Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 77-year-old woman underwent right fronto-temporal craniotomy for a right ruptured IC-PC aneurysm (case 1), and a 44-year-old woman underwent right fronto-temporal craniotomy for a right ruptured BA-SCA aneurysm (case 2). They were clipped completely without any troubles during surgery. But postoperative CT scan demonstrated contralateral cerebellar infarction. We recognized left-hand tremor as a neurological deficit caused by cerebellar infarction in case 1. Concerning the mechanism of contralateral cerebellar infarction after pterional craniotomy, we think that it could be; --1) changing of venous blood flow by overdrainage of cerebrospinal fluid, 2) destruction of the bridging vein because of cerebral transformation with rapid decompression, 3) ischemia caused by brain retraction and compression during operation, 4) hypertension or hypoxia during operation, 5) crossed cerebellar diaschosis, and so on. In our 2 cases, we believe that perioperative CSF overdrainage caused the contralateral cerebellar infarction or CCD. To avoid this kind of infarction, we should try to take more protective and careful procedures as well as closer perioperative management.
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PMID:[Contralateral cerebellar infarction after aneurysmal clipping with pterional craniotomy: report of two cases]. 1044 41

Endothelin-1 (ET-1), a vasoactive peptide, causes a significant rise in portal vein pressure, which is most likely a result of severe vasoconstriction in the liver. In this study, the effect of ET-1 on sinusoidal vasoconstriction in the liver after ischemia and reperfusion was directly investigated using intravital microscopy. In anesthetized female Sprague Dawley rats (200-250 g) ischemia of the median and left liver lobes was induced for 90 min by temporary ligation of the left pedicle. After declamping and a 90-min reperfusion period, the livers were exposed for intravital microscopy. Using a Nikon MM-11 fluorescence microscope (545 nm, 330x), a CCD camera (Cohu FK 6990), and a SVHS video recording unit, the hepatic microcirculation was directly investigated. Besides sham groups, two ischemia groups were studied, receiving ET-1 antiserum (anti-ET-1; 0.5 ml; Peptide Inst., Osaka, Japan) or NaCl 0.9% (0.5 ml) 5 min prior to reperfusion of the liver (n = 6/group). Following a transient drop in the mean arterial blood pressure in the anti-ET-1-treated groups, comparable systemic hemodynamic conditions among the four groups were noted during intravital microscopic assessment at the end of the 90-min reperfusion period. Reduction in the sinusoidal diameters during postischemic reperfusion (7.7 +/- 0.5 microm) was prevented by anti-ET-1 treatment (9.6 +/- 0.25 microm; P < 0.01; mean + SEM) back to control values (9.6 +/- 0.32 microm), while most of other microcirculatory parameters did not show significant differences. The results supported further the role of ET-1 in dysregulation of the sinusoidal vascular tone in the liver, e.g., after ischemia and reperfusion.
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PMID:Endothelin-1 is involved in hepatic sinusoidal vasoconstriction after ischemia and reperfusion. 1127 Dec 93

The alkaloid derivative vinpocetine (14-ethoxycarbonyl-(3alpha,16alpha-ethyl)-14,15-eburnamine; Cavinton) has a well known beneficial effect on brain function in hypoxic and ischemic conditions. While it increases CNS blood flow and improves cellular metabolism, relatively little is known about vinpocetine's underlying molecular mechanisms on the single cell level. Since apoptotic and necrotic cell damage is always preceded by an increase in [Ca2+]i, this study investigated the effect of vinpocetine on [Ca2+]i increases in acute brain slices. Sodium influx is an early event in the biochemical cascade that takes place during ischemia. The alkaloid veratridine can activate this Na+ influx, causing depolarization and increasing [Ca2+]i in the cells. Therefore, it can be used to simulate an ischemic attack in brain cells. Using a cooled CCD camera-based ratio imaging system and cell loading with fura 2/AM, the effect of vinpocetine on [Ca2+]i changes in single pyramidal neurons in the vulnerable CA1 region of rat hippocampal slices was investigated. Preperfusion and continuous administration of vinpocetine (10 microM) significantly inhibited the elevation in [Ca2+]i induced by veratridine (10 microM). When the drug was administered after veratridine, it could accelerate the recovery of cellular calcium levels. Piracetam, another nootropic used in clinical practice, could attenuate the elevation of [Ca2+]i only at a high, 1 mM, concentration. We have concluded that vinpocetine, at a pharmacologically relevant concentration, can decrease pathologically high [Ca2+]i levels in individual rat hippocampal CA1 pyramidal neurons; this effect might contribute to the neuroprotective property of the drug.
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PMID:The nootropic drug vinpocetine inhibits veratridine-induced [Ca2+]i increase in rat hippocampal CA1 pyramidal cells. 1169 36

