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

We exposed adult Rhesus (Macaca mulatta) to a transient global ischemia, which was induced by clipping the innominate and subclavian arteries that originated from the aortic arch. NHP1 received 20-min, while NHP2 and NHP3, were exposed to a 15-min transient global ischemia and were euthanized at day 1 (NHP1), day 5 (NHP2) or day 30 (NHP3) after ischemia, respectively. NHP1 displayed severe paralysis and rigidity, and intermittent convulsions over the next 24 h. Although histological examination of the brain revealed no detectable gross brain damage (i.e., swelling) and only minimal cell loss in the hippocampus, the acute survival time after surgery likely prevented the cerebral ischemia to fully develop and to be morphologically manifested. Nonetheless, the 20-min ischemia might have been too severe and caused a systemic multiple organ collapse that produced the abnormal behavioral symptoms. On the other hand, NHP2 and NHP3 which received 15-min ischemia only exhibited minor hindlimb paralysis. Indeed, by 48 h after ischemia, both animals appeared fully recovered with only fine motor deficits. Immunohistochemical examination revealed that NHP2 and 3, but not NHP1, had a marked neuronal cell loss in the hippocampal region, specifically the cornu Ammonis (CA1) region. The cell loss in these two ischemic NHP hippocampi was further confirmed by direct comparison with a normal Rhesus brain. These findings replicate the brain pathology seen in Japanese macaques exposed to the same ischemia model [T. Tsukada, M. Watanabe, T. Yamashima, Implications of CAD and DNase II in ischemic neuronal necrosis specific for the primate hippocampus, J. Neurochem. 79 (2001) 1196-1206; T. Yamashima, Implication of cysteine proteases calpain, cathepsin and caspase in ischemic neuronal death of primates, Prog. Neurobiol. 62 (2000) 273-295; T. Yamashima, Y. Kohda, K. Tsuchiya, T. Ueno, J. Yamashita, T. Yoshioka, E. Kominami, Inhibition of ischemic hippocampal neuronal death in primates with cathepsin B inhibitor CA-074: a novel strategy for neuroprotection based on calpain-cathepsin hypothesis, Eur. J. Neurosci. 10 (1998) 1723-1733; T. Yamashima, T.C. Saido, M. Takita, A. Miyazawa, J. Yamano, A. Miyakawa, H. Nishijyo, J. Yamashita, S. Kawashima, T. Ono, T. Yoshioka, Transient brain ischemia provokes Ca2+, PIP2 and calpain responses prior to delayed neuronal death in monkeys, Eur. J. Neurosci. 8 (1996) 1932-1944; T. Yamashima, A.B. Tonchey, T. Tsukada, T.C. Saido, S. Imajoh-Ohmi, T. Momoi, E. Kominami, Sustained calpain activation associated with lysosomal rupture executes necrosis of the postischemic CA1 neurons in primates, Hippocampus 13 (2003) 791-800]. The present minimally invasive transient global ischemia model using Rhesus shows many histopathological symptoms seen in human patients who experienced global ischemia, and should allow translational validation of experimental therapeutics for ischemic injury. Additional studies are warranted to reveal behavioral deficits associated with this ischemia model.
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PMID:Hippocampal CA1 cell loss in a non-human primate model of transient global ischemia: a pilot study. 1768 3

The goal of this study was to develop a new model of ischemia-induced seizures in immature rats using injection of vasoconstrictor Endothelin-1 (ET-1) into the brain. ET-1 (10, 20, or 40 pmol) was infused into the left dorsal hippocampus of freely moving Wistar rats 12 (P12) and 25 (P25) days old. Animals were then video/EEG-monitored for 100 min and monitoring was repeated 22 h later. Parameters of electrographic seizures (frequency and mean duration) as well as pattern of their behavioral correlates were evaluated. The pattern of behavioral seizures was used to develop model-specific scoring system. Cresyl violet and Fluoro Jade-B-staining were used to evaluate brain damage. Extension of the lesion was correlated with seizure severity. After ET-1-injection, seizures occurred in 83-100% animals of all age-and-dose groups and persisted for 24 h except P12 rats with 10 pmol. There were no differences in average seizure duration (18-40 s) or seizure frequency (3-7 seizures/100 min) among individual dose-groups. Between the 1st and 2nd observation period, total seizure duration decreased in 71% of P12 and 47% of P25 rats. Electrographic seizure activity was most frequently accompanied by clonus, incidence of more severe convulsions (barrel rolling or generalized clonic seizures) increased with dose of ET-1. Morphologic examination did not reveal any dose-related difference in damage severity, hippocampal damage was however more extensive in P12 compared to P25 animals. Seizure severity correlated positively with severity of the damage in both age groups. Our study presents focal injection of ET-1 into the brain as a new and practical model of ischemia-induced seizures in immature rats.
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PMID:Intrahippocampal injection of endothelin-1: a new model of ischemia-induced seizures in immature rats. 1791 May 75

