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

We have studied the development of the collateral circulation in the heart in response to gradual and progressive coronary artery occlusion. When the coronary stenosis becomes critical, tissue ischemia occurs, which we believe leads to the production (and probably to release from storage sites) of tissue hormones (mitogens) that lead to mitosis of endothelial and smooth muscle cells. We have identified from hearts several known mitogens (aFGF, bFGF), non-mitogenic angiogenic factors (TGF-beta), a new anti-mitogen, and a new myocyte-derived growth factor (structures of the last two not yet elucidated). An important principle in the development of collaterals is the remodeling of pre-existing small vessels into the much larger vascular structure. To accommodate new cells old structures have to be removed by controlled proteolysis (tPA, uPA, elastase).
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PMID:Angiogenesis in the adult heart. 171 53

The effects of exercise training on myocardial perfusion during the first 3 months after acute myocardial infarction (AMI) were assessed by exercise myocardial scintigraphy and fibrinolytic examinations. Symptom-limited treadmill exercise with thallium-201 myocardial single photon emission CT (SPECT) and fibrinolytic examinations (tissue plasminogen activator antigen: tPA, plasminogen activator inhibitor-1 antigen : PAI-1) were performed 2 and 14 weeks after AMI in 13 patients with exercise training and in 12 patients without exercise training. For quantitative analysis, counts of region of interest in the infarct area and normal reference area were calculated on a polar map obtained from myocardial SPECT. Severity of the hypoperfused myocardium was determined as an initial percent uptake (%IU) and a delayed percent uptake (%DU). The difference (%DU-%IU) was defined as a parameter of residual ischemia in the infarct area (%redistribution : %RD). Total treadmill exercise duration according to the Bruce protocol increased significantly in the training group (351 +/- 89 to 431 +/- 118 sec, p < 0.01); whereas, there was no significant change in the non-training group (340 +/- 95 to 356 +/- 123 sec). In the training group the pressure-rate product and %DU increased significantly (225 +/- 55 to 259 +/- 58 mmHg.beats/min x 100, 59 +/- 19 to 65 +/- 20%, p < 0.01, respectively), and %RD decreased significantly (8.8 +/- 6.7 to 4.8 +/- 4.5%, p < 0.01), but there was no significant change in the non-training group (231 +/- 89 to 240 +/- 86 mmHg.beats/min x 100, 56 +/- 17 to 57 +/- 12% and 7.4 +/- 5.5 to 6.2 +/- 6.5%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac rehabilitation in patients with acute myocardial infarction: assessments with T1-201 myocardial scintigraphy]. 184 44

Thrombolytic therapy in AMI restores infarct artery patency, preserves LV function, and decreases hospital mortality. Although hemorrhagic complications including stroke can occur, the incidence of stroke is not increased compared with control groups. Aspirin must be administered as soon as possible to inhibit platelet function, and an adjunctive role for early beta-blocker therapy may be important. Acute cardiac catheterization and coronary angioplasty need not be routinely performed in stable patients after tPA therapy, but should be considered in unstable patients. Two trials suggest that aggressive use of coronary angioplasty or bypass graft surgery before hospital discharge to preserve infarct artery patency and to prevent postinfarction ischemia is associated with an important improvement in long-term prognosis. Thrombolytic therapy should be considered standard care for patients whose ischemic chest pain lasts 20 min to at least 6 h in duration and who have an injury current on their ECG unless they are at increased risk for bleeding. The need for and timing of cardiac catheterization, coronary angioplasty, and surgical revascularization after AMI requires further evaluation.
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PMID:Thrombolytic therapy for acute myocardial infarction. 252 96

After reviewing the principles, results and complications of thrombolytic therapy with "classical" agents (Streptokinase and Urokinase) used via intravenous, intraarterial route, or intraoperatively, and with more "modern" agents (APSAC, scuPA, tPA), we discuss the future of thrombolysis in the treatment of arterial ischemia of the limbs. Several items need to be clarified: --indication of thrombolysis among other treatments, mainly surgery, of arterial ischemia depends on the clinical staging of ischemia, its causes and the site of arterial obstruction; --method of delivery of the thrombolytic agent must provide the highest local concentration and the lowest systemic side effects; --efficacy of each thrombolytic agent must be analyzed when used in peripheral arterial ischemia, but also in other diseases such as myocardial infarction.
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PMID:Results of thrombolysis in the treatment of arterial ischemia of the limbs according to mode of administration. 269 81

