The effects of 5-minute ischemia in mongolian gerbils: I. Blood-brain barrier, cerebral blood flow, and local cerebral glucose utilization changes

Suzuki, Ryuta; Yamaguchi, Takekane; Kirino, Takaaki; Orzi, Francesco; Klatzo, Igor

doi:10.1007/bf00691868

Cited by 255 publications

(67 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the present study, the feasibility of serial measurements of regional cerebral perfusion with arterial spin labeling was demonstrated in a feline model of prolonged CA and CPR. During post-CA resuscitation, variations of regional CBF that are consistent with the previously documented change from hyper-to hypoperfusion [6] were reliably monitored both in the cortex and in the basal ganglia. The combination of arterial spin tagging PWI with DWI and localized 1 H-MRS permitted simultaneous monitoring of regional cerebral perfusion and metabolic recovery.…”

Section: Discussionsupporting

confidence: 54%

“…The delayed hypoperfusion syndrome develops after a transient phase of reactive hyperaemia and is associated with a disturbed coupling between blood flow and metabolism [5]. After short periods of cerebral ischaemia post-ischaemic hypoperfusion is present already after 10 min of recirculation [6], and after prolonged global ischaemia the disturbances may last several days [7].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy

et al. 2003

View full text Add to dashboard Cite

Brain recovery after cardiac arrest (CA) was assessed in cats using arterial spin tagging perfusion-weighted imaging (PWI), diffusion-weighted imaging (DWI), and 1 H-spectroscopy ( 1 H-MRS). Cerebral reperfusion and metabolic recovery was monitored in the cortex and in basal ganglia for 6 h after cardiopulmonary resuscitation (CPR). Furthermore, the effects of an hypertonic/ hyperoncotic solution (7.5% NaCl/6% hydroxyl ethyl starch, HES) and a tissue-type plasminogen activator (TPA), applied during CPR, were assessed on brain recovery. CA and CPR were carried out in the MR scanner by remote control. CA for 15 Á/20 min was induced by electrical fibrillation of the heart, followed by CPR using a pneumatic vest. PWI after successful CPR revealed initial cerebral hyperperfusion followed by delayed hypoperfusion. Initial cerebral recirculation was improved after osmotic treatment. Osmotic and thrombolytic therapy were ineffective in ameliorating delayed hypoperfusion. Calculation of the apparent diffusion coefficient (ADC) from DWI demonstrated complete recovery of ion and water homeostasis in all animals. 1 H-MRS measurements of lactate suggested an extended preservation of post-ischaemic anaerobic metabolism after TPA treatment. The combination of noninvasive MR techniques is a powerful tool for the evaluation of therapeutical strategies on circulatory and metabolic cerebral recovery after experimental cerebral ischaemia. # 2003 Elsevier Ireland Ltd. All rights reserved.Keywords: Cardiac arrest; Cardiopulmonary resuscitation; Cerebral blood flow; Magnetic resonance techniques; Hypertonic solutions; Thrombolysis ResumoAvaliou-se a recuperação cerebral de gatos apó s paragem cardíaca (CA)..... com imagens de avaliação da perfusão (PWI) e imagens de avaliação da difusão (DWI) em espectrofotometria 1 H ( 1 H-MRS). A perfusão cerebral foi monitorizada no có rtex e nos gânglios da base durante seis horas a seguir à reanimação cardio-pulmonar (CPR). Avaliaram-se ainda os efeitos de uma solução hiperosmó tica e hiperoncó tica (NaCl hipertó nico 7.5% / hidroxi etil starch HES a 6%) e um activador tecidular do plasminogéneo (TPA), administrado durante a reanimação e avaliado na fase de recuperação. A CA e a RCP foram executadas, por controlo remoto, no scanner da ressonância magnética. A CA foi induzida, por descarga eléctrica, durante 15 Á/20 min, sendo a reanimação feita por colete pneumático. A PWI depois da CPR com sucesso evidenciou uma hiperperfusão cerebral inicial seguida de hipoperfusão. A recirculação cerebral inicial melhorou com a administração da solução osmó tica. O tratamento osmó tico e Abbreviations: ADC, apparent diffusion coefficient of water; ALS, advanced life support; CA, cardiac arrest; CBF, cerebral blood flow; CPR, cardiopulmonary resuscitation; Cr/PCr, creatine Á/phosphocreatine; DWI, diffusion-weighted imaging; HHS, hypertonic Á/hyperoncotic solution; 1 H-MRS, 1 H-proton spectroscopy; PWI, perfusion-weighted imaging; ROSC, return of spontaneous circulation; TPA, tissue-type plasminogen acti...

show abstract

Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy

et al. 2003

View full text Add to dashboard Cite

show abstract

“…, 1987), over 3-18 h (Kozuka et aI., 1989), up to 2 days (Pulsinelli et aI., 1982b;Suzuki et al , 1983). Two factors detract from the merits of these studies: Either they were performed at time points when glucose metabolism could not be assumed to be in a steady state, and hence pre sumably for this reason no quantitative data are provided (Diemer and Siemkowicz, 1980;lzu-miyama et aI., 1987), or no layer-specific data are given (Pulsinelli et aI., 1982b;Kozuka et aI.…”

Section: Discussionmentioning

confidence: 99%

“…They are also supported by semiquantitative data of augmented 2-deoxyglucose uptake in stratum oriens, radiatum, and pyramidale at 4 min of recir culation after a 10-min tourniquet-induced ischemia in the rat (Diemer and Siemkowicz, 1980). In a qual itative assay, Suzuki et al (1983) pointed out that at 10 min of recirculation after 5 min of ischemia in the gerbil, 2-deoxyglucose uptake was increased in the CAl sector, persisting in some animals up to 24 h post ischemia, but dropped below normal control levels at 2 days. Pulsinelli et al (l982b) measured a depression of hippocampal glucose utilization after Values are means ± SO of nine (control) or five (ischemic) rats.…”

