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

We evaluated the effect of increased heart rate on cardiac output and stroke volume in the stage 24 chick embryo (day 4 of a 21-day incubation). Blood flow was measured with a 20 MHz pulsed-Doppler flowmeter. Heart rate was increased by pacing with square wave stimuli (1 ms duration, less than 4 mA). The sinus venosus was paced from bipolar Teflon-coated silver electrodes in eight embryos and the ventricular apex was paced in three embryos. The pacing rates were at the intrinsic heart rate (P:I); 125% of intrinsic heart rate (P:125%I); and 150% of intrinsic heart rate (P:150%I). Physiologic measurements during pacing were compared to those obtained at the control intrinsic rate (I). We also evaluated the velocity profile of atrioventricular inflow and conotruncal outflow at intrinsic rate and during sinus venosus and ventricular pacing. With sinus venosus pacing, mean dorsal aortic blood flow was similar at control (1.07 +/- 0.05 mm3/s) and P:I (1.06 +/- 0.06 mm3/s) (mean +/- SEM). However, at P:125%I and P:150%I, mean dorsal aortic blood flow decreased significantly (P:125%I, 0.88 +/- 0.05 mm3/s; P:150%I, 0.67 +/- 0.07 mm3/s) (p less than 0.05). Stroke volume per beat also decreased with increasing heart rates (I, 0.41 +/- 0.02 mm3; P:I, 0.39 +/- 0.02 mm3; P:125%I, 0.28 +/- 0.02 mm3; P:150%I, 0.18 +/- 0.02 mm3) (p less than 0.05). With rapid sinus venosus pacing, the atrioventricular blood flow velocity profile showed a rate-dependent decrease in passive ventricular filling while active filling remained the same or increased slightly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of heart rate increase on dorsal aortic flow in the stage 24 chick embryo. 296 Sep 45

Different processes of microvascular wound healing under hypertension in comparison to normotension have been suspected. To explore these differences at the site of anastomotic wound repair, we performed microvascular anastomoses of the femoral arteries in 12-week-old, stroke-prone hypertensive rats (SHRSP) whose maximum blood pressure reached 238 mm Hg and in normotensive age-matched Wistar Kyoto (WKY) rats. Morphologic changes under hypertension were examined via light microscopy. The arrangement and number of endothelial cells were examined using the en face silver staining technique. The plasma activity levels of factor XIII were also measured in each group. Transitional healing at the microvascular anastomosis site was evaluated via scanning electron microscopy. The extent of endothelial migration over the exposed media around the needle holes was determined using a computerized graphic analysis system. Histologic cross sections demonstrated a thickened media, with altered shape and arrangement of the smooth muscle cell nuclei in SHRSP arteries compared with WKY arteries. En face silver staining showed small and spindle-shaped endothelial cells with an irregular cell arrangement and distribution in SHRSP arteries relative to WKY arteries. Factor XIII was increased 36% over baseline in SHRSP rats postoperatively; this was significantly higher than the increase in WKY rats (P < 0.05). Although both SHRSP and WKY arteries had similar wound healing responses to microvascular anastomosis, endothelial cell migration over the exposed media was significantly accelerated in the SHRSP rats.
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PMID:Effect of hypertension on arterial structure and wound repair at the microvascular anastomosis site using stroke-prone spontaneously hypertensive rats (SHRSP). 827 29

Post-ischemic treatment of di-Calciphor (16,16'-dimethyl-15- dehydroprostaglandin B1) significantly improves animal survival and prevents ischemia-induced neurodegeneration of vulnerable forebrain regions assessed with histochemical and biochemical techniques in gerbils. Neuronal degeneration seen by Cresyl violet staining and silver impregnation in the CA1 sector of the hippocampus and the dorso-lateral sector of the striatum was significantly reduced in animals treated with di-Calciphor. In addition, the early onset of selective degradation of calpain I substrates spectrin and microtubule-associated protein (MAP2) in these same vulnerable regions was prevented. The lack of adverse side effects may facilitate the potential therapeutic use of this drug in preventing neuronal damage caused by stroke.
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PMID:Neuroprotective activity of dimer of 16,16'-dimethyl-15-dehydroprostaglandin B1 (di-Calciphor) in cerebral ischemia. 846 94

