PMID- 7633696
OWN - NLM
STAT- MEDLINE
DCOM- 19950914
LR  - 20061115
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 152
IP  - 2
DP  - 1995 Aug
TI  - Anti-tumor necrosis factor-alpha prevents decreased ventricular contractility in 
      endotoxemic pigs.
PG  - 480-8
AB  - It is not known how the decrease in left ventricular contractility following 
      endotoxin exposure is mediated, or whether this decrease is preventable by 
      antibodies to tumor necrosis factor-alpha (TNF alpha). Four groups of six 
      anesthetized and instrumented pigs were pretreated with ovine polyclonal antibody 
      to human TNF alpha (anti-TNF alpha), nonspecific IgG, or saline, and then treated 
      with either endotoxin or saline. We measured hemodynamics and left ventricular 
      pressures (Millar catheter) and volumes (conductance catheter). Left ventricular 
      contractility was assessed using the slope (Emax) of the end-systolic 
      pressure-volume relationship. Four hours after the start of endotoxin infusion in 
      the nonspecific IgG pretreated group, Emax had decreased by 44 +/- 6% (p < 0.05), 
      mean arterial pressure had decreased from 115 +/- 7 mm Hg to 70 +/- 10 mm Hg (p < 
      0.05), and cardiac output was rapidly decreasing after an initial increase (p < 
      0.05). Anti-TNF alpha significantly reduced the decrease in Emax (11 +/- 9%, p < 
      0.05), and the systemic hypotension (108 +/- 15 mm Hg to 99 +/- 6 mm Hg, p < 
      0.05), at 4 h, and prevented the late decrease in cardiac output. This suggests 
      that TNF alpha is an important early mediator in sepsis leading to decreased left 
      ventricular contractility.
FAU - Herbertson, M J
AU  - Herbertson MJ
AD  - Pulmonary Research Laboratory, St. Paul's Hospital, University of British 
      Columbia, Vancouver, Canada.
FAU - Werner, H A
AU  - Werner HA
FAU - Goddard, C M
AU  - Goddard CM
FAU - Russell, J A
AU  - Russell JA
FAU - Wheeler, A
AU  - Wheeler A
FAU - Coxon, R
AU  - Coxon R
FAU - Walley, K R
AU  - Walley KR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Antibodies)
RN  - 0 (Endotoxins)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies/*immunology
MH  - Atrial Function, Right/immunology
MH  - Blood Pressure/immunology
MH  - Cardiac Output/immunology
MH  - Cardiac Volume/immunology
MH  - Endotoxins/*blood/immunology
MH  - Heart Rate/immunology
MH  - Humans
MH  - Immunoglobulin G/immunology
MH  - Myocardial Contraction/*immunology
MH  - Pulmonary Artery
MH  - Sheep
MH  - Shock, Septic/*immunology
MH  - Stroke Volume/immunology
MH  - Swine
MH  - Systole
MH  - Tumor Necrosis Factor-alpha/*immunology
MH  - Vascular Resistance/immunology
MH  - Ventricular Function, Left/*immunology
MH  - Ventricular Pressure/immunology
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - 10.1164/ajrccm.152.2.7633696 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 1995 Aug;152(2):480-8. doi: 
      10.1164/ajrccm.152.2.7633696.