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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the industrialized countries, diabetic retinopathy represents the most frequent cause of blindness during the period of active life. It occurs as two distinct clinical entities: non proliferating retinopathy characterized by dilatation of the retinal capillary bed and alterations in their vascular wall responsible for an increase in permeability, and proliferating retinopathy characterized by the appearance of pre-retinal neovessels secondary to the presence of vast zones of retinal ischemia. Numerous risk factors are implicated in the development of diabetic retinopathy: the primordial factor is the optimal equilibration of blood glucose levels. The primum movens of these diabetic lesions could be intoxication of the pericipets and endothelial cells of the retinal capillaries by an accumulation of sorbitol and fructose in this region. Additionally, the hyperglycemia suppresses the functioning of the retinal blood flow feed back system. An increase in systemic blood pressure will therefore be transmitted directly to the damaged capillary bed. In type II diabetes (NID), worsening of the diabetic retinopathy correlates with elevation of the systolic blood pressure. In type I diabetes (ID), worsening of the diabetic retinopathy correlates with an elevated diastolic blood pressure. A diastolic pressure of less than 74 mm Hg is a statistically significant protective factor against the worsening of type I diabetic retinopathy.
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PMID:[Influence of arterial hypertension on diabetic retinopathy]. 149 59

Five consecutive patients with proliferative diabetic retinopathy who were treated successfully with panretinal photocoagulation subsequently developed a central retinal artery obstruction. Iris neovascularization developed in the affected eye within one to three months after the obstruction in four of the five patients despite the previous laser treatment. Additional retinal ischemia, as occurs in central retinal artery obstruction, appears to promote marked iris neovascularization in a large percentage of patients, even when successful photocoagulation for proliferative retinopathy has been previously administered.
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PMID:Iris neovascularization after central retinal artery obstruction despite previous panretinal photocoagulation for diabetic retinopathy. 169 95

Much of the morbidity and mortality in sickle cell disease (SCD) is caused by tissue ischemia and infarction resulting from vascular occlusion. Research in this area has been dominated by the hypothesis that vascular occlusion in SCD is due primarily to microvascular obstruction by sickle erythrocytes (SS RBC), yet there is no direct evidence that microvascular occlusion is responsible for any of the vasocclusive complications of SCD. In this paper an alternate hypothesis is proposed: that thrombotic occlusion of larger arteries and veins is an important factor in many of the vasocclusive complications of SCD. Large-vessel cerebral arterial disease (intimal hyperplasia with superimposed thrombosis) has clearly been established as the most important cause of stroke in SCD, and considerable evidence suggests that pulmonary arterial thrombosis/embolism is a major cause of pulmonary infarction and hypertension. The involvement of large-vessel thrombosis in painful crisis, aseptic necrosis of bone, priapism, leg ulcers, retinopathy, and miscarriage has not been adequately investigated. Large-vessel occlusion in SCD is probably a consequence of the abnormal adhesive and procoagulant properties of SS RBC, which produce endothelial damage, secondary intimal proliferation, and thrombosis. Techniques currently used to treat large-vessel occlusion in other disorders (antiplatelet and anticoagulant agents, thrombolytic therapy, angioplasty, endarterectomy, and vascular bypass surgery) should be considered in sickle cell subjects with large-vessel occlusion, especially in the cerebral vasculature.
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PMID:Large-vessel occlusion in sickle cell disease: pathogenesis, clinical consequences, and therapeutic implications. 189 Sep 82

