.13 +/- 0.23; p < 0.01), and mean muscle infarct size, as determined by nitroblue tetrazolium staining, diminished from 47.6 +/- 11.3 percent in controls to 25.1 +/- 6.5 percent in diethylcarbamazine-treated animals and 7.3 +/- 4.8 percent in SC41930-treated animals (p < 0.05). These data indicate that leukotriene B4 plays a critical role in mediating neutrophil-dependent injury in postischemic skeletal muscle flaps.

Acquired protein S and antithrombin III deficiency caused by nephrotic syndrome: an unusual cause of graft thrombosis.

Thrombotic phenomena are well-recognized complications of nephrotic syndrome attributable to loss of intermediate-sized antithrombotic proteins in the urine, resulting in a hypercoaguable state. As such, nephrotic syndrome may be associated with a reduction in circulating antithrombin III and free protein S levels. Associated spontaneous thrombotic complications are generally venous in nature, with arterial thrombosis occurring less frequently. Hypercoagulability caused by acquired nephrotic syndrome has not generally been recognized as a cause of acute thrombosis of arterial bypass grafts. We report two patients who after having nephrotic syndrome sustained acute thrombosis of their arterial bypass grafts. Pathogenesis and management are discussed.

Mechanisms of cerebrovascular dysfunction.

Cerebrovascular dysfunction characterized by the loss of endothelial integrity has been observed following ischemic and traumatic insults to the brain, resulting in the net movement of fluid and solute out of the intravascular space and into the interstitium. Following traumatic brain injury, the development of intracranial hypertension secondary to cerebral edema plays a major role in the high morbidity and mortality in these patients. Although the precise mechanisms responsible for the disruption of the normally tightly regulated cerebrovascular tissue interface remain unclear, there is increasing evidence implicating inflammatory events in this process through the transient opening of tight junctional complexes. This article will examine the interaction of astrocytes, activated neutrophils, and inflammatory mediators in inducing endothelial contraction, thereby physically opening the permeability barrier and allowing the net movement of fluid out of the intravascular space.

Reperfusion injury of postischemic skeletal muscle is attenuated by the 21-aminosteroids U-74389F and U-74500A independent of iron binding.

BACKGROUND: Lazaroids (21-aminosteroids) are a novel class of compounds that have been shown to limit experimental ischemic injury of varied causes. The mechanism of action is uncertain but may include scavenging of lipid peroxy radicals, iron binding, or direct membrane interaction. The purpose of these experiments was to evaluate the capacity of the lazaroids U-74500A and U-74389F to modify ischemia/reperfusion injury of skeletal muscle in a well-characterized model of high-grade partial ischemia. METHODS: Nonfasted male Sprague-Dawley rats were anesthetized, a tracheostomy tube was placed, and the carotid artery and jugular vein were cannulated. Animals received heparin (1 unit/gm) and crystalloid (1 ml/hr) intravenously. The baseline group (n = 6) was allowed a 30-minute equilibration period, after which resting transmembrane potential (Em) was measured in a hindlimb muscle. Muscle biopsy specimen was obtained; conjugated diene and thiobarbituric acid reactive substances were measured as indexes of lipid peroxidation. Spectrophotometric determination of plasma iron and unsaturated iron-binding capacity were performed (total iron-binding capacity and percent saturation were calculated). Animals received U-74389F (2 mg/kg, n = 7), U-74500A (2 mg/kg, n = 6), or vehicle only (0.02 mol/L citrate acid/citrate; n = 7) intraarterially before infrarenal aortic clamping was performed for 120 minutes. An additional group of animals received U-74389F (2 mg/kg, n = 7), U-74500A (2 mg/kg, n = 7), or vehicle (n = 11) intraarterially before infrarenal aortic clamping was performed for 120 minutes, followed by reperfusion for 30 minutes. RESULTS: Depolarization of resting Em was noted during ischemia, with partial repolarization on reperfusion, which was enhanced by either lazaroid. As expected, iron delocalization occurred during ischemia and persisted on reperfusion, with U-74500A effectively binding iron, whereas U-74389 did not. Vehicle but not the 21-aminosteroids inhibited lipid peroxidation. CONCLUSIONS: High-grade partial ischemia of skeletal muscle is associated with iron delocalization, which persists on reperfusion. Each lazaroid achieved a similar "membranoprotective" effect during reperfusion only despite lack of iron binding by U-74389F, suggesting a direct interaction with the cell membrane. These data support the concept that ischemic injury and reperfusion injury occur through fundamentally different mechanisms.

