PMID- 8119146
OWN - NLM
STAT- MEDLINE
DCOM- 19940407
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 134
IP  - 3
DP  - 1994 Mar
TI  - Recombinant bovine somatotropin blunts plasma tumor necrosis factor-alpha, 
      cortisol, and thromboxane-B2 responses to endotoxin in vivo.
PG  - 1082-8
AB  - In vivo studies determined the effects of recombinant bovine somatotropin (bST; 
      sometribove) administration (0.1 mg/kg.day, im) to calves on the increases in 
      plasma immunoreactive tumor necrosis factor-alpha (TNF alpha), prostacyclin 
      [6-keto-prostaglandin F1 alpha (6KP)], thromboxane-B2 (TXB), and cortisol (C) 
      that occurred after endotoxin challenge (ET). Two ETs were administered 5 days 
      apart to test the effect of bST on the natural attenuation of hormone and 
      cytokine responses that occurs after repeated challenge with endotoxin. Calves (n 
      = 6) were treated with bST for 5 days. On day 6, the first ET was administered 
      (Escherichia coli; 055:B5; 0.2 microgram/kg, i.v.). Blood was sampled before and 
      hourly after ET through 6 h. For the next 4 days, bST injections continued, and 
      ET was repeated 1 day later. Six additional calves were treated with bicarbonate 
      buffer as contemporary controls for the bST and were similarly challenged with 
      endotoxin. Plasma TNF alpha, C, 6KP, and TXB were significantly increased after 
      each ET. The increases in TNF alpha, C, and TXB were blunted after the second Et 
      compared to those after the first in both untreated and bST-treated animals. The 
      increases in plasma TNF alpha and C and peak plasma TXB and TXB/6KP ratios were 
      smaller in bST-treated than in untreated after the first ET. TNF alpha receptor 
      binding was studied in hepatic microsomal fractions from three bST-treated and 
      three untreated calves. Microsomal fractions from bST-treated calves bound 40% 
      less TNF alpha (5.97 vs. 9.96 pmol/mg) than similar fractions from controls. The 
      data indicate that bST decreases TNF alpha, TXB, and C responses to ET and 
      reduces the TNF alpha-binding capacity of hepatic membranes, suggesting a 
      multiplicity of sites where bST might affect the physiological response to 
      endotoxin.
FAU - Elsasser, T H
AU  - Elsasser TH
AD  - Ruminant Nutrition Laboratory, U.S. Department of Agricultural, Agricultural 
      Research Service, Beltsville, Maryland 20705.
FAU - Fayer, R
AU  - Fayer R
FAU - Rumsey, T S
AU  - Rumsey TS
FAU - Hartnell, G F
AU  - Hartnell GF
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Endotoxins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 54397-85-2 (Thromboxane B2)
RN  - 58962-34-8 (6-Ketoprostaglandin F1 alpha)
RN  - 9002-72-6 (Growth Hormone)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - 6-Ketoprostaglandin F1 alpha/blood
MH  - Animals
MH  - Cattle
MH  - Endotoxins/*pharmacology
MH  - Growth Hormone/*pharmacology
MH  - Hydrocortisone/*blood
MH  - Male
MH  - Recombinant Proteins/pharmacology
MH  - Thromboxane B2/*blood
MH  - Tumor Necrosis Factor-alpha/*analysis
EDAT- 1994/03/01 00:00
MHDA- 1994/03/01 00:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 1994/03/01 00:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1210/endo.134.3.8119146 [doi]
PST - ppublish
SO  - Endocrinology. 1994 Mar;134(3):1082-8. doi: 10.1210/endo.134.3.8119146.