To elucidate the prevalence and features of painless myocardial ischemia among diabetic patients, 44 consecutive patients with angiographically-documented coronary artery disease and positive treadmill tests were examined. They were 26 with diabetes and 18 without it. Painless myocardial ischemia was defined as the absence of chest pain with 1 mm or more ST segment depression during the exercise stress tests. The severity of ischemia was determined by the magnitude of the ST segment depression. Painless myocardial ischemia was observed in 18 of the 26 (69%) diabetics, and in three of the 18 (17%) non-diabetics (p less than 0.005). The frequency of painless ischemia in the diabetics was relatively high regardless of the severity of ischemia, while painless ischemia was less frequent in the non-diabetics with severe ischemia. With a level of 2.5 mm ST depression, 11 of 12 (92%) diabetics were free of pain compared to four of 11 (36%) non-diabetics (p less than 0.01). Absence of chest pain during the exercise tests was not concordant with prior angina in diabetics, as opposed to non-diabetics in whom both clinical and exercise-induced angina developed concordantly. The diabetic patients without chest pain had a higher prevalence of three major diabetic complications such as neuropathy, nephropathy and retinopathy compared to those developing chest pain (p less than 0.025). It was concluded that in diabetics, painless myocardial ischemia is frequently observed during exercise stress tests and its prevalence is relatively high regardless of the severity of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia in diabetic patients with coronary artery disease: evaluations by treadmill exercise tests]. 210 4

Proliferative sickle retinopathy (PSR) is usually described as a peripheral neovascular tuft in a "sea fan" like configuration. While neovascularization of the disc (NVD) is a common finding in proliferative diabetic retinopathy (PDR), to our knowledge only one other case has been reported of NVD in an S-C patient in the absence of other contributing conditions. PSR has been shown to regress after treating hypoxic peripheral retina with peripheral circumferential retinal scatter photocoagulation (PCRSP). The following is a case report of an S-C patient with PSR and NVD/NVR which was originally treated elsewhere with scatter argon laser photocoagulation from the vascular arcades to just behind the equator. The peripheral "sea fan" and NVD did not regress. PCRSP to the zone of peripheral ischemia was then performed, and regression of the NVD and peripheral "sea fan" was achieved. This case illustrates the importance of concentrating laser treatment to the zones of retinal ischemia to achieve regression of associated neovascularization.
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PMID:Proliferative sickle retinopathy and neovascularization of the disc: regression following treatment with peripheral retinal scatter laser photocoagulation. 241 14

Rat urethane retinopathy produces sequential and progressive loss of the photoreceptor cells, proceeding from the posterior to the peripheral retina. The inner retina, the retinal pigment epithelium and the choriocapillaris are spared. After loss of the photoreceptor cells, a vasculopathy develops which includes progressive retinal capillary loss and formation of coil-like tufts of retinal vessels which are embedded in the retinal pigment epithelium. Some of the retinal vessels within the retinal pigment epithelium have changed their phenotype from continuous to fenestrated endothelial cells. To elucidate whether DNA synthesis was necessary for formation of the coil-like vessel tuft formation, an autoradiographic study was performed. At 12, 14, 16 and 20 weeks of age, times during which the vasculopathy is known to be forming, urethane and control rats were injected with 3 successive doses of methyl-3H-thymidine. Autoradiography of trypsin-digested retinal vessel preparations was compared with histological sections of the paired eye. The frequency of tritium labelled endothelial cells was much higher in the urethane rats than control animals, and were predominantly in the posterior pole, rather than the periphery. Labelled endothelial cells tended to be associated with, or near, the coil-like vessel tufts. Capillary dropout was observed in urethane, but not control animals. Frequently, adjacent endothelial cells were labelled, suggestive of mitosis. The occurrence of thymidine uptake and a change in phenotype of the endothelial cells leads us to suggest that new cell synthesis, or neovascularization, has occurred in these vessels. Since the retina is less than half the normal thickness and the choriocapillaris is intact, it appears unlikely that ischemia is responsible for inducing these pathological responses. We suggest that the retinal pigment epithelial cell is responsible for the increase in DNA synthesis and change in phenotype of the retinal endothelial cell.
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PMID:Neovascularization in urethane rat retinopathy demonstrated by thymidine labelling. 242 2