Reserving supraclavicular first rib resection for vascular complications of thoracic outlet syndrome.

BACKGROUND: The traditional approach to decompression of the thoracic outlet has been by transaxillary resection of the first rib. Recently, the trend has been toward a more selective and tailored surgical approach via the supraclavicular route. METHODS: During a 51-month period, 14 consecutive patients underwent decompressive surgery of the thoracic outlet via the supraclavicular approach. There were ten women and four men; mean age was 44 years. Indications for operation were arterial (n = 3), venous (n = 2) and neurogenic (n = 9). Mean follow-up was 31 months. Operation consisted of resection of the anterior scalene and medial aspect of the middle scalene muscles and brachial plexus neurolysis for neurogenic indication, with first rib resection reserved for vascular complications. RESULTS: Operations performed for vascular complication were successful and uncomplicated, with good clinical outcome. Seven of nine operations (78%) performed for neurogenic indication produced marked relief of symptoms, while two (22%) resulted in no clinical change. Complications consisted of transient scapular winging (n = 1) and transient diaphragmatic paralysis (n = 2). CONCLUSIONS: A selective approach to thoracic outlet decompression, consisting of anterior scalenectomy and brachial plexus neurolysis for neurogenic symptoms, and reserving first rib resection for arterial and venous indications, is a safe procedure and yields satisfactory results in appropriately selected patients.

The role of tumor necrosis factor and nitric oxide in the acute cardiovascular response to endotoxin.

OBJECTIVE: This study was designed to examine the differential effects of tumor necrosis factor (TNF) and nitric oxide on the acute cardiovascular changes that occur in response to endotoxemia. SUMMARY BACKGROUND DATA: Recent studies have suggested that some, if not all, of the cardiovascular effects of TNF are mediated through release of nitric oxide. However, the mechanisms through which TNF and nitric oxide induce hypotension and shock in vivo in response to systemic endotoxemia remain poorly characterized, despite current interest in the use of nitric oxide antagonists to ameliorate septic shock. METHODS: A reproducible model of endotoxemia was established in adult Sprague-Dawley rats. The acute cardiovascular changes that occur after bolus infusion of endotoxin was then determined in rats treated with either TNF antibody, N-methyl arginine, or both. RESULTS: Inhibition of either TNF or nitric oxide restores mean arterial blood pressure to normal after endotoxemia (p < 0.05). However, nitric oxide exerts its effects principally on the peripheral vasculature, whereas TNF appears to act on the myocardium. A combination of TNF antiserum pretreatment and N-methyl arginine administration is necessary to return mean arterial blood pressure to normal 60 minutes after endotoxin infusion. CONCLUSION: Tumor necrosis factor and nitric oxide mediate the acute cardiovascular effects of endotoxemia through distinct mechanisms. Nitric oxide is released as a result of both TNF-dependent and TNF-independent mechanisms, whereas the cardiovascular effects of TNF are only partially mediated through nitric oxide.

Neutrophil lipoxygenase activation and leukosequestration in postischemic myocutaneous flaps: role of LTB4.

Reperfusion of ischemic tissues leads to eicosanoid- and polymorphonuclear leukocyte (PMN)-dependent injury. The present experiments were undertaken to examine the effect of myocutaneous flap ischemia-reperfusion on neutrophil 5-lipoxygenase activity and to define the role of leukotriene B4 (LTB4) in postischemic PMN infiltration into such composite tissue grafts. Anesthetized Yorkshire pigs underwent 6 h of rectus abdominis myocutaneous flap ischemia or sham ischemia, and LTB4 generation was measured in calcium ionophore-stimulated neutrophils isolated from the circulation. At 30 min of reperfusion, neutrophil generation of LTB4 increased from a baseline value of 31.0 +/- 6.8 to 98.5 +/- 5.1 ng/5 x 10(6) PMN (P < 0.01) and was significantly greater than those neutrophils isolated from animals subjected to sham ischemia and reperfusion (54.3 +/- 4.1 ng/5 x 10(6) PMN; P < 0.01). Pretreatment of animals with the LTB4-receptor antagonist, SC-41930 (n = 5), significantly attenuated reperfusion-associated 5-lipoxygenase activation (60.3 +/- 11.6 ng LTB4/5 x 10(6) PMN; P < 0.01), suggesting the presence of a positive feedback mechanism for eicosanoid biosynthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary failure following lower torso ischemia: clinical evidence for a remote effect of reperfusion injury.

