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

Time-compressed Fourier analysis of the electroencephalogram has proven to be a useful analytical procedure during anesthesia and surgery which simplifies data interpretation by presenting the EEG in a time-compressed frequency domain rather than the conventional time domain. This method of data analysis graphically accentuates the electroencephalographic correlates of ischemia-induced cerebral dysfunction and other cerebral oxygen consumption abnormalities. The ability to accentuate trends in frequency and power is derived from sequential plotting of spectra to produce a graph with three dimensional axes of frequency, time, and power. In carotid endarterectomies the system has proven more useful than the conventional EEG in assessing the need for a vascular shunt to maintain internal carotid flow during endarterectomy. In open-heart surgery time-compressed EEG spectral analysis has allowed early recognition of cerebral ischemia resulting from arterial hypotension and venous hypertension. Five cases are presented which demonstrate the ability of our system to reflect developing cerebral ischemia.
Stroke
PMID:Monitoring of cerebral perfusion during anesthesia by time-compressed Fourier analysis of the electroencephalogram. 32 37

Using radioactive microspheres, we studied the quantitative and sequential distribution of myocardial blood flow during acute rejection of cardiac orthotopic allografts in 15 nonimmunosuppressed dogs. During rejection mean cardiac output per kilogram decreased 49 percent from control, stroke volume per kilogram decreased 40 percent, total left ventricular flow decreased 43 percent, and the subendocardial/subepicardial flow ratio (I/O) of the left ventricular free wall decreased 21 percent. Relative subendocardial hypoperfusion occurred despite an increase in the ratio of left ventricle subendocardial supply (diastolic pressure-time index) to demand (tension-time index). The data indicate that total left ventricular flow decreases severely and selective left ventricular subendocardial ischemia develops very early during acute cardiac rejection.
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PMID:Alterations in total and regional myocardial blood flow during acute rejection of orthotopic canine cardiac allografts. 34 80

Evidence is mounting that three drugs that inhibit platelet function--aspirin, dipyridamole, and sulfinpyrazine--have an antithrombotic effect in humans. Particularly in men, aspirin is beneficial in controlling transient ischemic attacks and stroke, and there is evidence that it may be effective in preventing thrombotic and embolic complication of hip surgery. It abolishes symptoms in peripheral ischemia associated with thrombocytosis and spontaneous platelet aggregation and may prove effective in coronary artery disease. When combined with oral anticoagulants, aspirin is more effective than oral anticoagulants alone in preventing systemic embolism in patients with prosthetic heart valves. Dipyridamole in combination with oral anticoagulants reduces the incidence of systemic embolism after prosthetic heart valve replacement. Sulfinpyrazone reduces the incidence of sudden death in the first year after myocardial infarction, decreases the incidence of arteriovenous shunt thrombosis in patients undergoing chronic hemodialysis, and when combined with anticoagulants, may be effective in reducing the frequency of episodes in recurrent venous thrombosis.
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PMID:Antiplatelet drugs in thromboembolism. 38 46

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

Twenty-seven heparinized dogs were exposed to 35 min of cerebrospinal fluid compression ischemia followed by 30 min of recirculation. The degree and distribution of post-ischemic reperfusion was then assessed by means of a 14C-antipyrine autoradiographic blood flow study. The animals were assigned to 5 groups by the administration of drugs as follows: 1) no additional drugs; 2) indomethacin 1.5 or 4 mg/kg prior to ischemia; 3) indomethacin 4 mg/kg 5 min after ischemia; 4) prostaglandin I2 (PGI2) infusion 30--180 ng/kg/min beginning 5 min after ischemia; and 5) indomethacin 4 mg/kg 5 min after ischemia plus PGI2 infusion 30--130 ng/kg/min beginning 5 min after ischemia. Animals receiving no additional drugs had relatively low post-ischemic blood flows with focal zones of greatly impaired reperfusion. Animals receiving either indomethacin or PGI2 after ischemia did not differ significantly from the no additional drug group. A significant enhancement of post-ischemic reperfusion occurred in animals receiving indomethacin prior to ischemia and those receiving the combination of indomethacin and PGI2 after ischemia. These observations implicate an imbalance in prostaglandin pathways at the blood-endothelial interface in the genesis of post-ischemic reflow impairment and suggest novel drug therapy for enhancing nutrient flow after ischemia.
Stroke
PMID:Prostaglandin I2 and indomethacin prevent impairment of post-ischemic brain reperfusion in the dog. 39 21

