Attenuation of Ischemic Brain EDEMA and Cerebrovascular Injury after Ischemic Preconditioning in the Rat

Masada, Tetsuya; Hua, Ya; Xi, Guohua; Ennis, Steven R.; Keep, Richard F.

doi:10.1097/00004647-200101000-00004

Cited by 112 publications

(85 citation statements)

References 42 publications

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“…Atropine and vagotomy blocked this promotion caused by intravenous injection of ghrelin. Masada et al (2001) reported that ghrelin regulates gastric kinetics via neuropeptide-Y1 receptor and nonselective corticotropin releasing factor receptor-1 in the paraventricular nucleus (Tebbe et al, 2005). Ghrelin is regulated by nutritional and hormonal factors.…”

Section: Serum Ghrelin and Small Intestinal Motilitymentioning

confidence: 99%

“…The concomitant effect causes decrease in enteric motility, and the increase of serum ghrelin is compensatory. Previous studies showed that once the middle cerebral artery was blocked for 15 min, heat shock protein 70 (HSP70) can be greatly synthesized to prevent ischemic brain edema and cerebrovascular damage in rats (Masada et al, 2001). We proposed that increased ghrelin may be released from the gut or the central nerve system such as thalamencephalon, pituitary, and hippocampus.…”

Section: Serum Ghrelin and Small Intestinal Motilitymentioning

confidence: 99%

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Changes in Serum Ghrelin and Small Intestinal Motility in Rats with Ischemic Stroke

Zhu

Chuai

2011

The Anatomical Record

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Ischemic stroke occurs as a result of an obstruction within a blood vessel supplying blood to the brain. Gastrointestinal mucosal damage not only induces local and systemic inflammatory reactions but may also result in multiple organ dysfunction syndrome. We studied whether the changes in serum ghrelin and small intestinal motility occur in cerebral ischemia. The focal cerebral ischemia rat models were produced by the middle cerebral artery occlusion (MCAO) method. The MCAO group was further equally divided into five subgroups at 3, 6, 12, 24, and 48 hr, and the sham operated rats were used as controls. Serum ghrelin level was analyzed using enzyme-linked immunosorbent assay, and small intestinal motility was measured by methylene blue staining. The ileum tissue was examined by light and electron microscopy. The neurologic scores were 0 for all the rats in the control group and 2-3 for those in the MCAO group, suggesting that rat models were established successfully. The serum ghrelin level was higher in the MCAO group when compared with the control group (P < 0.05). However, the impelling force in MCAO rats was significantly lower than that of the control group (P < 0.05), reaching the lowest level at 24 hr. Damage to the intestinal mucosa, including villus intestinalis, vacuolar degeneration of organelles, widened cell-cell junctions, and apoptotic cells could be found under the light and electron microscopy. Our results showed that higher level of serum ghrelin decreased gastrointestinal motility and damage to the intestinal mucosa existed in rats with MCAO. Anat Rec, 295:307-312, 2012. V V C 2011 Wiley Periodicals, Inc.

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Section: Serum Ghrelin and Small Intestinal Motilitymentioning

confidence: 99%

Section: Serum Ghrelin and Small Intestinal Motilitymentioning

confidence: 99%

Changes in Serum Ghrelin and Small Intestinal Motility in Rats with Ischemic Stroke

Zhu

Chuai

2011

The Anatomical Record

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“…Brains were rapidly removed and the cortex ipsi-and contralateral to the MCA occlusion was sampled as described previously (Masada et al, 2001). In brief, the hemisphere was divided, and the brain stem, hippocampus, cerebellum, and thalamus were removed.…”

Section: Blood-brain Barrier Disruptionmentioning

confidence: 99%

Effect of Sustained-Mild and Transient-Severe Hyperglycemia on Ischemia-Induced Blood–Brain Barrier Opening

