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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first generation of an integrated, totally implantable electrohydraulic total artificial heart was designed for long-term cardiac replacement. The system consists of an elliptical blood pump with an interatrial shunt, Medtronic-Hall 27 mm and 25 mm inflow and outflow valves, respectively, an energy converter consisting of an axial-flow, hydraulic pump driven by a brushless DC motor, and an electronics system with transcutaneous energy transmission and telemetry. Energy is supplied by internal nickel-cadmium rechargeable batteries that supply power for 20 min and external silver-zinc batteries that are designed to supply energy to run the system for 5 hr. The blood pump consists of a single layer diaphragm cast from Biolon, with joined right and left ventricles sharing a common base. The dynamic stroke volume is 84 ml, and maximum cardiac output is 9.2 L/min at a heart rate of 110 beats/min on the mock circulation. A 4.3 mm diameter interatrial shunt is used to balance the volumetrically coupled ventricles. The energy converter pumps hydraulic fluid alternately between ventricles, with controlled, active filling in one ventricle during the systolic phase of the other ventricle. Internal or external controllers adjust the heart rate and motor speed to maintain normal atrial filling pressures and full stroke. Electromagnetic induction is used to transfer energy through the skin and a bidirectional infrared data link incorporated within the transcutaneous energy transmission coils is used to transmit information. The entire system is being assembled and refined for long-term animal implant studies.
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PMID:Development of a totally implantable artificial heart. 145 55

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.
Stroke 1990 May
PMID:Neural damage in the rat thalamus after cortical infarcts. 169 45

Proton magnetic resonance (MR) imaging has been recommended as a diagnostic tool for the detection of focal cerebral ischemia. We compared microscopic MR images of rat brains after focal cerebral ischemia with evidence of histological damage found on corresponding silver-impregnated or cresyl violet-stained brain sections. Ten male Wistar rats were subjected to permanent unilateral occlusions of the right middle cerebral and common carotid arteries under halothane anesthesia. Twenty-four hours later the area of injury on MR images amounted to 26% of the total slice area, whereas only 9% of the total slice area was necrotic on histological sections from the same animals. The infarcted areas on tissue sections were surrounded by regions of selective neuronal injury in the cerebral cortex and occasionally in the hippocampus. The area of injury on MR images was larger than the combined areas of infarction and selective neuronal injury on histological sections. Areas of increased T2 values on MR images extended medially into noninfarcted striatum and laterally and dorsally into noninfarcted cortex. The lateral and dorsal areas on MR images frequently coincided with cortical areas in which considerable selective neuronal injury was present in the upper cortical layers. We hypothesize that the abnormal areas on MR images above histologically normal brain tissue represent the ischemic penumbra. If true, this is the first demonstration of the ischemic penumbra by MR imaging and may reflect our use of Wistar rats, a new image analysis technique, and ultra-high resolution MR imaging.
Stroke 1991 Feb
PMID:Quantitative proton magnetic resonance imaging in focal cerebral ischemia in rat brain. 200 91

Wear characteristics of hybrid denture teeth, plastic denture teeth which were partially reinforced with metal, was evaluated. The plane specimens were made up with resin and metal. Light curing veneering resin, new metacolor, heat curing veneering resin, Mitel-OM and PMMA (Poly methyl methacrylate) were used for resin parts, while gallium containing filling alloy, silver alloy, palladium alloy and titanium containing chromium cobalt alloy were used for metal parts. The specimens were abraded by the rod specimens of palladium alloy with abrasion test machine. The wear depth and width were measured at 1, 5, 10 and 20 x 10(4) times of abrasion which stroke was 10 mm each. The specimens of heat cured veneering resin reinforced with chromium cobalt alloy showed the least wear loss while the specimens of PMMA reinforced with silver alloy did the most. The difference of wear ratio between light cured and heat cured veneering resin was not statistically significant.
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PMID:[The evaluation of wear resistance of hybrid denture teeth]. 213 14

