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Titolo:
Regional dependence of cerebral reperfusion after circulatory arrest in rats
Autore:
Liachenko, S; Tang, P; Hamilton, RL; Xu, Y;
Indirizzi:
Univ Pittsburgh, Sch Med, Dept Anesthesiol & Crit Care Med, Pittsburgh, PA15261 USA Univ Pittsburgh Pittsburgh PA USA 15261 Care Med, Pittsburgh, PA15261 USA Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15261 USA Univ Pittsburgh Pittsburgh PA USA 15261 armacol, Pittsburgh, PA 15261 USA Univ Pittsburgh, Sch Med, Dept Neuropathol, Pittsburgh, PA 15261 USA Univ Pittsburgh Pittsburgh PA USA 15261 opathol, Pittsburgh, PA 15261 USA
Titolo Testata:
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
fascicolo: 11, volume: 21, anno: 2001,
pagine: 1320 - 1329
SICI:
0271-678X(200111)21:11<1320:RDOCRA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC-ARREST; BLOOD-FLOW; GLOBAL-ISCHEMIA; CARDIOPLEGIC ARREST; ARTERIAL WATER; BETA-BLOCKADE; NITRIC-OXIDE; BRAIN; RECOVERY; RESUSCITATION;
Keywords:
cerebral blood flow; global ischemia; heart arrest; magnetic resonance imaging; reperfusion; resuscitation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Xu, Y Univ Pittsburgh, Sch Med, Dept Anesthesiol & Crit Care Med, W-1358 Biomed Sci Tower, Pittsburgh, PA 15261 USA Univ Pittsburgh W-1358 Biomed SciTower Pittsburgh PA USA 15261 USA
Citazione:
S. Liachenko et al., "Regional dependence of cerebral reperfusion after circulatory arrest in rats", J CEREBR B, 21(11), 2001, pp. 1320-1329

Abstract

The severity of neurologic dysfunction after circulatory arrest depends oncerebral reperfusion during and after resuscitation. The objective of cur-rent study was to investigate the temporal and spatial patterns of the cerebral perfusion immediately after resuscitation. Precise control of circulatory arrest was achieved in rats by combination of asphyxia and transient blockage of cardiac-specific P-adrenergic receptors with esmolol, an ultra-short-acting P-blocker. Animals were randomized into 3 groups with resuscitation starting 0.5 (sham group, no asphyxia, n = 5), 4 (Group 2, n = 5), or 12 minutes (Group 3, n = 8) later by retrograde intraarterial infusion of donor blood along with a resuscitation mixture. Cerebral perfusion was measured by magnetic resonance imaging (MRI) using arterial spin labeling. The average perfusion before arrest was 163 +/- 27 mL 100 g(-1) min(-1) under isoflurane anesthesia. Resuscitation led to transient perfusion increase, which started from thalamus and hypothalamus and later shifted to the cortex. Severe hypoperfusion to as low as 6% to 20% of the normal level developed inthe first 10 to 20 minutes of reperfusion and lasted for at least 2 hours,On the fifth day after circulatory arrest, all animals showed a normal level of perfusion (159 +/- 57 mL 100 g(-1) min(-1)) and minimal neurologic deficit. Nevertheless, histologic examination revealed extensive changes in the CAI region of the hippocampus consistent with global ischemia and reperfusion damage. The combination of an improved circulatory arrest model and noninvasive MRI cerebral perfusion measurements provides a powerful tool forinvestigations of circulatory arrest and resuscitation, allowing for evaluation of therapies aimed at modulating cerebral reperfusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/10/20 alle ore 09:43:30