The use of glutamate antagonists and GABA agonists may protect neurons from the effects of transient ischemia. Felbamate is a new antiepileptic drug with glutamate antagonist and GABA agonist properties. We tested the efficacy of felbamate in a gerbil model of transient forebrain ischemia. Damage assessment was done with silver staining at 7 and 28 days after 5 min of bilateral carotid occlusion. Cerebral cortex, hippocampus (CA1 and CA4), thalamus and striatum were evaluated on a 4-point scoring system. The animals sacrificed at 28 days were also tested in a water-maze task to assess recovery of function. The initial dose of felbamate (300 mg/kg) was given 30 min before the ischemic insult in one set of animals and 30 min after the insult in another set of animals. There were 8 animals tested per group (total: 48 animals). There was significant neuronal protection with the use of felbamate, both before and after ischemia in all regions of the brain. Protection was seen in animals sacrificed at 7 and 28 days. Protection was moderate when felbamate was used before ischemia. It was highly significant when felbamate was given 30 min after the insult. Behavioral studies however did not show any difference in the felbamate treated animals versus the saline treated controls. The structural protection with felbamate was very significant when used in the post-ischemic period. This window for protection merits further evaluation in relation to the clinical setting of stroke.
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PMID:Neuroprotection with felbamate: a 7- and 28-day study in transient forebrain ischemia in gerbils. 884 83

This in vitro study evaluated the wear resistance of a high-strength resin posterior denture tooth against eight opposing dental materials. The tooth specimen was cusp shaped and the opposing materials were formed as a 10 x 10 x 5 mm plate. All material combinations were tested using a machine designed to produce sliding contact 20 x 10(4) times at 60 cycles per minute and a 4-mm sliding distance per stroke in the buccolingual direction under a load of 1 kg. Wear analysis was measured as the total height loss of each material combination and the volume loss of each material. Wear against human enamel was evaluated as a control. The least loss was observed opposing a gold-silver-palladium-copper alloy, and the greatest loss was observed opposing porcelain. The volume loss of high-strength resin against gold-silver-palladium-copper alloy was as small as that against human enamel. High-strength resin wear was more significant against castable ceramics and porcelain. The volume losses of high-strength resin against high-strength resin, polycarbonate, or cobalt-chromium alloy were significantly larger than those against polyethersulfone, poly(methyl methacrylate), gold-silver-palladium-copper alloy, or human enamel. These findings suggest that the were resistance of high-strength resin is influenced considerably by opposing dental materials, and that the best combination was high-strength resin-gold-silver-palladium-copper alloy, and the poorest combination was high-strength resin-porcelain.
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PMID:An in vitro study of high-strength resin posterior denture tooth wear. 948 67

The racemate 1, ((+/-)-(5-Chloro-2-methoxyphenyl)-1,3-dihydro-3-fluoro-6-(trifluoromethyl)- 2H-indol-2-one), is a potent, specific and novel opener of cloned large-conductance, calcium-activated (maxi-K) potassium channels. One of its enantiomers, BMS-204352 (MaxiPost), is undergoing clinical evaluation for efficacy in patients with suspected acute stroke. In the current study, we have prepared [(18)F]-labeled 1 using a silver assisted nucleophilic substitution to examine its distribution and disposition in the rat, with particular emphasis on the brain. Biodistribution studies in rats confirm that brain uptake is rapid and occurs at high levels, and indicate that a major fraction of the compound in the brain does not accumulate by a specific, saturable mechanism.
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PMID:Radiochemical synthesis and biodistribution of a novel maxi-K potassium channel opener. 1178 76

The effect of Trimetazidine (TMZ) as a potential neuroprotectant against stroke was studied in the gerbil model of transient forebrain global ischemia. Animals were subjected to a 5-min period of ischemia and assessed 4 and 21 days later. Gerbils were divided into two groups: in group one, gerbils were treated with TMZ at a dose of 25 mg/kg given by intraperitoneal injection prior to ischemia. In group two, gerbils were treated with TMZ at a dose of 25 mg/kg given intraperitoneally after ischemia. Saline-injected gerbils served as controls. Histological evaluation of neuronal damage was carried out using the silver staining technique in gerbils 4 and 21 days after the start of the experimental protocol. Behavioral functions were assessed in gerbils from the 14th to the 21st day after the start of the experimental protocol using the Morris water maze test. Results obtained from this study showed no significant difference between saline treated TMZ-treated gerbils when TMZ was administered after ischemia. When TMZ was administered prior to ischemia, there was a reduction in neuronal damage although it did not reach statistical significance and a statistically significant improvement in behavior. We conclude that TMZ shows signs of promise as a neuroprotective agent, and further studies should look at pre-treatment with different doses and different times.
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PMID:Trimetazidine as a potential neuroprotectant in transient global ischemia in gerbils: a behavioral and histological study. 1184 66