Mini-ischemia localized into a specific brain area has promoted understanding of the mechanisms underlying brain recovery in stroke. However, the conventional mini-stroke model adopted permanent arterial ligations but lacked controllable reperfusion, which is crucial for the outcome of delayed functional recovery. In this study, we devised a new rat mini-stroke model in which the vascular ligations can be easily reversed to induce targeted reperfusion. Specifically, a flexible ring was incorporated into the conventional small arterial ligations to tighten the ligating loops and facilitate cutting the ligatures for sufficient reperfusion afterwards. The distribution of cerebral blood flow was explored directly through a cranial window using laser speckle contrast imaging. A distinct ischemic core, which well fits the profile of the ligated ring, was bordered by a penumbral zone and then together surrounded by nonischemic tissue immediately after the arterial ligations involving the ring. After cutting the ligatures, post-recanalization hyperperfusion occurred in the previous ischemic core and to a greater extent at 24 h after reperfusion. In contrast, recirculation of common carotid artery in the conventional mini-stroke model hardly altered hypoperfusion status within the ischemic core. Evidence from two kinds of control groups indicated that the ring might produce a compression effect on the underlying cortex and then contribute to the more highly localized infarct that was identified by triphenyltetrazolium chloride staining. Our data suggest that this model provides opportunities for investigating the neurovascular dynamics in acute stroke and rehabilitation, especially with emerging optical imaging techniques.
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PMID:A modified mini-stroke model with region-directed reperfusion in rat cortex. 1807 74

Preeclampsia occurs in 3-14% of pregnancies and is defined by maternal hypertension with proteinurea, generally associated with edema, coagulation abnormalities, and disseminated intravascular coagulation. The conditions can lead to eclampsia, characterized by hyperreflexia and convulsions. Several organs are afflicted by the condition, most importantly the liver and kidneys. The direct cause of preeclampsia is unknown, but the initial events are linked to abnormalities of placentation. This implies abnormalities in trophoblast invasion and in physiological alterations of placental vessels required for adequate perfusion of the placenta, which leads to ischemia. The mechanisms that link the ischemic placenta to endothelial lesions and to stimulation of vasoconstrictors and inhibition of vasodilators are still subject of speculation. The only treatment of preeclampsia is delivery. Lowering of blood pressure and prevention of eclampsia with magnesium sulfate is indicated in severe preeclampsia. Despite numerous studies attempting to elucidate the exact etiopathogenesis of this complex multifactorial disease, prediction or prevention methods of preeclampsia are not available.
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PMID:Preeclampsia: a danger growing in disguise. 1849 5

We explore a method to quantitatively assess the ability of in vivo autofluorescence as a means to quantify the progression of longer periods of renal warm ischemia and reperfusion in a rat model. The method employs in vivo monitoring of tissue autofluorescence arising mainly from NADH as a means to probe the organ's function and response to reperfusion. Clinically relevant conditions are employed that include exposure of the kidney to ischemia on the order of tens of minutes to hours. The temporal profile during the reperfusion phase of the autofluorescence intensity averaged over an area as large as possible was modeled as the product of two independent exponential functions. Time constants were extracted from fits to the experimental data and their average values were found to increase with injury time.
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PMID:Quantification of in vivo autofluorescence dynamics during renal ischemia and reperfusion under 355 nm excitation. 1854 92

The rotating frame longitudinal relaxation magnetic resonance imaging (MRI) contrast, T(1 rho), obtained with on-resonance continuous wave (CW) spin-lock field is a sensitive indicator of tissue changes associated with hyperacute stroke. Here, the rotating frame relaxation concept was extended by acquiring both T(1 rho) and transverse rotating frame (T(2 rho)) MRI data using both CW and adiabatic hyperbolic secant (HSn; n=1, 4, or 8) pulses in a rat stroke model of middle cerebral artery occlusion. The results show differences in the sensitivity of spin-lock T(1 rho) and T(2 rho) MRI to detect hyperacute ischemia. The most sensitive techniques were CW-T(1 rho) and T(1 rho) using HS4 or HS8 pulses. Fitting a two-pool exchange model to the T(1 rho) and T(2 rho) MRI data acquired from the infarcting brain indicated time-dependent increase in free water fraction, decrease in the correlation time of water fraction associated with macromolecules, and increase in the exchange correlation time. These findings are consistent with known pathology in acute stroke, including vasogenic edema, destructive processes, and tissue acidification. Our results show that the sensitivity of the spin-lock MRI contrast in vivo can be modified using different spin-lock preparation blocks, and that physicochemical models of the rotating frame relaxation may provide insight into progression of ischemia in vivo.
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PMID:Quantitative assessment of water pools by T 1 rho and T 2 rho MRI in acute cerebral ischemia of the rat. 1882 34