The present study investigates the effects of the 5-hydroxytryptamine1A agonist ipsapirone on electroencephalography and somatosensory evoked potentials after middle cerebral artery occlusion in the rat. We implanted 17 silver ball electrodes symmetrically distributed over the skull in 14 rats and registered electroencephalography activity and somatosensory evoked potentials before, 1 hour, and 1 week after permanent occlusion of the left middle cerebral artery. Before vessel occlusion, a symmetric distribution of electroencephalography power was seen over both hemispheres. Middle cerebral artery occlusion caused a complete abolishment of electroencephalography power in the frontolateral aspects of the affected hemisphere. When electroencephalographic recordings 7 days after the insult were superimposed with three-dimensional-reconstructed pictures of the infarct, a close correspondence of the extention and spatial orientation was noted. Two negative and two positive peaks were consistently recorded before middle cerebral artery occlusion. In both control and ipsapirone-treated (30 mg/kg i.p. 30 minutes after induction of ischemia) animals, the vessel occlusion caused a severe reduction in amplitudes of somatosensory evoked potentials in all areas under record (p less than 0.05). One week after middle cerebral artery occlusion, amplitudes of somatosensory potentials over the lesioned hemisphere were still significantly (p less than 0.05) lower than preischemic values in the control group. When compared with the corresponding values 1 hour after middle cerebral artery occlusion, an albeit insignificant tendency toward increased amplitudes was observed in most areas under record. By contrast, in ipsapirone-treated animals, significant differences compared with preischemic values were no longer present 1 week after the vessel occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1990 Dec
PMID:Effects of ipsapirone on spatial and temporal changes in somatosensory evoked potentials after middle cerebral artery occlusion in the rat. 226 Jan 43

We studied eight anesthetized and physiologically monitored adult baboons (Papio cyanocephalus); four were subjected to hemorrhagic hypotension alone and four to hemorrhagic hypotension plus unilateral carotid artery occlusion. Cerebral blood flow was measured using xenon-133, the electroencephalogram was recorded using silver-silver chloride epidural electrodes, and histologic examination was carried out after perfusion-fixation. In the baboons subjected to hypotension alone (mean arterial blood pressure of 28 mm Hg) cerebral blood flow was 28.5 +/- 5.0 ml/100 g/min, whereas in the baboons subjected to hypotension plus unilateral carotid artery occlusion it was 21.8 +/- 1.8 ml/100 g/min at a mean arterial blood pressure of 27 mm Hg. There was no ischemic damage in the former group, but in the latter group there was necrosis in the arterial boundary zones of three baboons and in the distribution of the middle cerebral artery in one. We conclude that, when combined with hypotension, unilateral carotid artery occlusion may lead to hemodynamic ischemia accentuated in the arterial boundary zones of the ipsilateral cerebral hemisphere.
Stroke 1990 Mar
PMID:Neuropathologic consequences of internal carotid artery occlusion and hemorrhagic hypotension in baboons. 230 67

The roles of vasopressin and angiotensin II in the regulation of peripheral vascular tone were investigated in control rats and in rats with chronic (15 weeks) aortic stenosis, by intravenous application of a specific antagonist to the vascular receptors of vasopressin and the angiotensin-converting enzyme inhibitor teprotide. The application of a Silver clip (0.6 mm) on the aorta ascendens produced a hemodynamically effective aortic stenosis with an increase in left ventricular weight (38%), a reduction in mean arterial pressure, cardiac index, and stroke volume index, and an increase in peripheral vascular resistance. In both groups of rats, a bolus injection of 30 micrograms of the vasopressin inhibitor d (CH2) 5 Tyr (Me) arginine vasopressin (AVP) showed an agonistic effect by increasing arterial pressure by 11 and 15 mm Hg, respectively, and no antagonistic effect in the control animals. In the rats with chronic aortic stenosis we observed a significant fall in blood pressure (4.1 +/- 5.5 mm Hg; p less than 0.05) and a reduction in peripheral vascular resistance of 6.3% (p less than 0.02). Stroke volume index and heart rate did not change. Most of the animals with aortic stenosis had inappropriately elevated plasma levels of vasopressin and increased levels of plasma renin concentration. The rats with aortic stenosis and inappropriately increased values of vasopressin showed significantly lower plasma osmolality, cardiac index, and stroke volume index and increased peripheral vascular resistance compared with the stenosed rats with a normal osmoregulation of vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasoconstrictor role of vasopressin and angiotensin in experimental aortic stenosis in the rat. 245 39