Water movement between cells and interstitium in spinal cord and brain occurs during neural signal transduction and in response to injuries such as ischemia and blunt trauma. At least two aquaporin-type water channels are expressed in spinal cord: AQP1 in afferent sensory nerve fibers in the superficial layers of the dorsal horn, and AQP4 in glial cells throughout gray matter. An imaging method was developed to map thickness changes in viable spinal cord and brain slices cut by a vibratome, and applied to measure osmotically induced water transport in spinal cord slices from wildtype and aquaporin knockout mice. Spinal cord slices (300 microm thickness) were mounted in a perfusion chamber with < 2 s exchange time, and transmitted light (565 nm) was imaged by a CCD camera. Changes in slice thickness were mapped from the amount of light passing through a thin ( approximately 100 microm) layer of perfusate bathing the slice, in which hemoglobin (6 mg/ml) was added to the perfusate as an inert absorbing chromophore. In response to osmotic challenges imposed by changing perfusate osmolality by 100 mOsm, transmitted light intensity changed reversibly with approximately mono-exponential kinetics whose initial rate depended upon position in the slice. In the superficial dorsal horn where AQP1 is strongly expressed, the rate of osmotic swelling was 7.0 +/- 1.3 microm/s in wildtype mice and 2.0 +/- 0.2 microm/s in AQP1 null mice; osmotic swelling was slower in deeper lamina of dorsal horn, and was decreased in AQP4 but not AQP1 null mice. These results establish a simple imaging method to map changes in water content of spinal cord slices, and provide evidence that aquaporins facilitate osmotic water transport in functionally relevant areas of the spinal cord.
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PMID:Optical measurement of swelling and water transport in spinal cord slices from aquaporin null mice. 1174 25

The aim of the investigation was to estimate the peculiarities of myocardial remodelling on the conditions of experimental hypercholesterolemia. Experiments were carried out on chinchilla breed male rabbits weighing from 2.3 to 3.0 kilos and being of three-four months of age (15 rabbits). Rabbits were fed daily with 0.2 g/kilo of cholesterol during twelve months. We defined the percentage volume, perimeter and the number of separate fibers per field of collagenous matrix and the volume of cardiomyocytes by computerized image analysis system connected with the microscope by CCD camera. We defined that various degree of stenosis of epicardial coronary arteries and their intramural branches leading to absolute lumen narrowing due to long duration of hypercholesterolemia (12 months) is the cause of chronic ischemia and remodelling of the myocardial structures of left and right ventricles. In case of chronic ischemia, cardiomyocytes in the left ventricle are replaced by multifocal reparative fibrosis, in the right ventricle such changes were not observed. Percentage volume of interstitial collagenous fibres increases about 1.2 (p<0.05) in the left ventricle and 1.26 times (p<0.05) in the right ventricle, i. e. interstitial fibrosis is being formed.
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PMID:[Peculiarities of myocardial remodelling in rabbits' experimental hypercholesterolemia]. 1457 32

Although mannitol has been used as an osmotherapeutic drug on brain injury, the clinical efficiency of the drug are still controversial. In the present study, we examined the effects of mannitol on the edema in a hippocampal slice due to brief ischemia. To evaluate the effects, we employed an image analysis system that consists of an infrared-differential interference contrast (IR-DIC) microscope, an infrared CCD camera, and a computer with custom-made software. By this system, severity of the edema can be quantified as the coefficient of variation (CV) of digitalized slice images. The dose-dependent improvement on the deteriorated hippocampal slices could be obtained by administration of mannitol (10, 50, and 100 mM) after 10-min ischemia. However, field excitatory postsynaptic potentials (fEPSP) in CA1 stratum radiatum, which disappeared during 10-min ischemia, were never recovered by mannitol after more than 20-min treatment. fEPSP were blocked by the effective dose of mannitol for morphological recovery, but the effects found to be reversible. Although we failed to find positive rescuing effects of mannitol on the synaptic activities after ischemia, the protective effects of the drug on ischemic edema may rescue the secondary damages around the infarct area.
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PMID:Effects of mannitol on ischemia-induced degeneration in rat hippocampus. 1527 10

