Insulin-like growth factor-I and growth hormone administration in intestinal ischemia shock in the rat

• Published in: Shock (Augusta, Ga.) Ga.), 1998-07, Vol.10 (1), p.62-68
• Main Authors: HAGLIND, E, MALMLOF, K, JIE FAN, LANG, C. H
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Blood Glucose - analysis; Corticosterone - blood; Emergency and intensive care: digestive diseases. Bioartificial liver; Female; Growth Hormone - pharmacology; Insulin - blood; Insulin-Like Growth Factor Binding Protein 1 - blood; Insulin-Like Growth Factor Binding Protein 2 - blood; Insulin-Like Growth Factor Binding Protein 3 - blood; Insulin-Like Growth Factor I - analysis; Insulin-Like Growth Factor I - metabolism; Insulin-Like Growth Factor I - pharmacology; Intensive care medicine; Intestines - blood supply; Ischemia - drug therapy; Male; Medical sciences; Rats; Rats, Wistar; RNA, Messenger - analysis; Shock - drug therapy
• ISSN: 1073-2322; 1540-0514
• DOI: 10.1097/00024382-199807000-00011

The effect of exogenous insulin-like growth factor (IGF)-I and growth hormone (GH) was examined in a rat model of intestinal ischemia-reperfusion (I/R). Animals were anesthetized, vascular catheters were placed, and intestinal ischemia was induced for 60 min. Thereafter, the intestine was reperfused, and rats received a primed, constant infusion of either IGF-I or GH (500 microg/rat + 500 microg/day) for the remainder of the study; control rats received an equal volume of vehicle. The plasma IGF-I concentration gradually declined after I/R in the vehicle-shock group and was reduced 30% at 48 h. GH infusion completely prevented this reduction, whereas the effect of IGF-I was intermediate. The IGF-I content in liver was increased by IGF-I (78%) and further enhanced in the GH-treated group (140%). Comparable increases were seen for the abundance of IGF-I mRNA in liver in these two treatment groups, compared to the vehicle control. In contrast, while both IGF-I and GH elevated the IGF-I content in skeletal muscle similarly (80%), no increase in IGF-I mRNA expression was observed in this tissue. Neither treatment altered the IGF-I content in small intestine. At the time tissues were sampled (48 h), the plasma concentration of glucose and corticosterone was not different among the three groups. However, plasma insulin was reduced 50% in the IGF-I-infused animals, compared to values in either the shock-GH or shock-vehicle group. These data demonstrate that chronic administration of GH and, to a lesser extent, IGF-I, after intestinal I/R maintains levels of IGF-I in the blood, liver, and muscle. Thus, adjunct treatment with these anabolic agents may help blunt the increased catabolism observed in individuals following intestinal I/R.