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Updated: Oct 20, 2025

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
Published on: February 10, 2013
The Long-term Effect of Dobutamine on Intrinsic Myocardial Function and Myocardial Injury in Septic Rats with
Xiangxu Tang1, Yaqian Xu, Xiaomeng Dai
1Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, Guangdong, China.
Insights
Dobutamine (DOB) did not improve sepsis-induced heart dysfunction long-term. However, DOB increased survival in septic rats by boosting IL-10, suggesting a complex role in sepsis management.
Area of Science:
- Cardiology
- Sepsis Research
- Pharmacology
Background:
- Sepsis often causes myocardial depression, impacting cardiac output.
- Dobutamine (DOB) is a common inotrope for low cardiac output in sepsis.
- The long-term effects of DOB on sepsis-induced cardiomyopathy are not well understood.
Purpose of the Study:
- To investigate the long-term impact of DOB on myocardial dysfunction and injury in sepsis.
- To assess DOB's effects on hemodynamics, organ function, and inflammatory markers post-sepsis.
Main Methods:
- Rats underwent cecal ligation and puncture (CLP) to induce sepsis.
- Evaluated myocardial function (left ventricular ±dP/dt), organ function, hemodynamics, and inflammatory markers.
- Assessed serum biomarkers (cTnI, NT-proBNP, H-FABP), apoptosis, and vascular permeability.
- DOB was administered at 6 hours post-CLP, with assessments at later time points.
Main Results:
- Myocardial depression (decreased ±dP/dt) and cardiac inflammation occurred early (6h post-CLP).
- Hepatic dysfunction was observed later (9h post-CLP).
- DOB treatment did not improve cardiac function, hemodynamics, or reduce myocardial injury/apoptosis at 20h post-CLP.
- DOB increased serum IL-10 and improved survival in septic rats.
Conclusions:
- Sepsis-induced myocardial depression precedes hepatic and renal dysfunction.
- Standard cardiac biomarkers (cTnI, NT-proBNP, H-FABP) are not reliable early indicators of sepsis-induced myocardial dysfunction.
- While DOB improved survival, it did not ameliorate long-term myocardial dysfunction or injury in this sepsis model.
Abstract:
Dobutamine (DOB) is recommended as an inotrope for septic patients with low cardiac output, but its long-term impact on sepsis-induced cardiomyopathy remains unclear. This study investigated the long-term effect of DOB on septic myocardial dysfunction and injury. Rats were exposed to cecal ligation and puncture (CLP), the intrinsic myocardial function, other organ functions, hemodynamics, inflammatory response, serum myocardial injury biomarkers, myocardial apoptosis, and vascular permeability were determined. At 6 h after CLP, the left ventricular ±dP/dt were significantly depressed, cardiac tumor necrosis factor-α and vascular cell adhesion molecule-1 expression were increased, but not serum cardiac troponin I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (H-FABP), creatinine, and urea nitrogen concentrations in CLP group compared with controls. At 9 h after CLP, hepatic dysfunction was present in CLP rats compared with controls. At 6 h after CLP, DOB treatment did not affect hemodynamics, the left ventricular ±dP/dt, cytokine levels in serum and myocardium, as well as cardiomyocyte apoptosis and cardiac vascular hyperpermeability at 20 h after CLP. However, DOB (10.0 μg/kg) increased serum IL-10 level and improved survival in septic rats. These results indicate that the intrinsic myocardial depression occurs earlier than hepatic and renal dysfunction in sepsis and serum cTnI, NT-proBNP, and H-FABP are not suitable as early biomarkers for sepsis-induced myocardial dysfunction. Although DOB treatment (10.0 μg/kg) in the presence of myocardial dysfunction improves survival in septic rats, it neither improves myocardial function and hemodynamics nor attenuates myocardial injury at the later stage of sepsis.
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