Postischemic recovery from brain edema and of protein synthesis was examined following 1 h of middle cerebral artery (MCA) occlusion in rats. Recovery from brain edema and of protein synthesis showed a good correlation until 7 days after reperfusion in each area (cerebral cortex or lateral caudate) in the occluded MCA side. However, regional differences in the above types of recovery in the cortex and in the lateral caudate were found for the first time in this experiment. A profound inhibition of protein synthesis and formation of brain edema began sooner in the lateral caudate than in the cortex and continued long after reperfusion. Grades of cerebral blood flow during ischemia and the early period of reperfusion were almost the same in the two regions. Therefore, the regional differences in the above recoveries may not be due to the difference in the blood flow during ischemia and reperfusion, but may be partly attributable to the imbalance of excitatory and inhibitory innervation in the above two areas of the brain, may be due to a distinctive response to ischemic stress, and may be caused also by the potentiative effect of free arachidonate on the excitotoxic mechanism. 相似文献
Exact physiological mechanisms behind the potential positive treatment effects of pathological tissue swelling (edema), such as increased interstitial fluid flow, are poorly understood. Finite-element model was created and the model response was matched with the deformation data from the negative pressure (suction) measurements in human (N = 11) forearm. Two experimental suction protocols were simulated to evaluate their impact on interstitial fluid flow in soft tissues. Simulated continuous suction was up to 27 times more efficient in fluid transportation compared to the cyclic suction. The continuous suction that transports the interstitial fluid effectively may help to decrease soft tissue edema. 相似文献
Regional cerebral metabolite concentrations, principally of choline-containing compounds (Cho), total creatine (Cr), N-acetylaspartate
(Naa), and lactate (Lac), can be quantified by in vivo proton magnetic resonance spectroscopy. In order to estimate a metabolite
concentration, it is often necessary to measure the transverse relaxation time (T2). Metabolite T2s depend on cytosolic viscosity: as [adenosine triphosphate] falls leading to Na+/K+ pump failure, cytosolic water increases and T2s lengthen. In central grey-matter in human infants, Naa may be almost exclusively neuronal: Naa T2 may index neuronal edema and energy generation. In this preliminary report, metabolite concentrations and T2s have been measured in central grey matter in human infants suspected of perinatal hypoxic-ischemic cerebral injury. In infants
who developed serious cerebral injury or died, [Cho] and [Naa] were low (the latter suggesting neuronal loss), [Lac] and all
metabolite T2s were increased: the Naa T2 increase possibly reflected neuronal edema following failure of energy generation in a fraction of remaining neurons.
Special issue dedicated to Dr. Herman Bachelard. 相似文献
Resolution of inflammation is an emerging new strategy to reduce damage following ischemic stroke. Lipoxin A4 (LXA4) is an anti‐inflammatory, pro‐resolution lipid mediator with high affinity binding to ALX, the lipoxin A4 receptor. Since LXA4 is rapidly inactivated, potent analogs have been created, including the ALX agonist BML‐111. We hypothesized that post‐ischemic intravenous administration of BML‐111 would provide protection to the neurovascular unit and reduce neuroinflammation in a rat stroke model. Animals were subjected to 90 min of middle cerebral artery occlusion (MCAO) and BML‐111 was injected 100 min and 24 h after stroke onset and animals euthanized at 48 h. Post‐ischemic treatment with BML‐111 significantly reduced infarct size, decreased vasogenic edema, protected against blood–brain barrier disruption, and reduced hemorrhagic transformation. Matrix metalloproteinase‐9 and matrix metalloproteinase‐3 were significantly reduced following BML‐111 treatment. Administration of BML‐111 dramatically decreased microglial activation, as seen with CD68, and neutrophil infiltration and recruitment, as assessed by levels of myeloperoxidase and intracellular adhesion molecule‐1. The tight junction protein zona occludens‐1 was protected from degradation following treatment with BML‐111. These results indicate that post‐ischemic activation of ALX has pro‐resolution effects that limit the inflammatory damage in the cerebral cortex and helps maintain blood–brain barrier integrity after ischemic stroke.