The authors observed three cases (6 eyes) of vaso-occlusive retinopathy associated with the lupus anticoagulant and the related antiphospholipid antibody anticardiolipin. The disease occurred in patients who had no definable autoimmune disease such as systemic lupus erythematosus (SLE) and was characterized by severe bilateral retinal vascular occlusion. There was profound visual loss from intraretinal ischemia as well as vitreous hemorrhage from preretinal neovascularization. Results of laboratory testing showed a prolonged partial thromboplastin time (PTT) in two patients, and the presence of the lupus anticoagulant in all. Treatment with panretinal photocoagulation appeared to stabilize the neovascularization. The role of systemic anticoagulation and immunosuppressive therapy is uncertain.
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PMID:Vaso-occlusive retinopathy associated with antiphospholipid antibodies (lupus anticoagulant retinopathy). 232

Nonspecific aortoarteritis is a systemic autoimmune disease eventuating in gradual stenosis of the aorta and the main vessels with ischemia of the respective organs. Ophthalmologic symptoms have been examined in 54 patients with nonspecific aortoarteritis. Subjective disorders of vision (short-term binocular blindness, metamorphopsia, pain behind the eye, amaurosis fugax) have been detected in 52% of the examinees. Organic lesions of the eye have been diagnosed in 60% of the patients: hypertensive angiopathy (22%), venous stasis retinopathy (17%), occlusion of the central retinal artery (1%), etc. Three possible mechanisms of the development of ocular symptoms have been established: (1) a result of symptomatic hypertension, (2) chronic ocular ischemia, (3) acute hemodynamic ocular circulation insufficiency.
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PMID:[Ophthamologic pathology in non-specific aortoarteritis]. 256 80

Bidirectional laser Doppler velocimetry and monochromatic fundus photography were used to investigate retinal hemodynamics before and after panretinal photocoagulation (PRP) in 25 eyes of 23 diabetic patients with proliferative retinopathy. After PRP, there was a significant decrease in retinal volumetric blood flow rate and an increase in the retinal vascular regulatory response to hyperoxia (R). A significant association was found between the presence or absence of regression of neovascularization and the increase or decrease in R after PRP. Eyes that showed regression of neovascularization had significantly larger average R after PRP than eyes that did not show regression. Lack of improvement in R after PRP may be related to the presence of remaining ischemia or hypoxia in eyes that continue to show proliferation after PRP.
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PMID:Retinal blood flow regulation and the clinical response to panretinal photocoagulation in proliferative diabetic retinopathy. 258 47

Transplantation of the pancreas in late stages of type I diabetes has been performed increasingly frequently during recent years. By improved surgical techniques and immunsuppressive therapy including cyclosporin A, the 1-year graft function has increased to 60-70% and the patient survival to 85-95% in the institutions with greatest experience. These results are so good, that they nearly reach those from kidney transplantation. Most of the pancreas transplantations have been performed simultaneously with kidney transplantation in patients with end stage diabetic uremia. The results should therefore be evaluated according to these circumstances. In a few institutions transplantation of the pancreas is now performed in patients with persistent proteinuria and proliferative retinopathy in an attempt to avoid development of severe diabetic complications. The first pancreas transplantation in Denmark was performed Januar 31 st 1987, and since then, 17 further transplantations have been performed. All patients had severe diabetic nephropathy and received simultaneous kidney transplantation. According to the Danish heart death criteria the organs were perfused and cooled during the donor operation to keep the warm ischemia as brief as possible. The pancreatic vessels are anastomosed to the iliac vessels. In one group of patients the exocrine pancreatic function was preserved by anastomosis to the jejunum, and in another group of patients the exocrine function was abolished by injection of latex into the pancreatic duct system. The patients receive immunosuppression therapy with methylprednisolone, azatioprine and ciclosporin A and anti-coagulation therapy.
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PMID:[Simultaneous transplantation of the pancreas and kidney in terminal diabetic nephropathies]. 264 99


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