Ennis

Keep

2007

J Cereb Blood Flow Metab

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The purpose of this study was to examine what levels of hyperglycemia cause blood-brain barrier (BBB) disruption during permanent and transient middle cerebral artery occlusion in the rat and when the adverse effects of hyperglycemia occur. Cerebrovascular function was assessed by measuring the influx rate constant (K i ) for 3 H-inulin and by measuring cerebral plasma ( 14 C-inulin) and 51 Cr-labeled red blood cell (RBC) volume. Different glucose protocols were used to produce mild sustained hyperglycemia (blood glucose B150 mg/dL) or transient-severe hyperglycemia (with a spike in blood glucose of B400 mg/dL). As expected, transient-severe hyperglycemia at the time of occlusion induced marked BBB disruption in animals undergoing 2 h of ischemia with 2 h of reperfusion (25-fold increase in permeability compared with the contralateral core). However, the mild hyperglycemia model induced similar disruption. Similarly, after permanent occlusion, both hyperglycemia models enhanced disruption and they both produced marked (B50%) reductions in cerebral plasma volume. Apparent cerebral RBC volume also decreased when measured during the final 5 mins of 2 h of ischemia with transient-severe hyperglycemia. However, there was no decrease if the 51 Cr-labeled RBCs were circulated for the whole 2 h, indicating RBC trapping. The spike in blood glucose in the severe hyperglycemia model was used to examine when hyperglycemia induced BBB disruption. Hyperglycemia shortly after occlusion caused severe disruption. In contrast, hyperglycemia after 90 mins of occlusion caused little disruption. These results suggest that mild hyperglycemia has a profound effect on BBB function and that very early correction of hyperglycemia is necessary to prevent adverse effects.

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“…HSP-70 also increases the levels of anti-apoptotic proteins, Bcl-2 and Bcl-xL, thus serving as another mechanism to increase the anti:pro apoptotic ratio and push neurons toward cellular survival, especially in the setting of ischemia/reperfusion (Liebelt et al, 2010;Ohtsuka and Suzuki, 2000). Multiple studies have shown that ischemic preconditioning induces HSP-70 expression and promotes neuroprotection (Chen and Simon, 1997;Kirino et al, 1991;Masada et al, 2001). Despite these benefits, the effects of HSP-70 are limited.…”

Section: Heat Shock Proteinsmentioning

confidence: 99%

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Dornbos¹,

Ding²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia -Reperfusion Injury 301 neuroprotection after exercise has stopped.Another study revealed that the neuroprotective effects of exercise preconditioning appear to be long-lasting, showing that 3 weeks after cessation of exercise, rats still maintained lower levels of neurologic deficit and decreased stroke volume when compared to non-exercise rats (Ding et al., 2004b). Future human studies ought to determine the exact duration needed for maximal endogenous neuroprotection. Preconditioning modalitiesWhile various modalities, such as treadmill running, voluntary running, simple and complex exercise, have been shown to provide variable amounts of neuroprotection. When comparing forced exercise on a treadmill to voluntary running on a running wheel, rats forced to exercise on a treadmill tend to have better neurologic outcomes after stroke (Hayes et al., 2008). Previous studies have shown that forced exercise on a treadmill is slower but more constant than voluntary exercise occurs in shorter spurts with faster speed, although the total distance is equal in the two groups (Noble et al., 1999). This neuroprotection in forced exercise subjects led to decreased stroke volume, lessened neurologic deficit, upregulation of heat shock proteins, increased neurogenesis and cerebral metabolism (Hayes et al., 2008;Kinni et al., 2011;Leasure and Jones, 2008). These findings show that moderate exercise over a longer time period conveys more efficient and greater neuroprotection than more vigorous exercise over shorter time periods. In addition to the studies assessing forced and voluntary exercise, differences have also been established when comparing simple and complex exercise. This study analyzed simple exercise as the repetitive movements of treadmill running, whereas complex exercise constituted enriched activities which required both balance and coordination (Ding et al., 2003). Following ischemia/reperfusion injury, rats preconditioned with complex exercise demonstrated increased synaptogenesis and improved neurologic outcomes when compared to simple treadmill exercise (Ding et al., 2003;Jones et al., 1999). Simple exercise training also alleviates much of the injury following ischemia/reperfusion, but its benefit is less pronounced than what is observed with complex exercise training. Although no human studies have definitively shown the most effective means of exercise for enhanced neuroprotection, these animal studies provide a solid framework for the development of appropriate exercise regimens. Moderate exercise intensity, including components of balance, coordination and stress, taking place over a sustained duration seem to be the most neuroprotective when compared to other exercise modalities and intensities.

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Attenuation of Ischemic Brain EDEMA and Cerebrovascular Injury after Ischemic Preconditioning in the Rat

Cited by 112 publications

References 42 publications

Changes in Serum Ghrelin and Small Intestinal Motility in Rats with Ischemic Stroke

Changes in Serum Ghrelin and Small Intestinal Motility in Rats with Ischemic Stroke

Effect of Sustained-Mild and Transient-Severe Hyperglycemia on Ischemia-Induced Blood–Brain Barrier Opening

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

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