ISSN:
1435-1420
Keywords:
Key words Deep hypothermic Curculatory arrest – ischemia-reperfusion – rabbits – brain tissue oxygen pressure –cerebral blood flow
;
Schlüsselwörter Tiefe Hypothermie und Kreislaufstillstand – Ischämie-Reperfusion – Kaninchen – Hirngewebesauerstoffpartialdruck – zerebraler Blutfluß
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Description / Table of Contents:
Zusammenfassung In der vorliegenden Studie wurde ein Kaninchenmodell verwendet, um den Einfluß eines 60minütigen Kreislaufstillstandes in tiefer Hypothermie auf die intrakraniellen Veränderungen in der Verfügbarkeit von Sauerstoff im Hirngewebe sowie die Hindurchblutung untersuchen zu können. Mit der Dauer des totalen Kreislaufstillstandes nahm der Hirngewebe-Sauerstoffpartialdruck (ptiO2) kontinuierlich ab. In der Reperfusion und Erwärmung war die zerebrale Reoxygenierung mit subnormalen ptiO2-Werten stark verzögert. Am OP-Ende (nach Reperfusion und Entwöhnung von der EKZ) ergaben sich signifikant verminderte Werte für den ptiO2: 25±4 mmHg vs. Ausgangswert: 38±5 mmHg (p〈0,05) und den zerebralen Blutfluß: 43±8 ml/100 g/min vs. Ausgangswert: 68±11 ml/100 g/min (p〈0,05). Aufgrund der Ergebnisse kann angenommen werden, daß die temporär beeinträchtigte zerebrale Sauerstoffversorgungs- bzw. Utilisationsmöglichkeit mit einhergehender reduzierter Hirndurchblutung an der Pathogenese von neurologischen Störungen nach Operationen in tiefer Hypothermie und Kreislaufstillstand entscheidend beteiligt sein könnte.
Notes:
Summary We evaluated changes in brain tissue oxygen pressure (ptiO2) and global cerebral blood flow (CBF) during cardiopulmonary bypass (CPB) with deep hypothermic circulatory arrest (DHCA) in ten anesthetized New Zealand White rabbits (body weight 2.5±0.5 kg). CBF [hydrogen desaturation (clearance)-technique) and ptiO2 (Licox®-microsensor) right frontoparietal cortex] were determined. After median sternotomy, the animals were placed on CPB (standard roller pump, nonpulsatile, α-stat acid-base management, perfusion flow of 180–200 mL/kg/min, right atrial and aortic cannulation) for induction of DHCA by cooling to 15°C rectal temperature (1°C per minute). Rewarming period was started after 60 minutes of circulatory arrest and the rabbits were weaned from CPB without the use of any inotropic or vasoactive support. Under baseline conditions, ptiO2 was 38±5 mmHg and did not change significantly before DHCA. During DHCA the ptiO2 decreased within 15 minutes to 14±5 mmHg, after 30 minutes to 5±1 mmHg and after 40 minutes to zero. Neither the ptiO2 nor CBF recovered fully following restoration of bypass flow and reperfusion: ptiO2 (25±4 mmHg vs. baseline: 38±5 mmHg, p〈0.05) and CBF (43±8 vs. baseline: 68±11 ml/100 g/min, p〈0.05) were significantly reduced. Arterial and jugular-venous lactate levels increased after rewarming (p〈0.05) and corresponded to the appearance of a anaerobic metabolism. These data demonstrate significantly decreased levels of ptiO2 (brain tissue oxygenation) and CBF (oxygen supply) during and after rewarming from DHCA. The induced impairment of recovery persists after rewarming and generates a temporary low-flow situation with delayed brain tissue reoxygenation on the cellular/mitochondrial level. Thus, a direct influence on brain functional recovery by the active cooling and rewarming process about the bloodstream during CPB, resulting in disturbed tissue blood redistribution, mitochondrial dysfunction and/or excessive cerebral oxygen consumption (compensation of an oxygen debt) is a possible explanation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s003900050307
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