Literature DB >> 3961837

Cerebral blood flow and tissue metabolism in experimental cerebral ischemia of spontaneously hypertensive rats with hyper-, normo-, and hypoglycemia.

S Ibayashi, M Fujishima, S Sadoshima, F Yoshida, O Shiokawa, J Ogata, T Omae.   

Abstract

The present study was designed to clarify the effect of blood glucose level on cerebral blood flow and metabolism during and after acute cerebral ischemia induced by bilateral carotid ligation (BCL) in spontaneously hypertensive rats (SHR). Blood glucose levels were varied by intraperitoneal infusion of 50% of glucose (hyperglycemia), insulin with hypertonic saline (hypoglycemia) or hypertonic saline (normoglycemia). Cerebral blood flow (CBF) in the parietal cortex and thalamus was measured by hydrogen clearance technique, and the supratentorial metabolites of the brain frozen in situ were determined by the enzymatic method. In non-ischemic animals, blood glucose levels had no influence on the supratentorial lactate, pyruvate or adenosine triphosphate (ATP) concentrations. In ischemic animals, however, cortical CBF was reduced to less than 1% of the resting value at 3 hours after BCL. However, there were no substantial differences of CBF during and after ischemia among 3 glycemic groups. Cerebral lactate in the ischemic brain greatly increased in hyperglycemia (34.97 +/- 1.29 mmol/kg), moderately in normoglycemia (23.43 +/- 3.13 mmol/kg) and less in hypoglycemia (7.20 +/- 1.54 mmol/kg). In contrast, cerebral ATP decreased in hyperglycemia (0.93 +/- 0.19 mmol/kg) as much as it did in normoglycemia (1.04 +/- 0.25 mmol/kg), while ATP reduction was much greater in hypoglycemia (0.45 +/- 0.05 mmol/kg). At 1-hour recirculation after 3-hour ischemia, ATP tended to increase in all groups of animals, indicating the recovery of energy metabolism. Such metabolic recovery after recirculation was good in hypo- and normoglycemia, and was also evident in hyperglycemia. Our results suggest that hyperglycemia is not necessarily an unfavorable condition in acute incomplete cerebral ischemia.

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Year:  1986        PMID: 3961837     DOI: 10.1161/01.str.17.2.261

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  5 in total

1.  Hypoglycemia prevents increase in lactic acidosis during reperfusion after temporary cerebral ischemia in rats.

Authors:  D Sappey-Marinier; L Chileuitt; M W Weiner; A I Faden; P R Weinstein
Journal:  NMR Biomed       Date:  1995-06       Impact factor: 4.044

2.  Effect of selective brain hypothermia on regional cerebral blood flow and tissue metabolism using brain thermo-regulator in spontaneously hypertensive rats.

Authors:  S Ibayashi; K Takano; H Ooboshi; T Kitazono; S Sadoshima; M Fujishima
Journal:  Neurochem Res       Date:  2000-03       Impact factor: 3.996

3.  Does hyperglycaemia play a role on the outcome of acute ischaemic stroke patients?

Authors:  D Toni; M L Sacchetti; C Argentino; M Gentile; C Cavalletti; M Frontoni; C Fieschi
Journal:  J Neurol       Date:  1992-08       Impact factor: 4.849

4.  Cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma.

Authors:  H Yao; S Sadoshima; Y Nishimura; K Fujii; M Oshima; T Ishitsuka; M Fujishima
Journal:  J Neurol Neurosurg Psychiatry       Date:  1989-03       Impact factor: 10.154

5.  Changes in brain energy metabolism, neurotransmitters, and choline during and after incomplete cerebral ischemia in spontaneously hypertensive rats.

Authors:  M Kozuka
Journal:  Neurochem Res       Date:  1995-01       Impact factor: 3.996

  5 in total

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