The aim of the present work is to develop a non-destructive, non-invasive technique for the early diagnosis of an oncoming brain edema based on the variation of vibration characteristics of the head system (i.e. eigenfrequency spectrum and modal damping). Besides the theoretical model that supports the basic principle, the proposed technique has been verified experimentally in animal tests. The advantage of such an approach is that the relative information is available well in advance an increase of intracranial pressure is detected. The uncontrolled intracranial hypertension is associated with increased mortality or vegetative state in head trauma. Traumatic lesions located on temporal lobe render particularly impeding the transtendorial herniation. From the medical point of view, intracranial pressure (ICP) monitoring represents an effective way for early consideration of neurological decompensation in various neurosurgical conditions particularly in the head-injured setting. However, the use of ICP monitoring is not an effective way of brain edema detection, since ICP increase very often causes irreversible problems to the patient's brain. Therefore, the determination of an earlier, less invasive and more sensitive indicator of the oncoming intracranial hypertension and of the impeding neurological deterioration is of profound importance.
The present work aims at experimental verification of both eigenfrequency shifting and modal damping increase of the spectral response of the head system of rabbits, wherever a mass increase in the content of cranial shell appears. The conducted analysis concludes that the eigenfrequency spectrum and its modal damping characteristics are sufficiently sensitive parameters in order to characterize mass increase in the cranial shell.
Therefore the combination of both the above parameters could be used with confidence for the early diagnosis of brain edema. 相似文献
Cysteinyl leukotrienes (including LTC(4), LTD(4), and LTE(4)), potent inflammatory mediators, can induce brain-blood barrier (BBB) disruption and brain edema. These reactions are mediated by their receptors, CysLT(1) and CysLT(2) receptors. On the other hand, aquaporin 4 (AQP4) primarily modulates brain water homeostasis and edema after various injuries. Here, we aimed to determine whether AQP4 is involved in LTD(4)-induced brain edema. LTD(4) (1ng in 0.5mul PBS) microinjection into the cortex increased endogenous IgG exudation (BBB disruption) and water content (brain edema), and enhanced AQP4 expression in mouse brain. The selective CysLT(1) receptor antagonist pranlukast inhibited the IgG exudation, but not the increased water content and AQP4 expression induced by LTD(4). In the cultured rat astrocytes, LTD(4) (10(-9)-10(-7)M, for 24h) similarly enhanced AQP4 expression. The enhanced AQP4 expression was inhibited by Bay u9773, a non-selective CysLT(1)/CysLT(2) receptor antagonist, but not by pranlukast. LTD(4) (10(-9)-10(-7)M) also induced the mRNA expression of CysLT(2) (not CysLT(1)) receptor in astrocytes. These results indicate that LTD(4) modulates brain edema; CysLT(1) receptor mediates vasogenic edema while CysLT(2) receptor may mediate cytotoxic edema via up-regulating AQP4 expression. 相似文献
The antiinflammatory effect of low-intensity extremely-high-frequency electromagnetic radiation (EHF EMR, 42.0 GHz, 0.1 mW/cm2) was studied in comparison to the effects of the antiinflammatory drug sodium diclofenac and the antihistamine clemastine in acute inflammatory reaction in mice of NMRI outbred stock. The local inflammatory reaction was induced by intraplantar injection of zymosan to the left hind paw. Intraperitoneal injections of 2, 3, 5, 10, and 20 mg/kg of sodium diclofenac or 0.02, 0.1, 0.2, 0.4, and 0.6 mg/kg of clemastine were made 30 min after the initiation of inflammation. An hour after the initiation of inflammation, animals were whole-body exposed to EHF EMR for 20 min. The inflammatory reaction was assessed 3–8 h after initiation by measuring the footpad edema and hyperthermia of the inflamed paw. Sodium diclofenac (5–20 mg/kg) reduced the exudative edema by ~26% compared to the control. Hyperthermia of the inflamed paw decreased by 60% with an increase in the diclofenac dose to 20 mg/kg. EHF EMR reduced both the footpad edema and hyperthermia by ~20%. This was comparable to the effect of a single therapeutic dose of diclofenac (3–5 mg/kg). The combination of diclofenac and exposure to EHF EMR produced a partial additive effect. Clemastine (0.02–0.4 mg/kg) did not affect the exudative edema, but at a dose of 0.6 mg/kg, edema was reduced by 14–22% five to eight hours after zymosan injection. Clemastine caused a dose-dependent increase in hyperthermia of inflamed paw at doses 0.02–0.2 mg/kg and did not affect the hyperthermia at doses 0.4 and 0.6 mg/kg. A combination of clemastine and EHF EMR exposure resulted in a dose-dependent abolishment of the antiinflammatory effect of EHF EMR. Our results suggest that both arachidonic acid metabolites and histamine are involved in the achievement of the antiinflammatory effects of low-intensity EHF EMR. 相似文献