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Published on: September 22, 2017
Effect of cardiopulmonary bypass and calcium administration on the splanchnic circulation
1Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston 02114-2696, USA.
Insights
Gastrointestinal complications after cardiopulmonary bypass (CPB) are serious. This study found that reduced splanchnic perfusion is not the cause of CPB-related gastrointestinal injury.
Area of Science:
- Cardiovascular Surgery
- Gastroenterology
- Physiology
Background:
- Gastrointestinal complications post-cardiopulmonary bypass (CPB) are linked to high mortality.
- Prolonged CPB time and calcium administration are predictors of these complications.
- Decreased splanchnic perfusion is hypothesized as a potential mechanism.
Purpose of the Study:
- To investigate the impact of CPB on splanchnic organ perfusion.
- To determine if calcium chloride administration affects splanchnic blood flow post-CPB.
Main Methods:
- Mongrel dogs underwent CPB with controlled temperature and heart arrest.
- Radiolabeled microspheres were used to measure organ blood flow at baseline, during CPB, and post-CPB.
- Animals received either calcium chloride or saline after CPB.
Main Results:
- Splanchnic organ blood flow remained stable throughout all phases of CPB.
- Calcium chloride administration post-CPB did not alter splanchnic organ blood flow.
- The study did not find evidence supporting decreased splanchnic perfusion as a mechanism for CPB-induced gastrointestinal injury.
Conclusions:
- While CPB can cause gastrointestinal injury, reduced splanchnic perfusion is unlikely to be the primary mechanism.
- The mechanism of potential pancreatic injury from calcium chloride is not related to hypoperfusion.
Abstract:
Gastrointestinal complications following cardiopulmonary bypass (CPB) are associated with high mortality rates. The identification of prolonged CPB time and calcium administration as independent predictors of gastrointestinal complications suggests decreased splanchnic perfusion as a possible mechanism. To test this hypothesis, we evaluated splanchnic organ perfusion during CPB and after calcium chloride administration. Mongrel dogs were studied under anesthesia and were cannulated for bypass. CPB was begun at 37 degrees C, and the heart was fibrillated and vented. After 30 min, CPB temperature was reduced to 25 degrees C for 1 h with the heart arrested through cold crystalloid cardioplegia. After rewarming to 37 degrees C for 30 min, the heart was cardioverted, and CPB was weaned off. Calcium chloride (10 mg/kg) or saline was administered. Organ blood flow was determined with radiolabeled microspheres at baseline, during CPB, and after weaning from CPB. Splanchnic organ blood flow did not decrease during any phase of CPB. Calcium chloride administration after CPB had no effect on splanchnic organ blood flow. While gastrointestinal injury may result from CPB, this study suggests that the mechanism of injury is not decreased by splanchnic organ perfusion during bypass. While calcium chloride can cause pancreatic injury, the responsible mechanism is not calcium-induced hypoperfusion.
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