Post-Ischemic Resuscitation of the Brain: Selective Vulnerability Versus Global Resistance

Ka, Hossmann

doi:10.1016/s0079-6123(08)61971-8

Cited by 64 publications

(27 citation statements)

References 104 publications

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“…The first category of lesions is high incidence of thrombotic vascular occlusions in cliniconsistently produced by brief episodes of flow arrest in all cal stroke has prompted research into thrombolytic therapy models of global ischemia, whereas the manifestation of but previous attempts were of little benefit because imnecrotic lesions outside the vulnerable areas depends not provement of flow was offset by an increased rate of only on the duration, completeness and temperature of hemorrhagic transformation of the ischemic lesion. Only ischemia but also on the state of post-ischemic reperfusion recently, evidence has been provided that a carefully [76]. Therapeutic intervention may, therefore, lead to selected subgroup of patients responds favourably to greatly divergent results in different models of global ischemia, and have to be replicated in relevant disease the size of the thread has to be matched individually to the models to predict their usefulness for the treatment under body weight [65].…”

Section: Models For the Treatment Of Strokementioning

confidence: 99%

Experimental models for the investigation of brain ischemia

Hossmann

1998

Cardiovascular Research

143

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Section: Models For the Treatment Of Strokementioning

confidence: 99%

Experimental models for the investigation of brain ischemia

Hossmann

1998

Cardiovascular Research

143

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“…1 ' 5 Edema may thus compromise cerebral microcirculation and aggravate an ongoing ischemic process, or it may prevent adequate recovery of tissue blood flow during reperfusion. 5 ' 6 In addition, previous as well as more recent studies emphasize the possibility of localized cellular swelling and osmolytic damage of dendrites secondary to the release of glutamate or related excitatory amino acids. 7 -8 Postischemic brain edema has been suggested to be of two main types.…”

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confidence: 99%

Time course of early brain edema following reversible forebrain ischemia in rats.

Mellergård

Bengtsson

Smith

et al. 1989

Stroke

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Cerebral ischemia is known to be accompanied by brain edema. This increase in brain tissue water content probably influences the final outcome of an ischemic insult negatively. Despite extensive investigations on different aspects of brain edema, information on edema development during the early recirculation period following ischemia is sparse. We assessed changes in brain water content, as reflected by changes in tissue density, during the early recirculation period following severe forebrain ischemia. Fasted rats were subjected to 5,15, or 30 minutes of ischemia and 5 to 180 minutes of recirculation. The specific gravity of specimens from the caudoputamen, frontoparietal cortex, hippocampus, and mesencephalon were measured with a Percoll linear density gradient. Five minutes of ischemia followed by recirculation did not produce any significant regional brain edema. Received January 24, 1989; accepted June 23, 1989. cellular edema) is characterized by an intracellular accumulation of water, with or without a concomitant reduction of the extracellular space. 9 Later (on the order of hours) this early edema is followed by a second edema (vasogenic edema) associated with changes in the cerebral blood vessels, permitting leakage of large molecules such as proteins.2 -3 ' 10 ' 11The mechanisms of the two types of edema are still not fully understood. 2 -12 -15 Although much information is available on the pathophysiology of brain edema, only a few studies have explored the time course of edema during the early recirculation period following ischemia. Knowledge of this time course is required to allow better characterization of the mechanisms involved in the formation of edema. Therefore, we measured the time course of cerebral edema in four brain regions during the first 180 minutes of recirculation following severe forebrain ischemia in rats. Materials and MethodsTransient forebrain ischemia was induced in 81 male Wistar rats weighing 350-430 g (M0llegaard's Breeding Center, Copenhagen, Denmark). The rats were fasted overnight but had free access to tap water.

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“…curred can be traced back to the ischemic disrup tion of cellular energy state, and, at least to a first approximation, the density of damage is propor tional to the duration of energy depletion (see, how ever, Hossmann, 1985). Thus, although adverse mechanisms operating during recirculation may contribute to the final damage (see Siesjo, 198 1, 1988a;Siesjo and Wieloch, 1985), it has never been shown that damage affects brain areas whose met abolic state remains unperturbed during the primary insult.…”

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confidence: 99%

Focal and Perifocal Changes in Tissue Energy State during Middle Cerebral Artery Occlusion in Normo- and Hyperglycemic Rats

Folbergrová

Memezawa

Smith

et al. 1992

J Cereb Blood Flow Metab

154

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Summary:The objective of the present study was to as sess changes in cellular energy metabolism in focal and perifocal areas of a stroke lesion and to explore how these changes are modulated by preischemic hyperglycemia. A model for reversible occlusion of the middle cerebral ar tery (MCA) in rats was used to study changes in energy metabolism. Following MCA occlusion for 5, 15, or 30 min in normoglycemic rats, the tissue was frozen in situ, and samples from the lateral caudoputamen and from two neocortical areas were collected for metabolite analyses, together with a control sample from the contralateral, nonischemic hemisphere. Two other groups, subjected to 30 min of MCA occlusion, were made hyperglycemic by acute glucose infusion or by prior injection of streptozo tocin. Enzymatic techniques were used for measurements of phosphocreatine, creatine, ATP, ADP, AMP, glyco gen, glucose, pyruvate, and lactate. The neocortex of the contralateral, nonischemic hemisphere had labile metab olites that were similar to those measured in control an imals. Ipsilateral neocortex bordering the focus, and thus constituting the "penumbra," showed mild to moderate ischemic changes. In the "focus" (lateral caudoputamen plus the overlying neocortex), deterioration of energy state was rapid and relatively extensive (ATP content 20-There is little doubt that ischemia causes brain damage by disrupting or straining cellular energy metabolism (e.g., Siesjo, 1988a 2540% of control). After 5 min of occlusion, no further de terioration of metabolic parameters was observed. Sub strate levels were markedly reduced, and lactate content rose to � 10 mM kg -1. In the animals with the most se vere energy depletion, no additional accumulation of lac tate occurred, suggesting substrate depletion. This was confirmed by the results obtained in the hyperglycemic subjects whose tissue lactate contents rose to � 20 rnM kg -1. However, the energy state of the focus was better preserved in both hyperglycemic groups as compared with the normoglycemic group. It has been shown, in this model, that relatively brief occlusion periods are required to induce infarction. The present results demonstrate that this can occur in spite of the absence of pronounced de pletion of energy reserves. After 30 min of MCA occlu sion, infarction developed in the lateral caudoputamen, but not in the neocortex. Since a similar perturbation in metabolic state was demonstrated here, other factors must contribute to the degree of tissue damage. The present results suggest that damage is exaggerated by hy perglycemia because it allows additional lactate to accu mulate in the partially substrate-depleted tissue. Key Words: Ce rebral ischemia-Energy metabolites Hyperglycemia-Middle cerebral artery occlusion. curred can be traced back to the ischemic disrup tion of cellular energy state, and, at least to a first approximation, the density of damage is propor tional to the duration of energy depletion (see, how ever, Hossmann, 1985). Thus, although adverse mechanisms operating duri...

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Post-Ischemic Resuscitation of the Brain: Selective Vulnerability Versus Global Resistance

Cited by 64 publications

References 104 publications

Experimental models for the investigation of brain ischemia

Experimental models for the investigation of brain ischemia

Time course of early brain edema following reversible forebrain ischemia in rats.

Focal and Perifocal Changes in Tissue Energy State during Middle Cerebral Artery Occlusion in Normo- and Hyperglycemic Rats

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