Acute lung injury as a remote sequela of severe lower torso ischemia-reperfusion has been demonstrated experimentally, in a process involving leukosequestration and generation of the arachidonate derivatives thromboxane and leukotriene B4. However, contemporary clinical reports have been limited to development of transient, subclinical "reperfusion pulmonary edema" several hours after declamping in patients undergoing elective abdominal aortic aneurysm repair. This report refocuses attention on the clinical syndrome of severe, acute deterioration in pulmonary function occurring several hours after restoration of perfusion to an ischemic lower torso in two patients. The lung injury is characterized by progressive hypoxemia, pulmonary hypertension, decreased lung compliance, and non-hydrostatic pulmonary edema, consistent with adult respiratory distress syndrome (ARDS). This report reinforces the concept that humoral mediators generated at reflow may induce end-organ injury at a site remote from the focus of ischemia-reperfusion, and that the lung is a target organ.

Hypothermia during elective abdominal aortic aneurysm repair: the high price of avoidable morbidity.

PURPOSE: Adverse outcomes apparently associated with hypothermia led us to examine patients undergoing elective abdominal aortic aneurysm (AAA) repairs to test the hypothesis that hypothermia (temperature less than 34.5 degrees C) is associated with increased morbidity and excess mortality rates. METHODS: Two hundred sixty-two elective AAA repairs were retrospectively reviewed for preoperative and intraoperative risk factors. Core temperature, age, Acute Physiology and Chronic Health Evaluation (APACHE) II and APACHE III scores (raw and temperature-adjusted), fluid resuscitation, and perioperative organ dysfunction were recorded prospectively. Outcome measures included lengths of stay in the intensive care unit and in the hospital, and hospital mortality rates. RESULTS: Except for a higher risk of hypothermia in women (p < 0.05), by univariate analysis, preoperative risk factors were similar in patients in the hypothermic and normothermic groups. After operation, patients with hypothermia had significantly greater APACHE scores (p < 0.0001), and patients in the hypothermic nonsurvivor group took significantly longer to rewarm (p < 0.05), suggesting marked hypoperfusion. Patients with hypothermia had significantly greater fluid (p < 0.05), transfusion (p < 0.01), vasopressor (p < 0.05), and inotrope (p < 0.05) requirements, resulting in significantly higher incidences of organ dysfunction (53.0% vs 28.7%, p < 0.01) and death (12.1% vs 1.5%, p < 0.01) and markedly prolonged lengths of stay in the unit (9.2 +/- 2.0 vs 5.3 +/- 0.6, p < 0.05) and in the hospital (24.3 +/- 2.9 vs 15.0 +/- 0.08, p < 0.01). By multivariate analysis, female gender (p = 0.004) was the only predictor of intraoperative hypothermia, whereas initial hypothermia was significantly predictive of both prolonged hypothermia and development of organ failure (p < 0.05). Organ failure (p < 0.05) and acute myocardial infarction (p < 0.01) were independent predictors of death. CONCLUSIONS: After AAA repair, patients with hypothermia have multiple physiologic derangements associated with adverse outcomes. Although multiple etiologic factors are interacting, body temperature is one variable that should be controlled during aortic surgery.

Nitric oxide and cardiovascular dysfunction.

Prior to the mid-1980s, nitric oxide (NO) was viewed as an environmental pollutant but not as a compound of physiological significance. Thus, it was a skeptical audience that first heard the pronouncement at a scientific meeting in 1986, that NO was the identity of the elusive endothelium-derived relaxing factor, a mediator of vasorelaxation in response to numerous endogenous stimuli. Since then, the simple gas NO has gone from obscurity to center stage, being identified as a key player in physiologic processes as diverse as blood pressure maintenance, neural transmission, and immunologic defense. In addition to its physiological roles, NO has been implicated in the pathogenesis of a multitude of disease states, many of which are of primary interest to the cardiovascular surgeon: circulatory shock, atherosclerosis, diabetes mellitus, and ischemia-reperfusion injury. Recent years has seen NO biology emerge as an exciting and extremely fertile area of biomedical investigation. To fully understand the molecular basis of many clinical problems facing the cardiovascular surgeon, appreciation of NO's involvement is essential.

Iron and cardiovascular dysfunction: mechanisms and therapeutic implications.

It has been recognized for over three decades that tissue hypoperfusion is associated with the appearance of increased levels of iron in the plasma. Experimental observations have documented the liberation of iron into the circulation following reperfusion of ischemic myocardium and small intestine, and into the urine following renal ischemia-reperfusion. Similarly, we have recently demonstrated that iron is delocalized during ischemia of skeletal muscle, via a process which persists upon reperfusion. Other studies have demonstrated delocalization of iron in the parenchyma of postischemic brain, myocardium, and kidney.

