Volume 11, Issue 5pt1 pp. 420-425
Original article

Preservation of pancreatic endocrine function by hemodynamic stabilization following brain death

Hiroyoshi Yoshida

Hiroyoshi Yoshida

Department of Traumatology, Osaka University Medical School, 2-15 Yamadaoka, Suita City, Osaka, Japan

Search for more papers by this author
Atsushi Hiraide

Corresponding Author

Atsushi Hiraide

Department of Traumatology, Osaka University Medical School, 2-15 Yamadaoka, Suita City, Osaka, Japan

Atsushi Hiraide M.D., Department of Traumatology, Osaka University Medical School 2-15 Yamadaoka, Suita City, Osaka 565, Japan Tel:81-6-879-5707 Fax: 81-6-879-5632Search for more papers by this author
Atsushi Iwai

Atsushi Iwai

Department of Traumatology, Osaka University Medical School, 2-15 Yamadaoka, Suita City, Osaka, Japan

Search for more papers by this author
Naomasa Kawaguchi

Naomasa Kawaguchi

Department of Pathology, College of Biomedical Technology, Osaka University, Osaka, Japan

Search for more papers by this author
Toshiharu Yoshioka

Toshiharu Yoshioka

Department of Traumatology, Osaka University Medical School, 2-15 Yamadaoka, Suita City, Osaka, Japan

Search for more papers by this author
Tsuyoshi Sugimoto

Tsuyoshi Sugimoto

Professor emeritus, Osaka University

Search for more papers by this author
First published: 01 October 1997
Citations: 1

Abstract

A protocol achieving for long-term hemodynamic stability enabled us to evaluate pancreatic endocrine function for up to 1 wk following brain death. The glucose disappearance rate was significantly lower in brain-dead patients (N = 21) than in normal controls (N = 10) (p<0.001). In 19 brain-dead patients whose plasma epinephrine concentrations exceeded 0.4 ng/ml, the mean early insulin release was significantly lower than in controls, while early insulin release was markedly higher in the remaining two patients. It is possible that early insulin released may be due to increased plasma epinephrine concentrations following brain death. Late insulin release in brain-dead patients was not lower, but was higher than controls and was accompanied by a decrease in the glucose disappearance rate. No evidence of abnormalities in histopathology of pancreas was detected at autopsy. Our results indicate that intrinsic insulin secretory function can be preserved during the first week following brain death.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.