The Cortical Ischaemic Penumbra Associated with Occlusion of the Middle Cerebral Artery in the Cat: 1. Topography of Changes in Blood Flow, Potassium Ion Activity, and EEG

pH and K+ from the extracellular space, PO2, and CBF have been measured in the same region during progressive ischaemia of primate cerebral cortex. As blood flow was reduced, the other changes had the following sequence. PO2 fell rapidly to 30% of control levels at regional CBF (rCBF) of 30 ml 100 g−1 min−1. As CBF was further reduced, PO2 continued to fall. pH remained stable until around 20 ml 100 g−1 min−1, below which pH fell rapidly, with an exponential increase in H+ concentration. K+ showed the well-known relationship to CBF, remaining normal until around 10 ml 100 g−1 min−1, below which K+ rose rapidly. pHe and log K+ were linearly related and confirmed that pH fell by 0.3 U before K+ rose significantly, and fell by 0.6 U before the massive rise in K+. The mechanisms involved in this sequence of events and the role of pH changes in the development of the so-called “ischaemic penumbra” are discussed.

Section: Discussionsupporting

confidence: 87%

pH, K⁺, and PO₂ of the Extracellular Space during Ischaemia of Primate Cerebral Cortex

Harris

Richards

Symon

et al. 1987

“…Initial experience with the cat MCAO model of stroke indicated that in the majority of experiments the suprasylvian gyrus lies within the core from an early stage (Strong et al, 1983). This was confirmed in a pilot experiment for this series, in which microdialysate glucose concentration fell over some 5 mins to unrecordable levels soon after MCAO.…”

Section: Selection Of the Marginal Gyrus For Probe Locationsupporting

confidence: 63%

“…This was confirmed in a pilot experiment for this series, in which microdialysate glucose concentration fell over some 5 mins to unrecordable levels soon after MCAO. We therefore opted to locate the probe in the MG, which is known to lie within penumbra (Strong et al, 1983). There is evidence for diminished vasoreactivity on this gyrus (Strong et al, 1988), and for an appreciable incidence of PIDs there (Strong et al, 1996).…”

Section: Selection Of the Marginal Gyrus For Probe Locationmentioning

confidence: 99%

“…Recurrent, spontaneous depolarisations occur and propagate in the penumbra in a number of species including non-human primates (Branston et al, 1977;Strong et al, 2000), cat (Strong et al, 1983;Saito et al, 1995), and the rat (Nedergaard and Astrup, 1986;Gill et al, 1992;Iijima et al, 1992). These events-periinfarct depolarisations (PIDs)-appear to arise principally at the edge of the core area and spread into the peri-infarct zone (Strong et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Hopwood

Parkin

Bezzina

et al. 2005

114

Peri-infarct depolarisations (PIDs) contribute to infarct expansion in experimental focal ischaemia; furthermore, depolarisations propagate in the injured human brain. Glucose utilisation is increased under both conditions, and depletion of brain glucose carries a poor prognosis. We studied dynamics of cerebral glucose and lactate in relation to PID patterns in experimental stroke. The middle cerebral artery was occluded for 3 h in 23 cats under terminal chloralose anaesthesia. We used fluorescence imaging to detect occurrence of PIDs, and rapid-sampling online microdialysis (rsMD), coupled to a flow-injection assay, to examine changes in cerebral cortical extracellular glucose and lactate at intervals of 30 sec each. After 30 min' ischaemia, lactate had increased by 43.67s.d. 45.9 lmol/L, and stabilised in that range for 3 h. In contrast, glucose fell only slightly initially (11.979.7 lmol/L), but progressively decreased to a reduction of 56.7747.2 lmol/L at 3 h, with no evidence of stabilisation. There was a highly significant inverse relationship of frequency of PIDs with plasma glucose (Po0.001). The results also characterise a metabolic signature for PIDs for possible application in clinical work, and emphasise potential risks in the use of insulin to control plasma glucose in patients with brain injury.

“…Also, transient events occurred at the periphery of the infarct zone after MCAo in rat (Nedergaard and Astrup, 1986;Gill et al, 1992;Iijima et al, 1992) which resemble cortical spreading depression (CSD) (Leao, 1944). Similar events were recorded in other models of focal isch emia (Branston et al, 1977;Harris et aI., 1981;Strong et al, 1983). These CSD-like events were defined by criteria which characterized CSD in nor mal brain including a propagated wave of EEG sup pression, negative shifts in the extracellular direct current potential, large increases in extracellular potassium ion activity ([K + ]0) and decreases in the extracellular activities of Na + , CI-and Ca 2 + (Leao, 1944;Van Harreveld, 1959;Nicholson and Kraig, 1981;Hansen and Zeuthen, 1981;Hansen, 1985).…”

supporting

confidence: 56%

Photothrombotic Infarction Triggers Multiple Episodes of Cortical Spreading Depression in Distant Brain Regions

Dietrich

Feng

Leistra

et al. 1994

105

Summary:The purposes of this study were to determine whether cortical spreading depression occurs outside of the infarct produced by photothrombotic vascular occlu sion, and also the direction of spreading. Focal cerebral thrombotic infarction was produced by irradiating the ex posed skull of anesthetized rats with green light (560 nm) following systemic injection of rose bengal dye. At prox imal sites (-2 mm anterior to the infarct border), tran sient, severe hyperemic episodes (THEs) lasting 1-2 min were intermittently recorded. THE frequency was great est in the first hour and declined over a 3-h period. THEs were accompanied (and usually preceded) by a precipi tous rise in [K +]0 (from -3 to >40 mM) and were asso ciated with increases in local tissue oxygen tension Previous studies have defined marked differences between the consequences of severe focal and glob al cerebral ischemia. During global ischemia, elec trical, ion transport, and oxidative metabolic activ ities cease; this results in declines of creatine phos phate (PCr) and ATP, suppression of synaptic functioning, loss of transmembrane ion gradients, and accumulation of intracellular calcium ion (re view by Siesjo and Bengtsson, 1989).Following the onset of focal brain ischemia in many animal models, similar deteriorative changes ensue in the ischemic core as in tissue subjected to global ischemia (Hillered et al., 1989;Heiss et al.,