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Ann Thorac Surg 1989;48:798-802
© 1989 The Society of Thoracic Surgeons


Articles

Preservation of pancreatic beta cell function with pulsatile cardiopulmonary bypass

Hideo Nagaoka, MD*, Ryuichi Innami, MD, Masazumi Watanabe, MD, Motoaki Satoh, MD, Fumio Murayama, MD, Naoya Funakoshi, MD

Department of Cardiovascular and Thoracic Surgery, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan

Accepted for publication August 15, 1989.

* Address reprint requests to Dr Nagaoka, Department of Cardiovascular and Thoracic Surgery, Tsuchiura Kyodo General Hospital, 11-7 Manabeshinmachi, Tsuchiura, Ibaraki 300, Japan.

Pancreatic islet cell function and tissue metabolism were studied during and after crdiopulmonary bypass in 38 patients undergoing an open heart operation. Twenty patients were operated on with pulsatile cardiopulmonary bypass (group I) and 18, with nonpulsatile cardiopulmonary bypass (group II). Hyperglycemia was observed during and early after operation in both groups. In group I during cardiopulmonary bypass, the immunoreactive insulin and c-peptide levels and the insulin to glucagon molar ratio increased significantly compared with the preoperative values, but in group II, these variables did not alter significantly. An hour postoperatively, the immunoreactive insulin (71 ± 34 µIU/mL) and c-peptide (8.3 ± 3.0 ng/mU levels and the insulin to glucagon molar ratio (11.0 ± 5.2) in group I were significantly higher than those in group II (immunoreactive insulin, 29 ± 20 µIU/mL; c-peptide, 4.8 ± 1.8 ng/mt; insulin to glucagon molar ratio, 3.4 ± 2.6). The blood lactate level in group I (41 ± 22 mg/dL) was significantly lower than that in group II (78 ± 30 mg/dL) an hour postoperatively. In conclusion, pulsatile crdiopulmonary bypass is quite effective in preserving pancreatic beta cell function and tissue metabolism during and early after open heart procedures.




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