We used near-infrared spectroscopic (NIRS) imaging to assess the flow-dependence of both myocardial oxygenation and distribution of an intravascular tracer, indocyanine green (ICG). In open-chest pigs, nominal flow through the left anterior descending artery was reduced for 90 to 0 min (n = 6), 20 +/- 1 (n = 5) and 44% +/- 5% (n = 4) by variable occlusion and subsequently restored (to 219% +/- 71% at 45 min) for 120 min. Electrocardiogram-gated NIRS images of the heart were obtained using a CCD-array camera with a liquid crystal tunable filter, which acquired absorbance spectra in the range of 650-1050 nm for each of 256 x 256 pixels (0.4 x 0.4 mm each). Deoxy- and oxy-(hemoglobin (Hb) + myoglobin (Mb)) levels were determined independently by applying a spectral fitting algorithm to the spectra between 650 and 890 nm. Maps for oxygenation parameter (OP = oxy-(Hb + Mb)/deoxy-(Hb + Mb)) and oxygen saturation parameter (OSP) (oxy-(Hb + Mb)/total-(Hb + Mb)) were constructed. To visualize flow distribution, a bolus of ICG (8.3 mg/5 ml) was injected I.V. at each step of the protocol and gated images were acquired at 800 nm every second over 60 s period. The ratio of ICG wash-in velocity to equilibrium absorbance (V/DeltaA(tail)) was calculated. Changes in flow to 0%, 20%, 44%, 100% and 208% of baseline resulted in OP values of 1.46 +/- 0.25, 1.66 +/- 0.30, 2.22 +/- 0.45, 2.78 +/- 0.30 and 3.94 +/- 0.33 in the affected area. Flow rates of 20%, 44%, 100% and 220% of baseline corresponded to V/DeltaA(tail) values of 0.11 +/- 0.11, 0.39 +/- 0.13, 0.54 +/- 0.17 and 0.61 +/- 0.20, respectively. Thus, measurements of oxygenation and normalized ICG wash-in velocity correlated well with coronary flow, allowing for intraoperative optical assessment of the severity of regional ischemia.
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PMID:Mapping regional oxygenation and flow in pig hearts in vivo using near-infrared spectroscopic imaging. 1552 72

Generation of reactive oxygen species (ROS) and their detrimental effects on the brain after transient ischemia are widely recognized. We studied ROS production from mitochondria in human brain microvessel endothelial cells (HBEC) under chemical hypoxia. HBEC in confluent conditions were incubated for 30 min with 10 microM 5-(and-6)-carboxy-2',7'-dichlorodihydrofluorescein (DCF) diacetate, which was hydrolyzed and trapped inside the cells. ROS were measured with a fluorescent microscope, a CCD camera and an image analyzing system. Injury to mitochondrial respiratory chain was induced either with rotenone (an inhibitor of mitochondrial complex I) or with m-chlorocarbonyl cyanide phenylhydrazone (CCCP) (an uncoupler of ATP synthetase). Shortly after application of 10 microM rotenone, fluorescent intensity started to increase and the gradual increase continued for 10 min. Similarly, CCCP (10, 50 and 100 microM) dose-dependently increased the fluorescent intensity (p<0.01). Edaravone, a free radical scavenger widely used for treatment of cerebral infarction in Japan, at 100 microM successfully suppressed this ROS production (p<0.05). These data show that chemical hypoxia with normal concentration of oxygen in the medium induced free radicals generation in HBEC. Importance of endothelial mitochondria as a source of free radicals after reperfusion is suggested.
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PMID:Reactive oxygen species generated by mitochondrial injury in human brain microvessel endothelial cells. 1654 32

Rho-kinase modulates calcium sensitivity of the myosin light chain in smooth muscle cells and has been implicated as playing a pathogenetic role in cardiovascular disorders. This paper was aimed to determine whether hydroxyfasudil (a specific Rho-kinase inhibitor) exerts cardioprotective effect on coronary ischemia-reperfusion (I/R) injury, and if so, whether NO is involved. Canine subepicardial small arteries (diameter > or = 100 microm) and arterioles (diameter < 100 microm) were observed by a CCD intravital microscope during coronary I/R. Coronary vascular responses to endothelium-dependent (acetylcholine) and -independent (papaverine) vasodilators were examined after I/R under three conditions: control, preconditioning, and hydroxyfasudil. Coronary I/R significantly impaired coronary vasodilation to acetylcholine, whereas hydroxyfasudil completely preserved the responses, as did preconditioning. Hydroxyfasudil also significantly reduced myocardial infarct size. These results indicated that hydroxyfasudil exerts cardioprotective effects on coronary I/R injury in vivo, for which NO-mediated mechanism may be involved.
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PMID:Cardioprotective effect of hydroxyfasudil as a specific Rho-kinase inhibitor, on ischemia-reperfusion injury in canine coronary microvessels in vivo. 1654 34

Ischaemia, loss of neural tissue, glial cell activation and tissue remodelling are symptoms of anterior ischaemic as well as glaucomatous optic neuropathy leading to pallor of the optic nerve head. Here, we describe a simple method for the pallor measurement using a fundus camera equipped with a colour CCD camera and a special dual bandpass filter. The reproducibility of the determined mean pallor value was 11.7% (coefficient of variation for repeated measurements in the same subject); the variation over six healthy subjects was 14.8%. A significant difference between the mean pallor of an atrophic disc and that of the contralateral eye of the same individual was found. However, even the clinically unaffected eye showed a significantly increased pallor compared to the mean of the healthy control group. Thus, optic disc pallor measurement, as described here, may be helpful in the early detection and follow-up of optic neuropathy.
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PMID:Quantitative assessment of optic nerve head pallor. 1835 44


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