Introduction
Materials and methods
Induction of sepsis
Preparation of left ventricular papillary muscle
Intracellular recording from cardiomyocytes
Effects of tetrodotoxin and nifedipine on action potentials and contractility in healthy muscle
Data analysis and sample size
Results
Vrest(mV) | APA (mV) | AP threshold (mV) | dV/dt (mV/ms) | APD 50 (ms) | Number of rats studied (number of fibers) | |
---|---|---|---|---|---|---|
Healthy | −79.9 ± 1.0 | 85.5 ± 1.8 | −72.0 ± 0.5 | 59.6 ± 2.4 | 32.7 ± 2.5 | 11 (84) |
Septic | −78.3 ± 0.6 | 66.6 ± 5.6* | −65.0 ± 1.8* | 34.0 ± 5.7* | 29.1 ± 3.2 | 8 (108) |
TTX Studies | ||||||
Pre-TTX | −77.5 ± 1.3 | 88.5 ± 4.2 | −67.9 ± 2.5 | 57.1 ± 5.1 | 35.3 ± 3.9 | 3 (14) |
Post-TTX | −79.0 ± 2.4 | 69.1 ± 7.2 | −54.6 ± 4.0* | 22.1 ± 8.1* | 35.0 ± 0.5 | 3 (21) |
Nifedipine studies | ||||||
Pre-nifedipine | −82.5 ± 2.3 | 89.2 ± 2.6 | −70.5 ± 4.6 | 64.5 ± 5.0 | 38.5 ± 5.2 | 3 (15) |
Post-nifedipine | −85.2 ± 0.6 | 87.3 ± 2.0 | −70.5 ± 2.7 | 52.4 ± 2.8* | 34.3 ± 3.8 | 3 (22) |
Discussion
Downregulation of excitability during critical illness
The relationship between reduced cardiac excitability and contractility during sepsis
Conclusions
Key messages
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Cardiac excitability is reduced during sepsis in rats.
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The reduction in excitability appears to be primarily due to reduction of sodium current.
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The reduction in sodium current may be sufficient to explain most of the reduction in cardiac contractility during sepsis.
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Reduced excitability of electrically active tissues may be a unifying theme that accounts for the failure of a number of organ systems during sepsis and critical illness.