Cardiac Troponin I and cardiac Troponin T increases in pigs during ischemia-reperfusion damage

Bertsch, Thomas; Janke, Christoph; Denz, Christof; Weiss, Miriam; Luiz, Thomas; Ellinger, K.; Korth, Ulrike; Hannak, Dieter; Bartelt, U.; Krieter, H.

doi:10.1016/s0940-2993(00)80111-6

Cited by 12 publications

(8 citation statements)

References 6 publications

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“…It is reported that cTnT is significantly elevated in asphyxiated infants with heart failure and were not significantly different in asphyxiated newborns with neurological sequelae [2]. A recent study in an ischemia-reperfusion model of pigs showed that cTnT and cTnI is released into the bloodstream within 30 min after reperfusion and increases till 180 min [29]. The halflife of cTnI in serum is approximately 2 h and serum levels of this protein in patients with hypoxic cardiac injury remain increased for 7-10 days [30].…”

Section: Discussionmentioning

confidence: 98%

Cord Blood Cardiac Troponin I as an Early Predictor of Short-Term Outcome in Perinatal Hypoxia

et al. 2004

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Section: Discussionmentioning

confidence: 98%

Cord Blood Cardiac Troponin I as an Early Predictor of Short-Term Outcome in Perinatal Hypoxia

et al. 2004

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“…However, renal dysfunction and systolic left ventricular dysfunction were not predictive of high troponin level in our population. Besides, animals' studies demonstrated that high cTnI levels could be explained by coronary hypoperfusion and hypoxic phenomenon that occur during resuscitation procedure (33,34). The capacity of cardiac compression and defibrillation to provoke a blood release of cardiac enzyme had been previously investigated in several studies that have provided conflicted hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Can early cardiac troponin I measurement help to predict recent coronary occlusion in out-of-hospital cardiac arrest survivors?

Dumas

Manzo-Silberman

Fichet

et al. 2012

Critical Care Medicine

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In this large cohort of out-of-hospital cardiac arrest patients, isolated early cardiac troponin I measurement is modestly predictive of a recent coronary occlusion. Furthermore, the contribution of this parameter even in association with other factors does not seem helpful to predict recent occlusion. As a result and given the high benefit of percutaneous coronary intervention for such patients, the dosage of cardiac troponin I at admission could not help in the decision of early coronary angiogram.

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“…In animal studies, it has been reported that the level of cTnI starts to increase by 30 min with a peak value at 3h after cardiac arrest in adult pigs (30) and started to rise from 0.5-1h after induced cardiac injury and normalized within 48h after the insult in adult rodents (31). Our data confirms this rapid release of cTnI after acute injury as we observed the first rise in cTnI at 1h after a 45-min global (Fig 1) insult with a peak around 3-6h in the pilot study.…”

Section: Discussionmentioning

confidence: 99%

Immediate Hypothermia Reduces Cardiac Troponin I After Hypoxic-Ischemic Encephalopathy in Newborn Pigs

et al. 2011

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Neonatal hypoxic-ischemic encephalopathy (HIE) is a clinically defined neurological condition after lack of oxygen and often associated with cardiac dysfunction in term infants. Therapeutic hypothermia (HT) after birth is neuroprotective in infants with HIE. However, it is not known whether HT is also cardioprotective. Four newborn pigs were used in the pilot study and a further 18 newborn pigs [randomly assigned to 72 h normothermia (NT) or 24 h HT followed by 48 h NT] were subjected to global HIE insults. Serum cTnI was measured before and post the HIE insult. Blood pressure, inotropic support, blood gases, and heart rate (HR) were recorded throughout. Cardiac pathology was assessed from histological sections. Cooling reduced serum cTnI levels significantly in HT pigs by 6 h (NT, 1.36 ± 0.67; HT, 0.34 ± 0.23 ng/mL; p = 0.0009). After rewarming, from 24 to 30 h postinsult, HR and cTnI increased in the HT group; from HR[24 h] = 117 ± 22 to HR[30 h] = 218 ± 32 beats/min (p = 0.0002) and from cTnI[24 h] = 0.23 ± 0.12 to cTnI[30 h] = 0.65 ± 0.53 ng/mL, (p = 0.05). There were fewer ischemic lesions on cardiac examination (37%) in the HT group compared with the NT group (70%). HT (24 h) pigs did not have the postinsult cTnI increase seen in NT-treated pigs. There was a trend that HT improved cardiac pathology in this 3-d survival model.

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Cardiac Troponin I and cardiac Troponin T increases in pigs during ischemia-reperfusion damage

Cited by 12 publications

References 6 publications

Cord Blood Cardiac Troponin I as an Early Predictor of Short-Term Outcome in Perinatal Hypoxia

Cord Blood Cardiac Troponin I as an Early Predictor of Short-Term Outcome in Perinatal Hypoxia

Can early cardiac troponin I measurement help to predict recent coronary occlusion in out-of-hospital cardiac arrest survivors?

Immediate Hypothermia Reduces Cardiac Troponin I After Hypoxic-Ischemic Encephalopathy in Newborn Pigs

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