Key result
Expression of slow skeletal troponin I in adult transgenic mice protected left ventricular systolic function and enabled survival during 35% CO2 hypercapnia, whereas control mice died within 3-4 mins.
Why the study?
Does expression of slow skeletal troponin I in adult mouse heart maintain left ventricular systolic function during respiratory hypercapnia?
Population
Transgenic adult mice in which cardiac TnI was replaced with slow skeletal troponin I and nontransgenic…
Comparison
Ventilation with 35% CO2 balanced with oxygen… vs Nontransgenic littermates exposed to the same…
Design
Preclinical
Follow-up
Acute (minutes)
Authors
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May protect against hypercapnic LV dysfunction in mice; leaves open translation to human respiratory acidosis.
Does expression of slow skeletal troponin I in adult mouse heart maintain left ventricular systolic function during respiratory hypercapnia?
Specific replacement of cardiac TnI with slow skeletal TnI in adult mice protects left ventricular systolic function and improves survival during severe hypercapnic acidosis.
Urboniene et al. (2005) studied Respiratory hypercapnia. Expression of slow skeletal troponin I (ssTnI) vs. Nontransgenic (NTG) littermates was evaluated on Left ventricular systolic function and survival during hypercapnia. Expression of slow skeletal troponin I in adult transgenic mice protected left ventricular systolic function and enabled survival during 35% CO2 hypercapnia, whereas control mice died within 3-4 mins.
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