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Necrosis of skin flaps remains a significant clinical problem. This study examined whether steroids improve skin flap survival in rats. Random skin flaps were raised in 30 male Sprague-Dawley rats. Intramuscular methylprednisolone...
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Necrosis of skin flaps remains a significant clinical problem. This study examined whether steroids improve skin flap survival in rats. Random skin flaps were raised in 30 male Sprague-Dawley rats. Intramuscular methylprednisolone (n=15) or saline solution (n=15) were administered 1, 24, and 48 h after flap elevation. Surviving flap areas were measured after 7 days. The mean surviving flap area in the methylprednisolone group was greater than that in controls (916 vs. 675 mm). These results suggest that postoperative methylprednisolone improves skin flap viability in the ischemic rat flap model.
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Background: This study aims to determine the relationship between serum prolidase activity and ischemia duration in different ischemia types. Methods: Forty male Sprague Dawley rats were divided into five equal groups. The rats we...
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Background: This study aims to determine the relationship between serum prolidase activity and ischemia duration in different ischemia types. Methods: Forty male Sprague Dawley rats were divided into five equal groups. The rats were sacrificed and blood samples were obtained to determine the basal serum prolidase levels in group 1 (control group) without any intervention. In groups 2 and 3, the superior mesenteric arteries were clamped with simple laparotomy to induce mesenteric ischemia. In groups 4 and 5, the right common femoral artery was clamped to induce peripheral ischemia and blood samples were taken at 120 and at 360 minutes, respectively. The serum prolidase levels were measured using the samples obtained from each group. Results: The basal prolidase level in rats was found to be 266.8±20.5 U/L. The serum prolidase levels increased after two-hours of peripheral (404.0±105.6 U/L) and mesenteric ischemia (317.1±121.4 U/L). However, the serum prolidase levels decreased after six-hours of peripheral (346.1±104.9 U/L) and mesenteric ischemia (233.4±36.6 U/L). Although the serum prolidase levels were elevated in the second hour of mesenteric ischemia, they were lower than the enzyme levels obtained after twohours of peripheral ischemia (p=0.006). Conclusion: The serum prolidase level may be an important predictive biomarker for identifying the duration of ischemia.
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This article reviews the presentation, diagnosis, evaluation, and treatment of the various forms of mesenteric ischemia, including acute and chronic ischemia. In addition, nonocclusive mesenteric ischemia and median arcuate ligame...
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This article reviews the presentation, diagnosis, evaluation, and treatment of the various forms of mesenteric ischemia, including acute and chronic ischemia. In addition, nonocclusive mesenteric ischemia and median arcuate ligament compressive syndrome are covered. The goals are to provide a structured and evidence-based framework for the evaluation and management of patients with these intestinal ischemia syndromes. Special attention is given to avoiding typical pitfalls in the diagnostic and treatment pathways. Operative techniques are also briefly discussed, including an evidence-based review of newer endovascular techniques.
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Endovascular treatment of chronic mesenteric ischemia is currently the treatment of choice, regardless of the number of involved vessels. Unlike other anatomic areas, the hyperperfusion produced by revascularization and the consec...
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Endovascular treatment of chronic mesenteric ischemia is currently the treatment of choice, regardless of the number of involved vessels. Unlike other anatomic areas, the hyperperfusion produced by revascularization and the consecutive reperfusion syndrome is only described in cases of acute bowel ischemia, which is usually resolved with traditional surgery. We present a case of severe hyperperfusion syndrome secondary to endovascular correction with stents of a critical ischemia affecting the celiac trunk and superior mesenteric artery.
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We report a 33-year-old man with a history of chronic cannabis use who sustained myocardial infarction followed by cerebral infarction after a recent significant increase in cannabis use. This is the first case of cannabis-associa...
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We report a 33-year-old man with a history of chronic cannabis use who sustained myocardial infarction followed by cerebral infarction after a recent significant increase in cannabis use. This is the first case of cannabis-associated stroke of probable cardioembolic origin.
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Basic and clinical investigations have been performed, focusing on the mechanism of ischemic brain and spinal cord injuries, and preventive measures against ischemic insults such as drug therapy, hypothermia, maintenace of blood f...
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Basic and clinical investigations have been performed, focusing on the mechanism of ischemic brain and spinal cord injuries, and preventive measures against ischemic insults such as drug therapy, hypothermia, maintenace of blood flow to brain and spinal cord, preconditioning, and no use of high dose fentanyl. In this special issue, five experts have provided new relevant information concerning brain and spinal cord protection. Further research in brain and spinal cord protection will contribute to better understanding of ischemic central nervous system injuries and to the establishment of novel therapies for protection of central nervous system.
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White matter of the brain and spinal cord is susceptible to anoxia and ischemia. Irreversible injury to this tissue can have serious consequences for the overall function of the CNS through disruption of signal transmission. Myeli...
