Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to modify the photochemical stroke model of Watson et al. [23] so as to make possible microscopical investigation of the so-called penumbra, a tissue zone at risk that surrounds an infarction. The idea was to minimize photochemical challenge to endothelial membranes in such a way that thrombotic vascular obstruction is avoided but destabilization of the blood-brain barrier is still obtained. Morphological examination of the challenged area revealed open blood vessels, overt blood-brain barrier leakage over the entire area, severely swollen glial cells and structurally intact neurons. The lesion expanded over time due to progressive extravasation, formation of perivascular edema and consequent development of secondary ischemia through mechanical compression and microvascular congestion. In contrast to a photothrombotic infarct, in which the ischemic insult is more severe and blood vessels are completely congested by aggregated platelets, with this approach blood flow is partially preserved. In this way, an ischemic penumbra is created that mimics pathologic conditions secondary to stroke and trauma. The model may be useful in studying effects of drugs on pathologic phenomena that are characteristic of a penumbra, e.g. vasogenic and cellular edema, inflammation and infarction.
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PMID:Vasogenic oedema and brain infarction in an experimental penumbra model. 1144 86

Reactive angioendotheliomatosis (RAE) is a rare benign cutaneous vascular proliferation characterized by intravascular hyperplasia of endothelial cells and tuft-like proliferation of vessels. A 75-year-old man had erythematous and violaceous macules, some stellate and others arranged in a livedoid pattern, evolving toward necrosis with central areas having an "atrophie blanche" appearance spread on the trunk, inguinal folds, and right thigh. He was on hemodialysis and had a benign monoclonal gammopathy. Cutaneous biopsy revealed RAE characterized by the proliferation of epithelioid and spindle-shaped cells in superficial and middermis lining vascular channels, arranged in clusters, and sometimes displaying an intravascular growth pattern. These cells stained for CD31, CD34, and actin. Interestingly, prominent amyloid deposits were found in the wall of some vessels in deep dermis, often causing obstruction of their lumina. The cause of RAE is unknown, but it can be associated with infections, antiphospholipid syndrome, dysglobulinemia, cryoproteinemia, and lower extremities arteritis, and it may occur near arteriovenous fistulas. In this patient, we believe that RAE was caused by obliteration of dermal vessels by amyloid deposits. Indeed, it is thought that RAE could be caused by ischemia secondary to vascular obstruction. This is the first reported patient with RAE associated with amyloid deposits.
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PMID:Reactive angioendotheliomatosis secondary to dermal amyloid angiopathy. 1148 23

Sequestration of parasitized erythrocytes in the central nervous system microcirculation and increased cerebrospinal fluid lactate are prominent features of cerebral malaria (CM), suggesting that sequestration causes mechanical obstruction and ischemia. To examine the potential role of ischemia in the pathogenesis of CM, Plasmodium berghei ANKA (PbA) infection in CBA mice was compared to infection with P. berghei K173 (PbK) which does not cause CM (the non-CM model, NCM). Cerebral metabolite pools were measured by (1)H nuclear magnetic resonance spectroscopy during PbA and PbK infections. Lactate and alanine concentrations increased significantly at the terminal stage of CM, but not in NCM mice at any stage. These changes did not correlate with parasitemia. Brain NAD/NADH ratio was unchanged in CM and NCM mice at any time studied, but the total NAD pool size decreased significantly in the CM mice on day 7 after inoculation. Brain levels of glutamine and several essential amino acids were increased significantly in CM mice. There was a significant linear correlation between the time elapsed after infection and small, progressive decreases in the cell density/cell viability markers glycerophosphocholine and N-acetylaspartate in CM, indicative of gradual loss of cell viability. The metabolite changes followed a different pattern, with a sudden significant alteration in the levels of lactate, alanine, and glutamine at the time of terminal CM. In NCM, there were significant decreases with time of glutamate, the osmolyte myo-inositol, and glycerophosphocholine. These results are consistent with an ischemic change in the metabolic pattern of the brain in CM mice, whereas in NCM mice the changes were more consistent with hypoxia without vascular obstruction. Mild obstructive ischemia is a likely cause of the metabolic changes during CM, but a role for immune cell effector molecules cannot be ruled out.
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PMID:Is ischemia involved in the pathogenesis of murine cerebral malaria? 1154 3

