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

The importance of autacoidal substances in the genesis of cerebral vascular constriction and spasm is an unresolved issue. Comparative vasoactivity of 5-hydroxytryptamine (5HT) and norepinephrine (NE) on the human basilar artery was quantitatively assessed in vitro. 5HT was decidedly more vasoactive in this preparation. Three patterns of vasoactivity were noted with 5HT. Type I was an immediate sustained increase in tension lasting more than 30 minutes. Average increase in tension was 2988 mg (range 120-8600). Type II consisted of a sharp immediate increase in tension to average 1555 mg (range 240-4500) followed by gradual dissipation to base-line levels within 15 minutes. Type III pattern was a lesser immediate increase (372 mg; range 100-850) and more rapid dissipation over ten minutes. NE-induced Type I and Type III activity was present in only six of 20 segments. This study demonstrates that 5HT is vasoactive in human cerebral arteries. Type I sustained contractions may possibly be implicated in spasm. It is hypothesized that such autacoid-induced contraction may contribute to vascular wall ischemia, necrosis, and irreversible constriction as seen in human vasospasm.
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PMID:Quantitative in vitro vasoactivity of 5-hydroxytryptamine on the human basilar artery. 116 81

In a series of 19 patients with Volkmann's iscemia, 63 per cent had suffered skeletal trauma, whereas 38 per cent had received non-skeletal trauma. Non-specific trauma may trigger an ischemia-edema cycle, producing increased intracompartmental pressure. This cycle, if unrelieved, can involve all of the muscles in the compartment, via cyclic propagation and reinforcement of arterial spasm. The volar compartmental syndrome is not an all or none phenomenon. Localized ischemia may trigger a gradually spreading arterial spasm which results in slowly progressive clinical changes as late as 3-4 months after onset. Decompression not only of the compartment but of each individual muscle which shows evidence of vascular compromise, may reverse this destructive cycle even as late as 3-4 months but it should be performed promptly with the onset of symptoms, when its effect is rapid and dramatic. Induration of the compartment is pathognomonic of the compartmental syndrome. As long as it is present, benefit can be expected from decompression procedures. Regeneration of necrotic ischemic muscle is possible following restoration of circulation.
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PMID:Volkmann's ischemia. A volar compartment syndrome of the forearm. 119 76

Vessels of the microcirculatory bed of the heart in myocardial infarction were studied on the basis of the material of 21 section observations using histological, histochemical methods and the technique of impregnation of films of the epicardium developed by V. V. Kupriyanov. In the ischemic stage in the zone of ischemia and in perifocal areas there were noted signs of increased vascular permeability and impairment of hemodynamics: plethora of the venous department of the microcirculatory system, stasis of the blood in capillaries, spasm and paresis of vessels of the microcirculation. In the necrotic stage in the zone of necrosis there were observed destruction of vessels of the microcirculatory bed; in the peri-infarction zone--drastic plethora of veins, venules and capillaries, higher vascular permeability, leucostasis, leucopedesis, perivascular cellular infiltrates, destruction of vessels of the microcirculatory bed, dilatation of lymphatic vessels; in the intact zone--venous plethora and elevated permeability. In cases of shocks and collapses in vessels of the microcirculatory bed of the heart beyond the zone of necrosis aggregations of erythrocytes were found. In the reparative stage newly formed vessels in the granulation tissue were observed; In the post-infarction scars sinusoid vascular cavities and arteries of the closing type were noted.
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PMID:[Vessels of the microcirculatory bed of the heart in myocardial infarction]. 122 73

Paraplegia from spinal cord ischemia during thoracoabdominal aneurysm repair remains an unpredictable and unpreventable complication. In an effort to prevent spinal cord ischemia during aortic cross-clamping, preoperative angiographic localization of the blood supply to the spinal cord was performed in dogs. Sixteen animals underwent 60 minutes of thoracoabdominal aortic cross-clamping either without (control, n = 8) or with (shunted, n = 8) a selective shunt. Shunting was performed from the aortic arch to that isolated aortic segment angiographically shown to supply the thoracolumbar anterior spinal artery. Spinal cord blood flow was measured with microspheres just prior to cross-clamping, at 5 and 60 minutes after cross-clamping and at 5 minutes after restoration of aortic blood flow. Functional neurologic outcome was evaluated in animals at 24 hours postoperatively. Shunting did not decrease spinal cord injury. Seven of the 8 animals in the control group and 7 of the 8 in the shunted group developed paraplegia or paraparesis. Thoracic, but not lumbar spinal cord blood flow, was significantly increased in shunted animals. Spinal cord blood supply in dogs may be more segmental than previously believed. Technical problems in angiographic localization, spinal artery spasm, loss of spinal cord autoregulation or poor collateral circulation from the distal thoracic to the lumbar cord may also account for these results. Although shunting to aortic segments supplying the anterior spinal artery during thoracoabdominal aortic clamping may be attractive in humans, no benefit could be shown in this experimental model.
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PMID:Failure of selective shunting to intercostal arteries to prevent spinal cord ischemia during experimental thoracoabdominal aortic occlusion. 129 34

