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2017 ; 12
(11
): e0188144
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English Wikipedia
Adenosine, lidocaine and Mg2+ (ALM) fluid therapy attenuates systemic
inflammation, platelet dysfunction and coagulopathy after non-compressible
truncal hemorrhage
#MMPMID29145467
Letson H
; Dobson G
PLoS One
2017[]; 12
(11
): e0188144
PMID29145467
show ga
BACKGROUND: Systemic inflammation and coagulopathy are major drivers of injury
progression following hemorrhagic trauma. Our aim was to examine the effect of
small-volume 3% NaCl adenosine, lidocaine and Mg2+ (ALM) bolus and 0.9% NaCl/ALM
'drip' on inflammation and coagulation in a rat model of hemorrhagic shock.
METHODS: Sprague-Dawley rats (429±4 g) were randomly assigned to: 1) shams, 2)
no-treatment, 3) saline-controls, 4) ALM-therapy, and 5) Hextend®. Hemorrhage was
induced in anesthetized-ventilated animals by liver resection (60% left lateral
lobe and 50% medial lobe). After 15 min, a bolus of 3% NaCl ± ALM (0.7 ml/kg) was
administered intravenously (Phase 1) followed 60 min later by 4 hour infusion of
0.9% NaCl ± ALM (0.5 ml/kg/hour) with 1-hour monitoring (Phase 2). Plasma
cytokines were measured on Magpix® and coagulation using Stago/Rotational
Thromboelastometry. RESULTS: After Phase 1, saline-controls, no-treatment and
Hextend® groups showed significant falls in white and red cells, hemoglobin and
hematocrit (up to 30%), whereas ALM animals had similar values to shams (9-15%
losses). After Phase 2, these deficits in non-ALM groups were accompanied by
profound systemic inflammation. In contrast, after Phase 1 ALM-treated animals
had undetectable plasma levels of IL-1? and IL-1?, and IL-2, IL-6 and TNF-? were
below baseline, and after Phase 2 they were less or similar to shams. Non-ALM
groups (except shams) also lost their ability to aggregate platelets, had lower
plasma fibrinogen levels, and were hypocoagulable. ALM-treated animals had
50-fold higher ADP-induced platelet aggregation, and 9.3-times higher
collagen-induced aggregation compared to saline-controls, and had little or no
coagulopathy with significantly higher fibrinogen shifting towards baseline.
Hextend® had poor outcomes. CONCLUSIONS: Small-volume ALM bolus/drip mounted a
frontline defense against non-compressible traumatic hemorrhage by defending
immune cell numbers, suppressing systemic inflammation, improving platelet
aggregation and correcting coagulopathy. Saline-controls were equivalent to
no-treatment. Possible mechanisms of ALM's immune-bolstering effect are
discussed.