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.
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PMID:[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. 1156 26

The ability of organisms to spontaneously develop collateral vessels represents an important response to vascular occlusive diseases that determines the severity of residual tissue ischemia. Neovascularization of ischemic cardiac or skeletal muscle may be sufficient to preserve tissue integrity and/or function, and may thus be considered to be therapeutic. Innovative gene technologies and advances in animal modeling have enabled research scientists to develop therapeutic angiogenesis strategies applied in animal models of limb or myocardial ischemia and in treatment of patients with peripheral vascular obstruction or coronary artery diseases. Several therapeutic strategies have been proposed and tested even at the clinical level. Recent studies have established the feasibility of using recombinant angiogenic growth factors (mainly VEGF and FGF) to enhance angiogenesis in patients with limb or myocardial ischemia. Angiogenesis therapies using cells as a support for growth factor delivery or using endothelial progenitor cells which may directly participate in the angiogenic process have also been developed. Finally, one potential alternative strategy may be the use of drugs with pro-angiogenic activity, available in an oral formulation and which are currently administered to patients for treatment of different pathologies. All strategies of angiogenesis therapy currently being tested have the potential to be effective in the treatment of ischemic disease. However, such strategies may cause harmful side effects which emphasize the need to be aware of the biological effects of each angiogenic agent proposed for clinical studies.
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PMID:Angiogenesis therapy in ischemic disease. 1199 34

We report an autopsy case of acute pancreatitis with a high serum IgG4 concentration complicated by systemic amyloid A amyloidosis and rheumatoid arthritis (RA). The patient was a 42-year-old Japanese female with a 22-year history of rheumatoid arthritis. She was diagnosed with myasthenia gravis when she was 31-year old. At the onset of pancreatitis, the patient was anti-nuclear antibody-positive, and had high serum gamma globulin and IgG4 levels. Dexamethasone and conventional therapy induced clinical remission and significantly decreased the serum IgG4 and gamma globulin. However, despite the decreased disease parameters, the patient developed a bleeding pseudocyst and died of cardiac failure. In the autopsy examination, it was determined that pancreatitis was probably caused by ischemia due to vascular obstruction caused by amyloid deposition in the pancreas. Even though acute pancreatitis is a rare complication in RA patients, we speculate that an autoimmune pancreatitis-related mechanism and ischemia due to vascular obstruction by amyloid deposition might be attributable to a single source that leads to acute pancreatitis in our particular case.
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PMID:An autopsy case of acute pancreatitis with a high serum IgG4 complicated by amyloidosis and rheumatoid arthritis. 1580 Oct 1

Diabetic retinopathy is a frequently observed complication in both type 1 and type 2 diabetes, specially in patients with long term disease and poor glicemic control. Irreversible visual loss appears at the final stages of diabetic retinopathy and it is considered one of the most tragic of diabetic complications. It is also considered an important factor of morbidity and has a high economical impact once it is the leading cause of blindness. The pathophysiology of the retinal microvascular alterations is related to the chronic hyperglycemia that leads to the following circulatory disturbances: loss of vascular tonus, increase in vascular permeability, edema and exudation, with vascular obstruction and ischemia that stimulates neovascularization, which may lead to fibrous retraction and vitreous hemorrhages with retinal detachment. Recent studies have indicated that the strict glicemic and blood pressure controls are effective in reducing or blocking the progression of retinopathy. Up to now no pharmacological agents have shown to be effective in preventing or reducing neovascularization and visual loss. Presently, the most effective available treatment for proliferative retinopathy is laser photocoagulation. Further studies are needed to obtain new products and technologies that could effectively prevent or block retinopathy progression.
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PMID:[Diabetic retinopathy]. 1618 49