Significant current interest has focused on the possible value of fibrin-selective thrombolytic agents in acute stroke. Acute thrombosis contributes to carotid and vertebrobasilar arterial occlusions in the majority of acute stroke patients. Hence, fibrin(ogen)olytic agents may produce arterial recanalization and clinical benefit in thrombotic stroke. There are, however, unique features of cerebral tissue that suggest caution with the use of fibrin-selective agents in cerebral ischemia. The specific vascular anatomy and collateral flow suggest that salvage of the "ischemic penumbra" following vascular recanalization in focal ischemia is more likely to be successful than attempts in global ischemia. Recanalization may be associated with reperfusion injury and, more importantly, the risk of hemorrhagic transformation. There is little concrete information regarding the relative contribution of either event to post-thrombolysis cerebral injury. Early studies with exogenous fibrinolytic agents (urokinase, streptokinase) in completed stroke were regarded as inconclusive, demonstrating only an increased risk of intracerebral hemorrhage. Subsequent pilot studies in carotid and in vertebrobasilar territory thrombotic stroke have demonstrated that recanalization can result when exogenous agents are infused just proximal to the cerebral artery occlusion by interventional neuroradiological techniques. This experience and the advent of fibrin-selective agents (tissue plasminogen activator [tPA] and single-chain urokinase plasminogen activator) have led to the development of a multicenter prospective safety/dose-ranging study of tPA in acute (less than eight hours from symptom onset) thrombotic stroke. Following initial clinical assessment, computed tomography scan, and angiography, each patient with a documented cerebral artery occlusion appropriate to the clinical syndrome receives a preassigned intravenous dose of tPA over 60 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Investigational use of tPA in acute stroke. 314 17

After describing the mechanism of action, results and local and general complications of classical thrombolytic agents (streptokinase and urokinase) administered systemically, locally and peroperatively, then of modern thrombolytic agents (acyl enzyme, tPA and scuPA), the future perspectives of arterial fibrinolysis are discussed. These are based upon: analysis of the comparative efficacy of the different thrombolytic agents in the light of results seen, not only in peripheral arterial pathology but also in other indications, as in coronary pathology; discussion of the methods of administration of the thrombolytic agent in such a way as to obtain an optimal local concentration and at the same time reduced systemic fibrinolysis. better definition of the indications of thrombolysis in acute ischemia of the limbs in comparison with other therapeutic approaches, in particular surgery, taking into account the degree of ischemia, of etiological mechanism and the site of the arterial obstruction.
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PMID:[Arterial thrombolysis. Review and future prospects]. 314 94

Progesterone stimulation of the estradiol (E2)-primed human endometrium initiates DZ of the stromal cells around the spiral arterioles. Under continued steroid stimulation, DZ spreads wave-like to establish the decidual cell as a major cell type of the luteal phase and pregnant endometrium. Because of their widespread distribution throughout the endometrium and concentration at perivascular sites, decidual cells are spatially and temporally positioned to mediate the opposing requirements of maintaining hemostasis during endovascular trophoblast invasion, yet promoting menstrual hemorrhage in the absence of implantation. The experimental results summarized in this review indicate that the paradoxical properties manifested by endometrial stromal/decidual cells are controlled by several proteins with either hemostatic or ECM-degrading or vasoactive activity, and that their expression is altered in response to changes in levels of circulating ovarian steroids during the menstrual cycle. These conclusions are drawn primarily from studies with a well-characterized in vitro model of DZ using monolayers of stromal cells derived from specimens of predecidualized endometrium. Thus, progestins modify the expression of several DZ-related markers in the cultured stromal cells, and E2 enhances these effects despite the lack of response to E2 alone. These responses are consistent with the differential actions displayed by E2 and progesterone in vivo, by which E2 primes the endometrium for the decidualizing effects of progesterone by elevating progesterone receptor levels. Accordingly, during steroid-induced in vitro DZ, a marked increase in the expression of stromal cell TF and PAI-1 and reciprocal inhibition of tPA activity suggest mechanisms to account for the absence of hemorrhage during invasion of the endometrial vasculature by implanting trophoblasts. In contrast to steroid-induced DZ, the events of menstruation are initiated in response to a decline in circulating levels of ovarian steroids. Accordingly, subjecting in vitro decidualized stromal cells to steroid withdrawal results in pronounced reversal in the expression of all of the end points listed above. Consequently, the local hemostatic environment is transformed into a hemorrhage-promoting milieu. Taken together with vascular injury resulting from ischemia induced by spiral artery vasoconstriction, the net effect is attainment of two prerequisites for menstrual hemorrhage, vascular injury and inadequate hemostasis.
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PMID:Decidual cell regulation of hemostasis during implantation and menstruation. 932 39

