C. Bloechle et al., RAT-LIVER INJURY-INDUCED BY HYPOXIC ISCHEMIA AND REPERFUSION - PROTECTIVE ACTION BY SOMATOSTATINS IS INDEPENDENT FROM CHANGES IN GLUCOSE-METABOLISM, Hormone and Metabolic Research, 26(6), 1994, pp. 270-275
Changes in glucose metabolism mediated by natural somatostatin and two
derivatives (octreotide, 008) were studied in hypoxic ischemic cell i
njury of the isolated perfused rat liver. The tested somatostatin and
its analogues were previously shown to exert protective actions in liv
er damage induced by hypoxic ischemia and reperfusion. In isolated per
fused livers of rats starved for 24 hours and unstarved rats flow rate
was reduced and oxygen supply interrupted for 180 min. Then the liver
s were normoxically reperfused for 30 min. Glucose and lactate concent
ration, as well as LDH and GLDH activity, were determined in the efflu
ent. In starved and unstarved rat livers hypoxic ischemia resulted in
a substantial enzyme release. In livers harvested from unstarved rats
hepatic glucose release was noticed which ceased towards prolonged low
now ischemia. In livers harvested from starved rats containing low he
patic glycogen concentration only minimal hepatic glucose release was
present. In starved and unstarved rats pretreatment with somatostatin,
octreotide, and 008 significantly reduced LDH and GLDH release (p<0.0
01). In unstarved rats natural somatostatin and octreotide pretreatmen
t resulted in a substantial output of glucose during the hypoxic ische
mic perfusion period (p<0.001), whereas livers with 008 pretreatment d
id not show any difference in glucose release compared to controls. In
livers harvested from starved rats neither somatostatin nor octreotid
e nor 008 pretreatment led to a difference in glucose output observed
in controls. Natural somatostatin and octreotide cause a strong hepati
c glucose release even under hypoxic ischemic conditions in rat livers
with filled glycogen stores. The protective action of natural somatos
tatin, octreotide, and 008 is not mediated by changes in glucose metab
olism, and is not related to endocrine activity.