A German couple was struck by lightning. Both patients survived this event. Whereas the husband was unconscious for only a few minutes, his wife fell into coma for 24 h. The lightning stroke entered the body of the woman behind the left ear and left it at the left shoe. The stroke caused a partial evaporation of a gold ornamental chain on the neck, resulting in a tattoo of the neck skin. A biopsy of the skin 6 months after the event showed the accumulation of gold particles of different size in the dermis down to the subcutaneous fatty tissue. In semithin sections, histiocytes, multinucleated foreign giant cells, and fibroblasts were visible with uptaken metallic particles. In transmission electron microscopy, gold globules of up to 30 microm in diameter were visible outside the cells in the collageneous matrix of the connective tissue besides smaller metallic particles up to 5 nm inside lysosomes and residual bodies of phagocytic cells. Four different kinds of gold particles could be differentiated: globules, granular irregular particles, tubules, and tanglelike tracks. In scanning electron microscopy, gold particles were demonstrated by backscatter detection in the connective tissue of subcutis, where the EDX elemental analysis showed strong signals of aurum (Au), copper (Cu), and argentum (Ag). The detected metals were quantified by AAS as 70% gold, 21% silver, and 9% copper, which demonstrates the composition of gold alloy of the neck chain of the patient. Tanglelike tracks and elongated gold deposits represent crystals of gold salts, as detected by electron diffraction and polarization microscopy. Attempts to remove the gold particles from the skin to remove the tattoo should not be undertaken because the gold is deep and widespread.
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PMID:Detection of gold particles in the neck skin after lightning stroke with evaporation of an ornamental chain. 1218 73

Lesion size is an important outcome parameter in experimental stroke research. However, most methods of measuring the infarct volume in rodents either require expensive equipment or render the brain tissue unusable for further analysis. We report on an inexpensive, tissue-saving method for quantifying the infarct volume in small rodents. After 3 h of middle cerebral artery occlusion (MCAO) and 24 h of reperfusion in male Wistar rats, the lesion was first identified using MRI with T2-weighted sequences. The infarct was then visualized in unfixed brain cryosections using microtubule associated protein 2 (MAP2)-immunohistochemistry and silver infarct staining. The lesion areas detected by all three different methods completely overlapped. The infarct volume was calculated for each method from the lesion area size on serial sections and the distance between them. Significant differences in lesion size were found between the individual animals (p = 0.000056), but not between different methods (p > 0.05). MAP2 immunohistochemistry is a convenient and valid method to measure stroke lesion volume; in addition 98% of the brain tissue is saved and available for use in further histological, immunohistochemical, and biochemical analysis.
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PMID:Tissue-saving infarct volumetry using histochemistry validated by MRI in rat focal ischemia. 1239 11

Zinc ions seem to be important to several neurological functions and have been connected to the pathophysiology of epilepsy, neuronal cell death after seizure or stroke, and Alzheimer's disease. Both epilepsy and Alzheimer's disease are clinical conditions believed to involve the olfactory bulb. The mammalian olfactory bulb is densely innervated by zinc-enriched (ZEN) neurons, and the distribution of the ZEN terminals in the mouse olfactory bulb has previously been described. The aim of this study was to describe the origins of ZEN terminals projecting into the main olfactory bulb of the rat. Selective labeling of ZEN terminals was accomplished by intracerebral infusion of sodium selenide, whereby zinc selenium clusters are created in the ZEN terminals. Some of these clusters move by retrograde axonal transport to the somata where they can be silver-enhanced by autometallography (AMG). After infusion of sodium selenide into the main olfactory bulb, retrogradely labeled ZEN somata were found (1) ipsilaterally in all anterior olfactory nuclei, taenia tecta, piriform cortex and lateral entorhinal cortex, and (2) contralaterally in anterior olfactory nuclei except the external division. The ipsilateral anterior olfactory nucleus had the densest population of ZEN somata, and it was found that these somata originated mainly from pyramidal neurons in layers II and III of each area. The olfactory-related centrifugal afferents to the main olfactory bulb are discussed.
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PMID:Retrograde tracing of zinc-enriched (ZEN) neuronal somata projecting to the olfactory bulb. 1244 90


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