During reperfusion of previously ischemic cardiac tissue, oxygen-centered free radicals are generated and may result in peroxidative injury of cardiovascular cells and membranes. Since the occurrence of reperfusion injury in patients is unpredictable, particularly in those patients with chronic ischemic coronary artery disease, silent ischemia and those predisposed to significant coronary spasm, it would be advantageous to provide continuing therapy with antioxidant agents.
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PMID:Beta-blockers, calcium channel blockers and the sulfhydryl-ACE inhibitors demonstrate protection against free-radical-mediated injury of cardiovascular cells and membranes. 136 71

Acute coronary occlusion during PTCA represents a significant procedural complication occurring in approximately 4-5% of cases, most frequently because of coronary dissection, spasm, or thrombosis. In these cases the first step in the management of acute ischemia is 1) a brief evaluation of its hemodynamic consequences and 2) the assessment and treatment of its cause. Spasm and intracoronary thrombus formation are usually readily identifiable and treatable using intracoronary nitroglycerin and thrombolytic therapy. In our catheterization laboratory the current approach to occlusive coronary dissection is represented by the use of autoperfusion dilatation catheters and by stent application. The atherectomy devices and the laser "welding" of the dissected intimal segment represent other alternatives that are still under clinical evaluation in this particular setting. If coronary occlusion is refractory to these efforts and coronary blood flow is not reestablished rapidly, emergency coronary bypass surgery is required to salvage jeopardized myocardium. In this case myocardial ischemia may be lessened by the insertion of an intra-aortic balloon pump. In our experience, the incidence of death (4%) and myocardial infarction (37%) for emergency CABG after a failed angioplasty, is similar to that reported by other Authors. The duration of myocardial ischemia and the presence of cardiogenic shock before operation are the most important determinants of major complications such as death and acute myocardial infarction.
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PMID:[Surgical indications and results of myocardial revascularization in complications of PTCA]. 142 76

Along with organic involvement of the coronary arteries their spasm is one of the mechanisms of development of acute myocardial ischemia. Transesophageal electrocardiostimulation in 314 patients with non-stable stenocardia revealed in 32 (10.2%) increased vasospastic activity. Holter monitoring allowed to find essential differences in patients with vasospasm manifested in a significant increase of the frequency and duration of nonpainful myocardial ischemia in the absence of distinct changes in painful ischemia. Two-week treatment with calcium antagonists allowed to reduce the ischemia level in the group of patients with vasospasm tendencies.
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PMID:[The characteristics of the Holter monitoring data on patients with a vasospastic reaction during the performance of transesophageal electrocardiostimulation]. 147 17

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

The study of the epidemiological data (published since 1952) seems to show an increasing frequency of the coronary disease for 15 last years. But this incidence seems to reach a stable level about 6 to 7% of the cardiovascular diseases at the Abidjan Institute of Cardiology; and 3.17% in a study in 13 countries but without coronarography (except at the Abidjan Institute). The study of the risk factors show that they are the same ones than in Europa. The risk index in Black Africa was 2.1 to 2.7 risk factor patient. These numbers are lesser than the risk index noted in France (3.6 in coronary patients and 1.9 in non-coronary subjects). The signs of the disease show that myocardial infarctions were frequent (48.8%) and often were the first manifestations of the coronary disease (40%). Angina pectoris was observed in 32.2%, an ischemic cardiomyopathy in 6.6% and a ventricular aneurysm in 6.6%. A silent ischemia was observed in 5.5% among at risk diabetic patients. The in-hospital mortality after myocardial infarction was 15% and was the same in European and African patients. But the mortality in Africans was greater than in Europeans the next years. Coronarography showed that 18.8% of the patients with coronary disease had normal coronary arteries. The arteries were also normal in 19.9% of the patients examined after an infarction. These high percentages can be related to coronary arterial spasms or to recanalized thrombosis. A spontaneous spasm was observed in 6.6% of the patients (a provoked coronary arterial spasm was not studied. The coronary arterial lesion was an one artery disease in 38.8% of the coronary patients and 50% of the patients with infarction. The stenosis were frequently proximal (82.6%) and the anterior descending artery was interested in 45.6%. Ventricular aneurysms were observed in 56.6% and the ejection fraction was lower than 0.50 in 63.3%. These data permit to compare the myocardial infarction of Blacks with the myocardial infarction of the young occidental men. We can think that thrombolysis or angioplasty would be very useful but they are often impossible in the Black African conditions.
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PMID:[Coronary disease in black Africans: epidemiology, risk factors, clinical symptomatology and coronarography, evolution]. 150 58

Acute ischemia of the extremity may be due to arterial occlusion from spontaneous thrombosis, embolus, arterial bypass graft thrombosis, trauma, or spasm. The presence of occlusion or stenosis can be determined noninvasively with the use of duplex Doppler ultrasonography. Most patients will require arteriography prior to thrombolytic or surgical therapy. New techniques, such as percutaneous aspiration thrombolectomy, expand the role of radiologic percutaneous therapy of the acutely ischemic limb. Prompt diagnosis and therapy are required to avoid limb loss or systemic metabolic complications from reperfusion of a dying limb.
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PMID:Acute limb ischemia. 153 Oct 45


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