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White matter of the brain and spinal cord is susceptible to anoxia and ischemia. Irreversible injury to this tissue can have serious consequences for the overall function of the CNS through disruption of signal transmission. Myelinated axons of the CNS are critically dependent on a continuous supply of energy largely generated through oxidative phosphorylation. Anoxia and ischemia cause rapid energy depletion, failure of the Na(+)-K(+)-ATPase, and accumulation of axoplasmic Na+ through noninactivating Na+ channels, with concentrations approaching 100 mmol/L after 60 minutes of anoxia. Coupled with severe K+ depletion that results in large membrane depolarization, high [Na+]i stimulates reverse Na(+)-Ca2+ exchange and axonal Ca2+ overload. A component of Ca2+ entry occurs directly through Na+ channels. The excessive accumulation of Ca2+ in turn activates various Ca(2+)-dependent enzymes, such as calpain, phospholipases, and protein kinase C, resulting in irreversible injury. The latter enzyme may be involved in "autoprotection," triggered by release of endogenous gamma-aminobutyric acid and adenosine, by modulation of certain elements responsible for deregulation of ion homeostasis. Glycolytic block, in contrast to anoxia alone, appears to preferentially mobilize internal Ca2+ stores; as control of internal Ca2+ pools is lost, excessive release from this compartment may itself contribute to axonal damage. Reoxygenation paradoxically accelerates injury in many axons, possibly as a result of severe mitochondrial Ca2+ overload leading to a secondary failure of respiration. Although glia are relatively resistant to anoxia, oligodendrocytes and the myelin sheath may be damaged by glutamate released by reverse Na(+)-glutamate transport. Use-dependent Na+ channel blockers, particularly charged compounds such as QX-314, are highly neuroprotective in vitro, but only agents that exist partially in a neutral form, such as mexiletine and tocainide, are effective after systemic administration, because charged species cannot penetrate the blood-brain barrier easily. These concepts may also apply to other white matter disorders, such as spinal cord injury or diffuse axonal injury in brain trauma. Moreover, whereas many events are unique to white matter injury, a number of steps are common to both gray and white matter anoxia and ischemia. Optimal protection of the CNS as a whole will therefore require combination therapy aimed at unique steps in gray and white matter regions, or intervention at common points in the injury cascades.
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Abstract Purpose Chronic mesenteric ischemia (CMI) is a rare but life-threatening disease. This study reviewed outcomes in patients treated surgically for CMI by open treatment (OT) and endovascular treatment (ET), analyzing risk ...
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Abstract Purpose Chronic mesenteric ischemia (CMI) is a rare but life-threatening disease. This study reviewed outcomes in patients treated surgically for CMI by open treatment (OT) and endovascular treatment (ET), analyzing risk factors for endovascular failure.Methods Clinical data for 36 patients treated for CMI from 2007 to 2017 were retrospectively analyzed. The study’s primary endpoint was symptom-free survival. The secondary endpoint was the primary technical success for endovascular and open surgical treatments. Risk factors for endovascular failure were identified by using univariate analysis.Results Patients were analyzed as treated: 21 patients (58.3%) in the ET and 15 (41.6%) in the OT group. Overall, 20 patients (56%) presented with abdominal angina, 9 (25%) with rest pain, and 7 (19%) without symptoms. An ET was initially attempted in 31 patients (86.1%). The conversion rate from ET to OT was 32.3%, which resulted in a primary technical success of 67.6% in ET and 100% in OT. Six patients from the ET group (19.3%) required surgical revision due to restenosis. One-year (OT 91.6% vs. ET 96.8%; n.s.) and three-year primary patency (OT 91.6% vs. ET 80.6%; n.s.) as well as 3-year symptom-free survival did not differ between the groups (OT 62.5% vs. ET 69.4%; n.s). Overall, in-hospital mortality was 2.8% (n?=?1), which was not statistically different between the groups (OT 6% vs. ET 0%; n.s.). High-grade stenosis of the superior mesenteric artery tended to be associated with higher technical failure (P?=?0.06).Conclusions ET showed a comparable perioperative outcome with higher technical failure. OT was distinguished by excellent early and late technical success.
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Mesenteric ischemia is classified as either acute or chronic. The former is a life-threatening emergency in which a sudden reduction in intestinal blood flow may ultimately result in bowel infarction. The most common causes are ar...
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Mesenteric ischemia is classified as either acute or chronic. The former is a life-threatening emergency in which a sudden reduction in intestinal blood flow may ultimately result in bowel infarction. The most common causes are arterial embolism, arterial thrombosis, nonocdusive mesenteric ischemia, and mesenteric venous thrombosis. A high index of suspicion, early diagnosis and rapid intervention are necessary so that normal mesenteric perfusion is restored before fatal bowel infarction can occur. Chronic mesenteric ischemia is usually caused by stenotic or occlusive disease involving the proximal segments of the mesenteric arterial supply to the bowel, usually as a result of atherosclerosis. Intestinal angina is the classic presentation, defined as recurrent postprandial abdominal pain that subsides in 1 to 2 hours, with associated weight loss and aversion to food. When combined with the clinical presentation, physical examination, and laboratory data, imaging plays a key role in the diagnosis of either acute or chronic mesenteric ischemia. Recognition of pertinent imaging findings and various treatment options may aid in preventing the serious and possibly fatal sequelae that may occur in cases of mesenteric ischemia.
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摘要 :
Mesenteric ischemia is classified as either acute or chronic. The former is a life-threatening emergency in which a sudden reduction in intestinal blood flow may ultimately result in bowel infarction. The most common causes are ar...
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Mesenteric ischemia is classified as either acute or chronic. The former is a life-threatening emergency in which a sudden reduction in intestinal blood flow may ultimately result in bowel infarction. The most common causes are arterial embolism, arterial thrombosis, nonocdusive mesenteric ischemia, and mesenteric venous thrombosis. A high index of suspicion, early diagnosis and rapid intervention are necessary so that normal mesenteric perfusion is restored before fatal bowel infarction can occur. Chronic mesenteric ischemia is usually caused by stenotic or occlusive disease involving the proximal segments of the mesenteric arterial supply to the bowel, usually as a result of atherosclerosis. Intestinal angina is the classic presentation, defined as recurrent postprandial abdominal pain that subsides in 1 to 2 hours, with associated weight loss and aversion to food. When combined with the clinical presentation, physical examination, and laboratory data, imaging plays a key role in the diagnosis of either acute or chronic mesenteric ischemia. Recognition of pertinent imaging findings and various treatment options may aid in preventing the serious and possibly fatal sequelae that may occur in cases of mesenteric ischemia.
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