Persistent hypoglossal artery: diagnostic and therapeutic considerations concerning carotid thromboendarterectomy.

Fetal anastomotic connections between the developing internal carotid and basilar arterial systems are via the three presegmental arteries: the otic artery, the hypoglossal artery, and the trigeminal artery. After formation of the posterior communicating artery from the caudal branch of the internal carotid artery, the presegmental arteries are generally obliterated. Rarely, however, these primitive carotid-basilar anastomoses will persist into adult life, and may be detected as incidental findings at the time of cerebral angiography during evaluation of the patient with suspected cerebrovascular disease. In addition, persistence of such anastomoses may result in the coexistence of anterior and posterior circulation symptoms, precipitating diagnostic confusion. Two patients with symptoms and persistent hypoglossal artery undergoing carotid thromboendarterectomy are discussed, with emphasis on clinical presentation, diagnostic criteria and intraoperative management.

Neutrophil leukotriene generation and pulmonary dysfunction after abdominal aortic aneurysm repair.

BACKGROUND: The purpose of this study was to assess the role of polymorphonuclear neutrophil (PMN)-generated leukotriene B4 (LTB4) as an etiologic agent in the pulmonary dysfunction seen after operation in patients undergoing abdominal aortic aneurysm repair. METHODS: Blood was analyzed in 10 consecutive patients undergoing elective infrarenal abdominal aortic aneurysm repair for plasma thromboxane B2, lactoferrin, C3a, and PMN-generated LTB4. RESULTS: There was a close linear correlation (r = 0.88; p < 0.001) between aortic clamp time and PMN LTB4 production. Conversely, aortic clamp time and the ratio of arterial oxygen pressure to fraction of inspired oxygen, a measure of pulmonary function, were inversely related (r = -0.80; p < 0.008). PMNs from patients with long aortic cross-clamp times generated three times more LTB4 than those patients with short cross-clamp times (194 +/- 29.6 vs 64.9 +/- 9.7 ng per 5 x 10(6) PMN; p < 0.05). Similarly, the pressure/inspired oxygen ratio was significantly lower on admission to the intensive care unit in patients with long cross-clamp times as compared with patients with short cross-clamp times (237 +/- 14 vs 342 +/- 5; p < 0.005). In addition, patients with long cross-clamp times remained intubated longer than patients with short times (1.6 +/- 0.2 vs 0.6 +/- 0.4 days; p < 0.05). CONCLUSIONS: These data suggest a causal role for LTB4 in the generation of pulmonary dysfunction in patients undergoing abdominal aortic aneurysm repair, similar to what has been shown in animal models.

Iron delocalization occurs during ischemia and persists on reoxygenation of skeletal muscle.

Attenuation of oxidative reperfusion injury in skeletal muscle by the administration of iron-chelating compounds suggests that ischemia-reperfusion is associated with delocalization of iron with subsequent catalysis of hydroxyl radical generation. To test this hypothesis we examined the extent of iron liberation and lipid peroxidation in a well-established model of high-grade partial hindlimb ischemia and reperfusion. Laparotomy was performed on heparinized male Sprague-Dawley rats with isolation of the infrarenal aorta. Resting membrane potential (Em) and conjugated diene content in hindlimb skeletal muscle were determined along with plasma iron concentration and percent saturation of transferrin in five groups of animals. Baseline animals (n = 6) underwent a 30-minute postoperative stabilization period before data collection; Sham ischemia animals (n = 10) underwent aortic exposure without clamping for 120 minutes; ischemia animals (n = 8) underwent aortic clamping for 120 minutes; sham reperfusion animals (n = 8) underwent aortic exposure without clamping for 150 minutes; reperfusion animals (n = 8) underwent aortic clamping for 120 minutes followed by 30 minutes of reperfusion. Iron delocalization occurred during ischemia, as indicated by a significant rise in percent saturation of transferrin over that of the corresponding sham group (35% +/- 2% vs 25% +/- 2%; p < 0.05) and persisted during reperfusion (39% +/- 5% vs 27% +/- 3%; p < 0.05). Depolarization of resting Em was noted during ischemia (-75.7 +/- 1.7 mV vs - 92.6 +/- 0.4 mV in the corresponding sham group; p < 0.01), with only partial repolarization demonstrated after reperfusion (-82.2 +/- 1.7 mV; p < 0.01 vs all other groups).(ABSTRACT TRUNCATED AT 250 WORDS)