PMID- 8779822
OWN - NLM
STAT- MEDLINE
DCOM- 19961220
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 270
IP  - 2 Pt 2
DP  - 1996 Feb
TI  - Serum tumor necrosis factor-alpha does not mediate endotoxin-induced myocardial 
      depression in rabbits.
PG  - H485-91
AB  - Tumor necrosis factor-alpha (TNF-alpha) is an endogenous mediator for several 
      effects of endotoxin. To evaluate whether TNF-alpha mediates endotoxin-induced 
      left ventricular (LV) dysfunction, we measured LV function (sonomicrometers) and 
      serum TNF-alpha (cytolytic assay) in anesthetized rabbits given endotoxin (100 
      micrograms/kg iv). In the control group (n = 8), systolic depression (defined by 
      a > 10% increase in end-systolic volume at a matched end-systolic pressure) 
      developed in four rabbits and diastolic dilation (> 10% increase in end-diastolic 
      volume at a matched end-diastolic pressure) developed in three rabbits. Neither 
      the increase in end-systolic volume nor the increase in end-diastolic volume 
      correlated with the increase in TNF-alpha, which reached a peak of 2,875 +/- 762 
      U/ml. In a second group of rabbits (n = 7), a goat polyclonal anti-rabbit 
      antibody to TNF-alpha was given 30-60 min before endotoxin. Anti-TNF-alpha 
      antibody alone did not alter LV function. Although the TNF-alpha response to 
      endotoxin was effectively blunted (peak TNF-alpha remained < 100 U/ml), all seven 
      rabbits developed systolic depression (P = 0.08 compared with control group) and 
      diastolic dilation (P = 0.03). We conclude that serum TNF-alpha does not mediate 
      endotoxin-induced LV systolic depression or diastolic dilation in this model.
FAU - Nishikawa, Y
AU  - Nishikawa Y
AD  - Department of Medicine, Department of Veterans Affairs Medical Center, San Diego, 
      California, USA.
FAU - Mathison, J
AU  - Mathison J
FAU - Lew, W Y
AU  - Lew WY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antibodies)
RN  - 0 (Endotoxins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology
MH  - Blood Pressure
MH  - Blood Volume
MH  - Endotoxins/*pharmacology
MH  - Heart/*drug effects
MH  - Rabbits
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism
MH  - Ventricular Function, Left
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 10.1152/ajpheart.1996.270.2.H485 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 Feb;270(2 Pt 2):H485-91. doi: 
      10.1152/ajpheart.1996.270.2.H485.