Abstract:-Objective: to evaluate the neuroprotective effect of mild hypothermia during temporary focal ischemia in cats. Method: 20 cats underwent middle cerebral artery 60 minutes occlusion and 24 hours reperfusion: 10 under normothermia and 10 under mild hypothermia (32º c). Brain coronal sections 2mm thick were stained with 2,3,5-triphenyltetrazolium hydrochloride, photographed and evaluated with software for volume calculation. Results: cortical ischemia was found in 7 and basal ganglia ischemia in 8 animals of gro… Show more
“…This model therefore leads to a focal ischemic insult, followed by reperfusion injury affecting neuronal populations in specific arterial territories. In contrast to the limited and inconsistent beneficial results seen with permanent MCA occlusion, moderate hypothermia has been shown to be protective in several models of transient MCA occlusion when initiated immediately (Ridenour et al, 1992;Zhang et al, 1993;Huh et al, 2000;Nakano et al, 2007) or in a delayed fashion after occlusion (Karibe et al, 1994;Maier et al, 1998;Corbett et al, 2000). Morikawa et al (1992) demonstrated that selective brain hypothermia (308C) during a period of 2 h of reversible MCA occlusion reduced infarct volume.…”
For the past 20 years, various laboratories throughout the world have shown that mild to moderate levels of hypothermia lead to neuroprotection and improved functional outcome in various models of brain and spinal cord injury (SCI). Although the potential neuroprotective effects of profound hypothermia during and following central nervous system (CNS) injury have long been recognized, more recent studies have described clinically feasible strategies for protecting the brain and spinal cord using hypothermia following a variety of CNS insults. In some cases, only a one or two degree decrease in brain or core temperature can be effective in protecting the CNS from injury. Alternatively, raising brain temperature only a couple of degrees above normothermia levels worsens outcome in a variety of injury models. Based on these data, resurgence has occurred in the potential use of therapeutic hypothermia in experimental and clinical settings. The study of therapeutic hypothermia is now an international area of investigation with scientists and clinicians from every part of the world contributing to this important, promising therapeutic intervention. This paper reviews the experimental data obtained in animal models of brain and SCI demonstrating the benefits of mild to moderate hypothermia. These studies have provided critical data for the translation of this therapy to the clinical arena. The mechanisms underlying the beneficial effects of mild hypothermia are also summarized.
“…This model therefore leads to a focal ischemic insult, followed by reperfusion injury affecting neuronal populations in specific arterial territories. In contrast to the limited and inconsistent beneficial results seen with permanent MCA occlusion, moderate hypothermia has been shown to be protective in several models of transient MCA occlusion when initiated immediately (Ridenour et al, 1992;Zhang et al, 1993;Huh et al, 2000;Nakano et al, 2007) or in a delayed fashion after occlusion (Karibe et al, 1994;Maier et al, 1998;Corbett et al, 2000). Morikawa et al (1992) demonstrated that selective brain hypothermia (308C) during a period of 2 h of reversible MCA occlusion reduced infarct volume.…”
For the past 20 years, various laboratories throughout the world have shown that mild to moderate levels of hypothermia lead to neuroprotection and improved functional outcome in various models of brain and spinal cord injury (SCI). Although the potential neuroprotective effects of profound hypothermia during and following central nervous system (CNS) injury have long been recognized, more recent studies have described clinically feasible strategies for protecting the brain and spinal cord using hypothermia following a variety of CNS insults. In some cases, only a one or two degree decrease in brain or core temperature can be effective in protecting the CNS from injury. Alternatively, raising brain temperature only a couple of degrees above normothermia levels worsens outcome in a variety of injury models. Based on these data, resurgence has occurred in the potential use of therapeutic hypothermia in experimental and clinical settings. The study of therapeutic hypothermia is now an international area of investigation with scientists and clinicians from every part of the world contributing to this important, promising therapeutic intervention. This paper reviews the experimental data obtained in animal models of brain and SCI demonstrating the benefits of mild to moderate hypothermia. These studies have provided critical data for the translation of this therapy to the clinical arena. The mechanisms underlying the beneficial effects of mild hypothermia are also summarized.
“…Even more, while neuroprotection by deep hypothermia can be explained by a decrease in cerebral blood flow and metabolic demand for oxygen, this by itself cannot fully explain the equal protection that has been shown when the temperature is lowered by only a few degrees, 17 . A high degree of neuroprotection was conferred by postischemic cooling (2h) to 32ºC which is virtually equivalent to that observed with intraischemic cooling at the same level in focal cerebral ischemia4 Nakano et al have demonstrated the neuroprotective effect of mild hypothermia in the temporary brain ischemia in cats 20 . Hypothermia was induced with an ice bag over the chest/abdomen.…”
Section: Discussionmentioning
confidence: 78%
“…Over the last 20 years a large number of studies have demonstrated that mild hypothermia (31-33ºC) can have the same neuroprotective effect provided by deep hypothermia in ischemic brain 1,2,3,5,6,9,14,16,19,20,22,21,28 .…”
Introduction: Less than 30% of Middle Cerebral Artery (MCA) aneurysms are amenable for endovascular coiling. Microvascular surgery still carries a large number of complications, since many perforators arteries arise near to the neck of the aneurysm and, in many cases, one or more branches of bifurcation or trifurcation of the MCA originate in the aneurysm wall. Temporary clipping of the proximal MCA avoids the aneurysmal rupture, facilitates the aneurysm dissection and clip placement but long term temporary clipping carries a great risk of ischemic complications. Objective: We developed a protocol of brain protection based on the neuroprotective properties of mild hypothermia which would intend to permit a more extended time of temporary clipping. Methods: Sixty-eight cases of MCA incidental aneurysms or after the 12nd day of hemorrhage were operated on. Brain temperature was dropped at levels that varied from 29.5ºC at 15mm parenchymal depth to 32.5ºC at ventricular level. There was no change in the patient’s body temperature. Temporary MCA clipping varied from 8 to 28 minutes. Results: There was no intraoperative aneurysm rupture. All 68 patients were alive and neurologically unchanged at the 90th and 180th follow-up days. Conclusion: Loco-regional mild hypothermia may be effective in protecting cerebral parenchyma in cases of temporary clipping over 8 minutes up to 28 minutes in MCA aneurysms surgery.
In recent years, metabolomics analyses have been widely applied to cerebral ischemia research. This paper introduces the latest proceedings of metabolomics research on cerebral ischemia. The main techniques, models, animals, and biomarkers of cerebral ischemia will be discussed. With analysis help from the MBRole website and the KEGG database, the altered metabolites in rat cerebral ischemia were used for metabolic pathway enrichment analyses. Our results identify the main metabolic pathways that are related to cerebral ischemia and further construct a metabolic network. These results will provide useful information for elucidating the pathogenesis of cerebral ischemia, as well as the discovery of cerebral ischemia biomarkers.
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