Section: Figmentioning

confidence: 99%

Glucose Utilization in Rat Hippocampus after Long-Term Recovery from Ischemia

Beck

Wree

Schleicher

1990

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary:The influence on hippocampal glucose utiliza tion of a transient lO-min forebrain ischemia was quanti fied in male Wi star rats after 2 and 3 weeks as well as after 3 months by application of the [14C]2-deoxyglucose tech nique. Ischemia was induced by occlusion of the carotid arteries and simultaneous lowering of the blood pressure to 40 mm Hg. For identification of the hippocampal ar chitecture, sections were stained for perikarya (cresyl vi olet) and for acetylcholinesterase. The hippocampal re gions clearly showed different responses to the ischemic insult. The necrotic pyramidal cells being almost com pletely removed, significant increases in glucose utiliza tion occurred in most layers of the CAl sector at 2 and 3For over 100 years it has been a well-documented fact that cell populations in the brain do not suc cumb to an ischemic insult uniformly (Sommer, 1880; Bratz, 1899). This concept of selective vulner ability has been addressed in numerous experimen tal studies. Recently, evidence has been presented that accumulation of Ca 2 + on cellular as well as on subcellular levels (Dienel, 1984; Simon et aI., 1984a; Hossmann et aI. , 1985; Sakamoto et aI. , 1986; van Reempts et aI. , 1986; Deshpande et aI., 1987; Dux et aI. , 1987) and excessive excitatory in put due to excitatory amino acids (Benveniste et aI. , 1984; Simon et aI., 1984b; Lodge et aI. , 1986) are interwoven and play a key role in ischemic cell damage. These studies as well as work on postisch emic capillary perfusion (lmdahl and Hossmann, 1986), impaired protein synthesis (Thiel mann et aI., Received November 2, 1989; revised December 12, 1989; ac cepted December 22, 1989. Address correspondence and reprint requests to Dr. T. Beck at Laboratory of Cellular and Molecular Neurobiology, Depart ment of Pathology, Columbia University College of Physicians and Surgeons, 630 W. 168 St., New York, NY 10032, U.S.A.Abbreviations used: NMDA, N-methyl-D-aspartate. 542weeks post ischemia, while widespread reductions pre vailed in all other sectors and the dentate gyrus. At 3 months after the ischemic insult, glucose utilization was reduced in all hippocampal structures including the CAl region. The increases in glucose utilization in the CAl sector are suggested to indicate long-lasting presynaptic hyperexcitation, while the widespread reductions in glu cose utilization demonstrate that neuronal activity is also altered in hippocampal areas that do not show major his tological damage. Key Words: Cerebral ischemia Hippocampus-Local cerebral glucose utilization Long-term recovery.1986), and impaired normalization of pH in the CAl sector (Munekata and Hossmann, 1987) cover a time range that extends up to 7 days post ischemia. The same holds true for the extensive histological work characterizing the temporal profile of isch emic damage in gerbil and rat models of cerebral ischemia (Kirino, 1982; Pulsinelli et aI. , 1982a; Kirino et aI., 1984; Smith et aI., 1984;Schmidt Kastner and Hossmann, 1988), the respective time points ranging from 3 ...

show abstract

“…The kinetics of anticonvulsant drug uptake into the brain during epileptic seizures are markedly dif ferent from those of nonconvulsing patients. Early in status epilepticus BBB opening is likely due to ictal hypertension and increased CBF (Petito et al, 1977;Suzuki et al, 1983;Suzuki et al, 1984) with resultant increased entry of polar anticonvulsants. Hypoxia, a common association of spontaneous seizures, will also open the BBB (Slobody et al, 1957).…”

Section: Discussionmentioning

confidence: 99%

Brain Phenobarbital Uptake during Prolonged Status Epilepticus

Simon

Copeland²,

Benowitz

et al. 1987

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: The brain uptake of phenobarbital during pro longed status epilepticus (3 h) was studied in paralyzed, ventilated sheep. The first 30 min of status epilepticus was characterized by systemic hypertension, increased CBF, increased peripheral vascular resistance, a fall in brain pH, and an elevation in brain lactate concentra tions. Subsequently, hemodynamic factors normalized and brain acidosis persisted. Phenobarbital administered during the early phase of status epilepticus produced higher levels of brain phenobarbital concentration, which was greatest at the earliest sample time (5 min followingThe kinetics of anticonvulsant medications ad ministered during status epilepticus are poorly un derstood. Metabolic perturbations during status epilepticus, e. g. , alteration of blood-brain barrier (BBB) permeability (Petito et aI. , 1977), ictal hy pertension (Johansson et aI. , 1970; Suzuki et aI. , 1984), hypoxia (Suzuki et aI. , 1983), hypercapnia (Johansson and Nilsson, 1977), systemic corticoste roid and catecholamine release (Long and Holaday, 1985), as well as the effect of the drug itself (Jo hansson, 1983) may influence brain uptake of anti convulsants. Recently, the influence of the blood brain pH gradient on brain uptake of the weak acid phenobarbital (Simon et aI. , 1985) and the weak base lidocaine (Simon et aI. , 1982; Simon et aI. , 1984) during bicuculline-induced status epilepticus

show abstract

The effects of 5-minute ischemia in mongolian gerbils: I. Blood-brain barrier, cerebral blood flow, and local cerebral glucose utilization changes

Cited by 255 publications

References 26 publications

Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy

Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy

Glucose Utilization in Rat Hippocampus after Long-Term Recovery from Ischemia

Brain Phenobarbital Uptake during Prolonged Status Epilepticus

Contact Info

Product

Resources

About