Preparation of rescue nurses to work in trauma team in Poland. RK in trauma team in Poland

Mikuła-Mazurkiewicz, Agnieszka; Chilimoniuk, Beata; Nogalski, Adam; Chemperek, Ewa

doi:10.1016/j.resuscitation.2010.09.430

Cited by 1 publication

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“…In general, NHE-1 inhibition is thought to be a pharmacological tool for the treatment of various detrimental cardiac conditions such as ischemia/reperfusion injury, arrhythmias, hypertrophy, and HF. In many pre-clinical studies, NHE-1 inhibition has been shown to reduce ischemia/reperfusion injury (Lee et al, 2005; Ayoub et al, 2010). In clinical trials, however, the cardioprotective effects of NHE-1 inhibition were less clear and the treatment with the NHE-1 inhibitor cariporide was associated with significantly greater incidence of stroke (Fliegel and Karmazyn, 2004).…”

Section: Discussionmentioning

confidence: 99%

Dietary Omega-3 Polyunsaturated Fatty Acids Suppress NHE-1 Upregulation in a Rabbit Model of Volume- and Pressure-Overload

Borren¹,

Ruijter²,

Baartscheer³

et al. 2012

Front. Physio.

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Background: Increased consumption of omega-3 polyunsaturated fatty acids (ω3-PUFAs) from fish oil (FO) may have cardioprotective effects during ischemia/reperfusion, hypertrophy, and heart failure (HF). The cardiac Na+/H+-exchanger (NHE-1) is a key mediator for these detrimental cardiac conditions. Consequently, chronic NHE-1 inhibition appears to be a promising pharmacological tool for prevention and treatment. Acute application of the FO ω3-PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibit the NHE-1 in isolated cardiomyocytes. We studied the effects of a diet enriched with ω3-PUFAs on the NHE-1 activity in healthy rabbits and in a rabbit model of HF induced by volume- and pressure-overload. Methods: Rabbits were allocated to four groups. The first two groups consisted of healthy rabbits, which were fed either a diet containing 1.25% (w/w) FO (ω3-PUFAs), or 1.25% high-oleic sunflower oil (ω9-MUFAs) as control. The second two groups were also allocated to either a diet containing ω3-PUFAs or ω9-MUFAs, but underwent volume- and pressure-overload to induce HF. Ventricular myocytes were isolated by enzymatic dissociation and used for intracellular pH (pHi) and patch-clamp measurements. NHE-1 activity was measured in HEPES-buffered conditions as recovery rate from acidosis due to ammonium prepulses. Results: In healthy rabbits, NHE-1 activity in ω9-MUFAs and ω3-PUFAs myocytes was not significantly different. Volume- and pressure-overload in rabbits increased the NHE-1 activity in ω9-MUFAs myocytes, but not in ω3-PUFAs myocytes, resulting in a significantly lower NHE-1 activity in myocytes of ω3-PUFA fed HF rabbits. The susceptibility to induced delayed afterdepolarizations (DADs), a cellular mechanism of arrhythmias, was lower in myocytes of HF animals fed ω3-PUFAs compared to myocytes of HF animals fed ω9-MUFAs. In our rabbit HF model, the degree of hypertrophy was similar in the ω3-PUFAs group compared to the ω9-MUFAs group. Conclusion: Dietary ω3-PUFAs from FO suppress upregulation of the NHE-1 activity and lower the incidence of DADs in our rabbit model of volume- and pressure-overload.

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Section: Discussionmentioning

confidence: 99%