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- Open Access
0738. Mortality is associated with early tachycardia and cardiac troponin release in a fluid-resuscitated rat model of sepsis
© Khaliq and Singer; licensee Springer. 2014
Published: 26 September 2014
Tachycardia and high troponin levels prognosticate for poor outcomes in human sepsis . Reducing cardiac stress with beta-blockade has been proposed as an important therapeutic strategy as high catecholamine levels are injurious . We have characterized a 72h fluid-resuscitated rat model of faecal peritonitis where prognostication can be made with high sensitivity and specificity at 6h from heart rate and stroke volume .
To determine whether non-survival is associated with early changes in troponin release and circulating catecholamine levels.
Male Wistar rats (325±15g) underwent insertion of tunneled carotid arterial and jugular venous lines under isoflurane anaesthesia, followed by immediate i.p. injection of 4µl/g faecal slurry. Control animals were treated identically but without i.p. injection of slurry. Once awake, attachment to a swivel-tether system allowed animals to move freely and access food and water ad libitum. Fluid resuscitation (50:50 mixture of 5% dextrose/Hartmann's; 10ml/kg/h) was commenced at 2h. At 6h, echocardiography was used to measure heart rate and stroke volume. Animals were observed until 72h to assess survival. In a second experiment septic animals underwent echocardiography at 6h followed by sacrifice and blood and tissue sampling. We here report plasma catecholamine and troponin T levels (measured by ELISA) in predicted survivors and non-survivors, and sham-operated controls.
Predicted survival (n=6)
Predicted non-survival (n=6)
Heart rate (bpm)
390 ± 21
442 ± 17
488 ± 18*
Stroke volume (mL)
0.40 ± 0.03
0.25 ± 0.02
0.18 ± 0.02*
8.56 ± 0.42
9.44 ± 0.23
10.3 ± 0.18
1.60 ± 0.25
3.21 ± 0.23
2.98 ± 0.27
171 ± 24
168 ± 15
311 ± 47*
An association was seen between eventual non-survival and tachycardia, low stroke volume and myocardial injury (denoted by high troponin) at 6h after induction of sepsis. The impact of modulating cardiac stress on outcome merits further study.
UK Intensive Care Foundation and NIHR
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