Selective embolization of the internal carotid artery bifurcation (ICA bifurcation) was performed in monkeys (Macaca mulatta) to study acute regional cerebral ischemia in the middle cerebral artery (MCA) territory with minimum surgical intervention in the neck under sedated conditions. The anthropomorphic similarity in angio-anatomy of the carotid system of monkeys and the use of silastic spheres, as artificial emboli, of the critical diameter of 1.2 to 1.4 mm resulted in the overall success rate of 87% in localizing the site of embolization to the ICA bifurcation, producing ischemia in the whole middle cerebral artery territory. All the animals with ICA-bifurcation embolization had contralateral deep motor weakness and conjugate eye deviation with nystagmus toward the site of embolization. Simultaneous EEG recording showed flattening of the basic background activities over the affected MCA area and cerebral arteriograms showed definite retrograde filling of the proximally occluded MCA. Clinical recovery was observed in a few animals within two to five hours of embolization. Gross ischemic swelling in the affected MCA territory, particularly in the gray matter, became obvious in six of eight animals which were exposed to four to five hours of ischemia. The angio-anatomical study of the carotid system of this experimental animal as a background for this MCA stroke model confirmed the previous observations of other investigators that the extremely abundant leptomeningeal anastomoses would be one of the major factors leading to the variability in the clinicopathological pictures seen in the models of proximal MCA occlusion. In addition, the pre-parenchymal anastomoses in the base of brain between the medial striate arteries from the proximal anterior cerebral (ACA) and lateral lenticulostriate arteries from the MCA were observed and described as a possible functional collateral to the basal ganglia in case of proximal MCA occlusion.
Stroke
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 1: Angio-anatomy and description of an experimental model with selective embolization of the internal carotid artery bifurcation. 40 41

We developed a monkey model of 16 minutes global brain ischemia (GBI) resulting in reproducible, severe, permanent functional neurologic deficit with long term (7 days) postischemic (PI) survival made possible by standardized intensive care with 24 hour coverage by trained personnel. Quantitated neurologic deficit (ND) and brain histopathological examinations were developed. Fifteen minutes GBI resulted in rapid recovery within12--24 hours PI without residual neurologic sequelae. Twenty minutes GBI caused severe neurologic deficit and within 4 days PI, a delayed Cushing response eventually leading to cardiac arrest. Sixteen minutes GBI resulted in severe neurologic deficit (monkeys unable to sit, stand, walk, or feed themselves), but with long term survival. Brain histopathological analyses revealed a combination of cortical and brainstem lesions. Severest changes were observed in the occipital (calcarine) cortex with less severe damage in the frontal and temporal regions. Oculomotor nuclei and medial longitudinal fasciculus in the midbrain were regularly affected. With this model we can test the efficacy of promising therapies in terms of clinically relevant variables.
Stroke
PMID:Global brain ischemia: a reproducible monkey model. 41 Jan 21

The capacity of delayed barbiturate administration to limit brain damage after unilateralcerebral ischemia was examined histologically in gerbils. The right common carotid artery was occluded in 50 animals under brief (3-minute) halothane anesthesia; 18 animals (36%) developed motor abnormalities consistent with stroke. The arterial clasps were removed after 1 hour and the abnormal animals were divided into treatment and placebo groups. Treated gerbils received sodium pentobarbital (70 mg/kg) intarperitoneally 1 hour after clasp removal and a smaller dose (50 mg/kg) 2 hours later; these animals lost corneal reflexes but retained spontaneous respiration and were kept normothermic. Animals in the placebo group received equivalent volumes of normal saline. Except for the period of anesthesia, both groups had similar postischemic motor behavior. Neuropathological examination of animals killed by perfusion-fixation after 24 hours revealed fewer pentobarbital-treated animals with shift of midline structures and with ipsilateral ischemic damage (including infarction). Compared with the placebo group, there was less extensive neuronal ischemic cell change in five regions of the ipsilateral cerebral hemispheres of the pentobarbital-treated animals (p less than 0.05). The results suggest that barbiturates administered as long as 1 hour after the end of an ischemic insult can still limit brain damage.
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PMID:Delayed pentobarbital administration limits ischemic brain damage in gerbils. 42 68

Unilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h-1, and the paramedian region (PM) of the hippocampus. In typical SC the nucleus was eccentric and the Nissl substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3-5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.
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PMID:Selective chromatolysis of neurons in the gerbil brain: a possible consequence of "epileptic" activity produced by common carotid artery occlusion. 42 76

The pathophysiology of post-cardiac arrest brain damage is not well understood. Many of the model systems presently used to study global ischemia have serious limitations. A new model system for total cerebral ischemia (TCI), using aortic and inferior vena caval occlusion balloons, is described. This model system produces verifiable TCI and avoids surgical invasion of the thorax or the use of vasoactive drugs. It does not impede cerebral venous return and protects the cardiopulmonary system from damage. This model system can be used to study the efficacy of various therapeutic interventions following a standardized CNS global ischemic insult.
Stroke
PMID:Total cerebral ischemia: a new model system for the study of post-cardiac arrest brain damage. 43 99


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