Дексаметазон может быть не полезен при операциях с ИК....

[Евгений Хоменко]

Операции с ИК как известно несут в себе риск неврологического повреждения, основной вклад в которое вносит значительная эмболическая нагрузка в период каннюляции аорты, снятия зажима, начала изгнания из сердца, эмболы могут иметь разные хар-ки (размеры, состав - воздух, тканевой детрит, кальций) однако все они вызывают то, что неврологи кличут фокальной ишемией. В 1999 году в журнале анестезиология было опубликовано исследование японских ученых, которое заставляет задуматься о дальнейшей практике использования стероидов вообще и ДЕКСАМЕТАЗОНА в частности...


АБСТРАКТ

Dexamethasone Changes Brain Monoamine Metabolism and Aggravates Ischemic Neuronal Damage in Rats

LABORATORY INVESTIGATION
AUTHOR(S): Tsubota, Shinzo, M.D.*; Adachi, Naoto, M.D., Ph.D.†; Chen, Junfeng, M.D.‡; Yorozuya, Toshihiro, M.D.†; Nagaro, Takumi, M.D.§; Arai, Tatsuru, M.D.
* Senior Resident in Anesthesiology and Resuscitology.
† Lecturer in Anesthesiology and Resuscitology.
‡ Visiting Researcher of Anesthesiology and Resuscitology.
§ Associate Professor in Anesthesiology and Resuscitology. Professor in Anesthesiology and Resuscitology. Received from the Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Ehime, Japan.

Submitted for publication January 6, 1998. Accepted for publication October 8, 1998. Supported in part by the Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Ehime, Japan. Address reprint requests to Dr. Adachi: Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Shitsukawa, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan.

ABSTRACT: Background: Glucocorticoids have been reported to aggravate ischemic brain damage. Because changes in the activities of various neuronal systems are closely related to the outcome of ischemic damage, the authors evaluated the effects of dexamethasone on the monoaminergic systems and ischemic neuronal damage.
Methods: The right middle cerebral artery was occluded for 2 h, and the tissue concentrations of monoamines and their metabolites were determined in the cerebral cortex and the striatum of rats. The turnover of 5-hydroxytryptamine was compared in animals injected with saline and those injected with dexamethasone twice (2 mg/kg in each injection) by evaluating the probenecid-induced accumulation of 5-hydroxyindoleacetic acid. The turnovers of norepinephrine and dopamine were estimated from the a-methyl-p-tyrosine—induced depletion of norepinephrine and dopamine, respectively. The effect of dexamethasone on the infarct volume was evaluated by triphenyltetrazolium chloride stain in rats subjected to 2 h of occlusion.
Results: Dexamethasone did not affect the cortical 5-hydroxytryptamine or 5-hydroxyindoleacetic acid contents. However, it suppressed the turnover of the cortical 5-hydroxytryptamine on both sides. Dexamethasone reduced the turnover of the striatal 5-hydroxytryptamine and facilitated the dopamine turnover. In rats subjected to 2 h of occlusion and 2 h of reperfusion, the infarct volume was 10.5 times greater in the group that received dexamethasone than in the animals that received saline.
Conclusions: Dexamethasone suppresses the inhibitory serotonergic system and facilitates the excitatory dopaminergic system in the rat telencephalon. This may be a mechanism by which dexamethasone aggravates ischemic neuronal injury.

Anesthesiology 90:515-23, 1999

[Евгений Хоменко]

Dexamethasone Changes Brain Monoamine Metabolism and Aggravates Ischemic Neuronal Damage in Rats
(Laboratory Investigations)

[minin sergey]

[Ярослав Липатов]

Получается, что глюкокортикоиды вредны при фокальной ишемии как и при травматическом повреждении мозга?

[Alexey Dyachkov]

Насколько я помню, их польза была доказана только при травмах с поражениями спинного мозга в течение нескольких часов от момента травмы

[minin sergey]

а при DHCA?

статейка 99-го продолжения мысли более нигде нет?

[Alexey Dyachkov]

Вот, например:

Anesthesia and Analgesia
Volume 101, Issue 5, November 2005, Pages 1311-1318

Large-dose pretreatment with methylprednisolone fails to attenuate neuronal injury after deep hypothermic circulatory arrest in a neonatal piglet model

Schubert, S.a , Stoltenburg-Didinger, G.d , Wehsack, A.a , Troitzsch, D.a , Boettcher, W.c , Huebler, M.c , Redlin, M.b , Kanaan, M.a , Meissler, M.e , Lange, P.E.a , Abdul-Khaliq, H.a f

a Department of Paediatric Cardiology and Congenital Heart Disease, Deutsches Herzzentrum Berlin, Berlin, Germany
b Department of Anesthesiology, Deutsches Herzzentrum Berlin, Berlin, Germany
c Department of Thoracic and Cardiovascular Surgery, Deutsches Herzzentrum Berlin, Berlin, Germany
d Department of Neuropathology, University Clinic Benjamin Franklin, Free University of Berlin, Berlin, Germany
e Animal Experimental Laboratory, Charité, Humboldt University, Berlin, Germany
f Department of Paediatric Cardiology and Congenital Heart Disease, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany

Abstract

Conflicting results have been reported with regard to the neuroprotective effects of steroid treatment with cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA). We evaluated the mode and severity of neuronal cell injury in neonatal piglets after prolonged DHCA and the possible neuroprotective effect of systemic pretreatment (>6 h before surgery) with large-dose methylprednisolone (MP). Nineteen neonatal piglets (age, <10 days; weight, 2.1 ± 0.5 kg) were randomly assigned to 2 groups: 7 animals were pretreated with large-dose systemic MP (30 mg/kg) 24 h before surgery, and 12 animals without pharmacological pretreatment (saline) served as control groups. All animals were connected to full-flow CPB with cooling to 15°C and 120 min of DHCA. After rewarming to 38.5°C with CPB, animals were weaned from CPB and survived 6 h before they were killed, and the brain was prepared for light and electron microscopy, immunohistochemistry, and TUNEL-staining. Quantitative histological studies were performed in hippocampus, cortex, cerebellum, and caudate nucleus. Systemic pretreatment with large-dose MP lead to persistent hyperglycemia but no significant changes of cerebral perfusion. Necrotic and apoptotic neuronal cell death were detected in all analyzed brain regions after 120 min of DHCA. In comparison to the control group, large-dose pretreatment with systemic MP lead to an increase of necrotic neuronal cell death and induced significant neuronal apoptosis in the dentate gyrus of the hippocampus (P = 0.001). In conclusion, systemic pretreatment with large-dose MP fails to attenuate neuronal cell injury after prolonged DHCA and induces regional neuronal apoptosis in the dentate gyrus.
©2005 by the International Anesthesia Research Society.

[Alexey Dyachkov]

Ну и противоположная

Annals of Thoracic Surgery
Volume 72, Issue 5, 2001, Pages 1465-1472

Systemic steroid pretreatment improves cerebral protection after circulatory arrest

Shum-Tim, D.a e Email this author, Tchervenkov, C.I.a , Jamal, A.-M.a , Nimeh, T.b , Luo, C.-Y.a , Chedrawy, E.a , Laliberte, E.a , Philip, A.b , Rose, C.P.c , Lavoie, J.d Correspondence address

a Division of Cardiovascular Surgery, Montreal Children's Hospital, McGill University Health Center, Montreal, Que., Canada
b Division of Plastic Surgery, Montreal General Hospital, McGill University Health Center, Montreal, Que., Canada
c Division of Cardiology, Montreal General Hospital, McGill University Health Center, Montreal, Que., Canada
d Division of Anesthesia, Montreal General Hospital, McGill University Health Center, Montreal, Que., Canada
e Cardiovascular Surgery, Montreal Children's Hospital, 2300 Tupper St, Montreal, Que. H3H 1P3, Canada

Abstract

Background. This study evaluates whether systemic steroid pretreatment enhances neuroprotection during deep hypothermic circulatory arrest (DHCA) compared with steroid in cardiopulmonary bypass (CPB) prime. Methods. Four-week-old piglets randomly placed into two groups (n = 5 per group) were given methylprednisolone (30 mg/kg) into the pump prime (group PP), or pretreated intravenously 4 hours before CPB (group PT). All animals underwent 100 minutes of DHCA (15°C), were weaned off CPB, and were sacrificed 6 hours later. Postoperative changes in body weight, bioimpedance, and colloid oncotic pressure (COP) were measured. Cerebral trypan blue content, immunohistochemical evaluation of transforming growth factor-β1 (TGF-βl) expression, and caspase-3 activity were performed. Results. Percentage weight gain (group PP 25.0% ± 10.4% versus group PT 12.5% ± 4.0%; p = 0.036), and percentage decrease in bioimpedance (PP 37.2% ± 14.5% versus PT 15.6% ± 7.9%; p = 0.019) were significantly lower, whereas postoperative COP was significantly higher in group PT versus group PP (PT 15,3 ± 1.8 mm Hg versus PP 11.6 ± 0.8 mm Hg; p = 0.003). Cerebral trypan blue (ng/g dry tissue) was significantly lower in group PT (PT 5.6 × 10-3 ± 1.1 × 10-3 versus PP 9.1 × 10-3 ± 5.7 × 10-4; p = 0.001). Increased TGF-β1 expression and decreased caspase-3 activity were shown in group PT. Conclusions. Systemic steroid pretreatment significantly reduced total body edema and cerebral vascular leak and was associated with better immunohistochemical indices of neuroprotection after DHCA.
© 2001 by The Society of Thoracic Surgeons.

[minin sergey]

http://www.experts.scival.com/umichigan ... &u_id=1273

[Alexey Dyachkov]

Думаю, надо вникать в дизайн исследований, чтобы понять, почему у одних одно, а у других другое

[minin sergey]

да... а то так можно доказать что микроструйное введение протамина после инициации CPB снижает риск кровотечения на piglets, rats and mf roaches///