Eclampsia is characterized by generalized convulsions in pregnant women with hypertension and proteinuria. Little is known about what triggers the convulsions in this syndrome. The prevailing view is that convulsions are caused by cerebral vasospasm and cerebral edema. However, many important clinical findings argue against cerebral edema or hypertensive encephalopathy as the sole causes of convulsions in eclampsia. The utero-placental ischemia causes the release of certain molecules such as neurokinin B, inflammatory cytokines, endothelins, and tissue plasminogen activator. These molecules stimulate excitatory neuronal receptors and alter neuronal excitability, synaptic transmission, and neuronal survival independent of any vascular effects. Highlighting the neuromodulatory and the convulsive effects of each of these molecules which are elevated in pre-eclampsia, offers a new perspective on the mechanisms of convulsions in eclampsia.
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PMID:Mechanisms of convulsions in eclampsia. 1884 Mar 93

We report the clinical-radiological case of a 25 year-old female patient who developed reversible posterior leukoencephalopathy syndrome (RPLS) in the postpartum period, without evidence of preeclampsia-eclampsia or chronic arterial hypertension. RPLS is associated with diverse clinical entities including eclampsia. Ten days after giving birth, the patient presented with clinical symptoms of headache, elevated blood pressure and seizures. Reversible vasogenic oedema affecting the white matter in the posterior regions was the characteristic finding in magnetic resonance imaging (MRI) of the brain. Although the prognosis is favourable, treatment needs to be early and aggressive, with rapid control of the convulsions and arterial hypertension, with the aim of preventing ischemia and cerebral infarct from developing. There is a need to be highly alert and to consider the diagnosis of RPLS in women presenting with convulsions and other neurological symptoms in postpartum.
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PMID:[Posterior reversible leukoencephalopathy in a patient with postpartum eclampsia]. 1884 28

Pre-eclampsia is a pregnancy-associated disease of the second part of the pregnancy, occurring mainly after 20th weeks gestation. The prevalence of hypertension in pregnancy is between 5 to 11% and affects mainly women under 20 years of age. An inadequate invasion of trophoblasts with consequential placental ischemia as a result of insufficiently dilated uterine spiral arteries is thought to be an initial cause in the pathogenesis of pre-eclampsia. The clinical symptoms of pre-eclampsia, such as loss of intravascular volume and edema, are caused by generalized endothelial dysfunction. These symptoms are potentiated by hypertension and reduced colloid osmotic pressure in the plama. The organs being affected by pre-eclampsia are those of the vascular-, hepatic-, renal-, cerebral- and coagulatory systems. The prognosis is much more severe when pre-eclampsia develops very early in the pregnancy. The symptoms include elevated blood pressure (over 140 mmHg systolic, 90 mmHg diastolic) combined with proteinuria. Frequent symptoms are hyperreflexia and edema. The etiology of pre-eclampsia has not been clearly defined. Risk factors/triggers for the development of pre-eclampsia can include chronic hypertension, advanced maternal age at first pregnancy (over 35 y), nephropathy, thrombophilia (heterozygous factor V Leiden mutation, antiphospholipid syndrome, heterozygous prothrombin mutation and homozygous MTHFR), multiple gestation and prior pregnancy with preeclampsia. The incidence of preeclampsia is higher in nulliparous than multiparous women. In many countries pre-eclampsia is still most frequent cause of maternal perinatal mortality. HELLP-Syndrome (haemolysis-elevated liver enzyme- low platelets) is a severe progressive course of this disease. Eclampsia, characterized by generalized tonic-clonic convulsion, is the most dangerous complication of pre-eclampsia, and may develop before or after delivery. This form of pre-eclampsia is associated with higher maternal and fetal mortality. Constant maternal hypertension potentially alter vascular integrity of the placenta with further consequences in fetal blood supply leading to growth restriction or zero growth and subsequently resulting in low birth weight or fetal death. The sooner the disease is detected and confirmed, the better the maternal and fetal prognoses are. This is the reason why it is major importance, together with the employment of preventive measures, to identify patients with risk factors with pre-eclampsia though an adequate screening method, thereby detecting the disease earlier and ensuring better pregnancy outcomes for both mother and child.
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PMID:[Pre-eclampsia screening in first and second trimester]. 1897 29

This prospective study was done to determine the predisposing factors and outcome of stroke in Bangladeshi children. It was carried out in Khulna Medical College Hospital from July 2002 to June 2007. Admitted children with acute neurological deficit attributable to a vascular cause were included in the study. Forty two children were finally diagnosed with stroke; 73.8% were male. Apart from paresis/paralysis in 35 (83.3%) cases, headache/vomiting/convulsion was the presenting problem in 28 (66.7%) cases at the onset. Infection in 17 (40.5%) children and trauma in 11 (26.2%) were the important predisposing factors. CT scan revealed ischemia and hemorrhage in 18 (42.8% and 8 (19.1%) cases, respectively. Twenty two (52.4%) of the children recovered fully and 3 (7.2%) expired.
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PMID:Predisposing factors and outcome of stroke in childhood. 1917 36


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