Several CNS disorders feature microglial activation. Microglia are known to have both restorative and cytotoxic capabilities. Neuronal apoptosis has been noted after an acute insult such as ischemia. Microglia may participate in this event. We previously showed that conditioned medium (CM) harvested from peritoneal macrophages or from activated microglia triggered apoptosis in rat hippocampal neurons in culture. We wished to characterize the factor responsible for triggering neuronal death. Quiescent microglia produced CM that did not disrupt hippocampal neurons. Lipopolysaccharide-activated microglia produced CM which resulted in neuronal death. This effect was blocked by plasminogen activator inhibitor-1, by tPA STOP, and by co-incubation with tPA antibody. Recombinant human tPA exaggerated the neurotoxic effects of microglial CM, while tPA alone was toxic only at very high concentrations. This in vitro system, which probably excludes any significant impact of microglial free radicals, suggests that microglial tPA may contribute significantly to hippocampal neuronal death.
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PMID:Microglial tissue plasminogen activator (tPA) triggers neuronal apoptosis in vitro. 1065 44

Recent experimental observations indicate that tPA plays a key role in the development of neuronal damage that follows cerebral ischemia and excitotoxicity. In an attempt to clarify how tPA favors ischemia-induced neuronal damage, we performed in vitro electrophysiological experiments in striatal slices by using mice selectively lacking this serine protease.We found that tPA ablation did not affect the membrane depolarization of striatal neurons exposed to combined oxygen and glucose deprivation but fully prevented the induction of NMDA-dependent post-ischemic long-term synaptic potentiation. The absence of striatal post-ischemic pote ntiat ion observed in tPA-lacking mice may account for the significant neuroprotection observed in these animals after the occlusion of middle cerebral artery.
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PMID:Tissue plasminogen activator is required for striatal post-ischemic synaptic potentiation. 1192 71

During a period of nine years, 10 patients, ages 42 to 66 years (55 +/- 7, mean +/- SD) underwent upper extremity bypass for ischemic changes to the hand not responsive to conservative management. Patients were referred from the vascular department at the authors' institution. Preoperative angiograms were performed and attempts at angioplasty or intravenous attempts to dissolve clots were carried out (with tissue plasminogen activator-tPA) when appropriate. Patients with persistent upper extremity ischemia and an obvious occlusion with reconstitution in the hand were candidates for upper extremity bypass to the palmar arch. All patients had upper extremity bypasses performed with reverse saphenous vein grafts. The proximal anastomoses (end-to-side) were performed by either the vascular or plastic surgery team, while all distal anastomoses (end-to-side) were performed by plastic surgery team microscopic magnification to the deep or superficial palmar arch. Postoperative follow-up ranged from 3 months to 3 years. The bypass graft to the hand resulted in improved pain and resolution of tissue ischemia in all cases. Patients with preoperative ulcers were completely healed by 3 months. The results are in accordance with previous studies demonstrating that improved blood flow afforded by the procedure can improve the healing of recalcitrant ulcers and mitigate the symptoms of ischemic changes. In addition, end-to-side anastomosis to the palmar arch offers significant advantages, in that the continuity of the arch is maintained with all possible outflow vessels, and the problems associated with size discrepancy in the anastomosed vessels are eliminated.
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PMID:Palmar arch revascularization for arterial occlusion of the distal upper extremity. 1597 Nov 64


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