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Hyperglycaemia increases S 100β after short experimental cardiac arrest
Author(s) -
MOLNAR M.,
BERGQUIST M.,
LARSSON A.,
WIKLUND L.,
LENNMYR F.
Publication year - 2014
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.12209
Subject(s) - medicine , resuscitation , hemodynamics , anesthesia , perfusion , shock (circulatory) , cardiac output , cerebral perfusion pressure , cardiology
Background Hyperglycaemia is associated with aggravated ischaemic brain injury. The main objective of this study was to investigate the effects on cerebral perfusion of 5 min of cardiac arrest during hyperglycaemia and normoglycaemia. Methods Twenty triple‐breed pigs (weight: 22–29 kg) were randomised and clamped at blood glucose levels of 8.5–10 mM [high ( H )] or 4–5.5 mM [normal ( N )] and thereafter subjected to alternating current‐induced 5 min‐cardiac arrest followed by 8 min of cardiopulmonary resuscitation and direct current shock to restore spontaneous circulation. Results Haemodynamics, laser Doppler measurements and regional venous oxygen saturation ( HbO 2 ) were monitored, and biochemical markers in blood [S100β, interleukin ( IL )‐6 and tumour necrosis factor ( TNF )] quantified throughout an observation period of 3 h. The haemodynamics and physiological measurements were similar in the two groups. S100β increased over the experiment in the H compared with the N group ( P < 0.05). IL ‐6 and TNF levels increased across the experiment, but no differences were seen between the groups. Conclusions The enhanced S100β response is compatible with increased cerebral injury by hyperglycaemic compared with normoglycaemic 5 min of cardiac arrest and resuscitation. The inflammatory cytokines were similar between groups.