We studied functional disturbances following left middle cerebral artery occlusion in rats. Neuronal function was evaluated by [14C]2-deoxyglucose autoradiography 1 day after occlusion. We analyzed the mechanisms of change in glucose utilization outside the infarct using Fink-Heimer silver impregnation, axonal transport of wheat germ agglutinin-conjugated-horseradish peroxidase, and succinate dehydrogenase histochemistry. One day after occlusion, glucose utilization was remarkably reduced in the areas surrounding the infarct. There were many silver grains indicating degeneration of the synaptic terminals in the cortical areas surrounding the infarct and the ipsilateral cingulate cortex. Moreover, in the left thalamus where the left middle cerebral artery supplied no blood, glucose utilization significantly decreased compared with sham-operated rats. In the left thalamus, massive silver staining of degenerated synaptic terminals and decreases in succinate dehydrogenase activity were observed 4 and 5 days after occlusion. The absence of succinate dehydrogenase staining may reflect early changes in retrograde degeneration of thalamic neurons after ischemic injury of the thalamocortical pathway. Terminal degeneration even affected areas remote from the infarct: there were silver grains in the contralateral hemisphere transcallosally connected to the infarct and in the ipsilateral substantia nigra. Axonal transport study showed disruption of the corticospinal tract by subcortical ischemia; the transcallosal pathways in the cortex surrounding the infarct were preserved. The relation between neural function and the neuronal network in the area surrounding the focal cerebral infarct is discussed with regard to ischemic penumbra and diaschisis.
Stroke 1989 Sep
PMID:Neuronal network disturbance after focal ischemia in rats. 247 23

We studied histopathologic changes in cerebral cortex of 20 rats after middle cerebral artery occlusion by using the Fink-Heimer suppressive silver impregnation method and conventional stains. At 6 hours after occlusion, Fink-Heimer-stained sections revealed abundant coarsely granular, intensely argyrophilic neurons in the ischemic cortex. These distinctive argyrophilic neurons could be clearly differentiated from neurons that suffered postmortem changes; argyrophilic neurons were present in all layers of the lateral parietal cortex but in only the superficial cortical layers II and III in the parasagittal area of the frontoparietal cortex and the temporo-occipital area. At 24 hours after occlusion as the ischemic region progressed to pannecrosis, argyrophilic neurons were still evident in peri-infarct regions, with more prominent neuritic silver deposits but no changes in number or spatial distribution. Over 2-7 days, the argyrophilic neurons gradually disappeared while many fine silver-impregnated degenerating terminals appeared in the peri-infarct regions. At 3-6 weeks after occlusion, no more argyrophilic neurons were seen in the cortex although degenerating axons were still present in the deep white matter. Our results indicate selective neuronal damage in the superficial cortical layers and massive axonal degeneration in the cerebrum surrounding infarcts. The neuronal damage does not appear to progress beyond 6 hours after middle cerebral artery occlusion. The Fink-Heimer method has many advantages over existing conventional stains for documenting selective neuronal damage in focal cerebral ischemia.
Stroke 1989 Nov
PMID:Selective cortical neuronal damage after middle cerebral artery occlusion in rats. 247 27

We used the Fink-Heimer method to study degenerating corticofugal axons after unilateral middle cerebral artery occlusion in 14 adult male Long-Evans hooded rats. Axonal degeneration in the pyramidal tracts was prominent at 1-3 weeks, manifesting in well-defined silver-impregnated axonal bundles coursing from the internal capsule to the pyramids and crossing completely to the contralateral spinal cord. In half of eight rats examined at 1-3 weeks, the cortical infarct included the forelimb region of the sensorimotor cortex, and degenerating corticospinal axons could be traced to the lower cervical segments; in rats with involvement of the hindlimb cortical area as well, axonal degeneration extended to the lumbosacral segments. Terminal degeneration products were present in the forebrain, midbrain, and brainstem within 2 days after arterial occlusion; the number of degenerating terminals peaked at 7 days and decreased gradually thereafter up to 6 weeks. Dense terminal degeneration was observed in the trigeminal nuclear complex of all seven rats studied at 2 and 7 days. In these seven rats, five had small cortical infarcts, and silver-impregnated terminals were observed in the lateral reticular formation; in two rats with large cortical lesions, terminal degeneration was prominent in the medial reticular formation as well. We conclude that infarcts produced by middle cerebral artery occlusion cause axonal degeneration in the brainstem and spinal cord. The Fink-Heimer method may be useful for evaluating the rat middle cerebral artery occlusion model.
Stroke 1989 Oct
PMID:Corticofugal axonal degeneration in rats after middle cerebral artery occlusion. 279 71


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