Intravascular accumulation of blood cells after brain ischemia-reperfusion can cause obstruction of cerebral blood flow and tissue hypoxia/ischemia as a consequence. In the present study, we examined temporal and topographic changes of tissue hypoxia/ischemia after occlusion of the middle cerebral artery (MCA) for 60 min in rats with immunohistochemical staining for hypoxia (2-nitroimidazole hypoxia marker: hypoxyprobe-1 adducts). Our results showed that tissue hypoxia expressed as positive staining for hypoxyprobe-1 adducts preceded neuronal degeneration. Platelets and granulocytes were detected close to the hypoxyprobe-1 adducts positive area. These results suggested that the hypoxic environment could persist even after reperfusion of MCA, because of vascular obstruction with accumulation of platelets and granulocytes.
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PMID:Temporal and topographic profiles of tissue hypoxia following transient focal cerebral ischemia in rats. 1695 79

Vascular occlusion is still the main reason for flap loss and occurs mostly within the first hours after performing anastomoses. Many surgeons still prefer to perform reconstruction and close the defect before starting to anastomose. The aim of this investigation was to find out if detection of early vascular occlusion is facilitated with a prolonged observation period. Between January 2000 and August of 2006, 350 consecutive free flap transfers for reconstruction in maxillofacial surgery were analyzed. In all flaps vascular anastomoses were performed prior to definite flap insertion. The flaps were controlled continuously during soft tissue or bony reconstruction until final wound closure at the neck. Complete operation time, ischemia time of the flap, and time from reperfusion to wound closure (direct pedicle observation time) were registered for each flap. In 350 flaps (138 radial forearm, 94 fibular, 53 ALT, 23 DCIA, 26 soleus perforator, 9 lateral arm, 5 lat. dorsi, and 2 scapular), operation time in average was 8.5 h, ischemia time varied between 78 and 139 min (average 104 min), and direct pedicle observation time of the flaps was 144 min in average (93-192 min). Four arteries and 2 veins showed immediate failure within 5 min after clamp removal, 10 arteries and 6 veins developed thromboses during the direct pedicle observation time. Out of these 16 vascular complications, 15 developed later than 15 min, 7 of them later than 30 min, and 2 of them later than 45 min. The overall complication rate including secondary revision of the pedicle was 16.8%, and an overall flap survival rate resulted in 95.4%. We conclude that microvascular anastomoses should be controlled for at least 45 min before definite wound closure. By performing anastomoses first and flap insertion second, this can be easily warranted.
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PMID:Incidence and time of intraoperative vascular complications in head and neck microsurgery. 1828 59

We describe our technique of achieving transient vascular occlusion utilizing Hem-o-Lok clips during robotassisted laparoscopic partial nephrectomy (RLPN) A once-folded vascular loop is threaded through a 2-cm feeding tube. After passing around the renal vessel, its tail goes through the U-loop, creating a tourniquet. Vascular occlusion begins when the tube slides towards the vessel and a Hem-o-Lok clip is applied on the vascular loop next to the exposed end of the tube. When no longer needed, it is released. Since July 2006, 25 patients underwent RLPN utilizing this technique, which required <15 seconds to deploy for any vessel size. There were eight patients with multiple vessels. The mean operative time was 82.6 minutes, and the mean warm ischemia time was 22 minutes (range 17-27 minutes). There were no cases of intraoperative or postoperative bleeding. The technique is simple, inexpensive, and applicable to multiple vessels. It is a viable alternative to standard vascular occlusion techniques, such as laparoscopic bulldog or Satinsky clamps.
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PMID:Another novel application of Hem-o-Lok clips for transient vascular occlusion in robot-assisted laparoscopic partial nephrectomy: an alternative to laparoscopic bulldog and Satinsky clamps. 1872 Oct 46


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