Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo
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Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo. / Hansen, P R; Svendsen, Jesper Hastrup; Høyer, S; Kharazmi, A; Bendtzen, K; Haunsø, S.
I: American Journal of Physiology (Consolidated), Bind 266, Nr. 1 Pt 2, 01.01.1994, s. H60-7.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo
AU - Hansen, P R
AU - Svendsen, Jesper Hastrup
AU - Høyer, S
AU - Kharazmi, A
AU - Bendtzen, K
AU - Haunsø, S
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Tumor necrosis factor-alpha (TNF-alpha) is a primary mediator in the pathogenesis of tissue injury, and high circulating levels of TNF-alpha are found in a variety of pathological conditions. In open-chest anesthetized dogs, the effects of intracoronary recombinant human TNF-alpha (rTNF-alpha; 100 ng/kg for 60 min) on myocardial microvascular transport of a small hydrophilic indicator was examined by the single-injection, residue-detection method. Intracoronary infusion of rTNF-alpha increased myocardial microvascular transport after 120 min. This increase was preceded by a sustained decline in cardiac output and was associated with the appearance of areas with myocardial necrosis in the regional left ventricular wall. The myocardial plasma flow rate and maximum plasma flow rate in response to a 30-s coronary occlusion were not influenced by rTNF-alpha, although a decrease in the myocardial plasma flow rate was observed after 180 min. Circulating neutrophil counts were increased by rTNF-alpha, but the increase in myocardial capillary permeability could not be ascribed to regional neutrophil infiltration. We conclude that picomolar levels of rTNF-alpha can influence the movement of small hydrophilic molecules across the myocardial microvascular barrier in vivo and induce a prolonged decrease in cardiac performance. These effects may be important elements in myocardial pathophysiology.
AB - Tumor necrosis factor-alpha (TNF-alpha) is a primary mediator in the pathogenesis of tissue injury, and high circulating levels of TNF-alpha are found in a variety of pathological conditions. In open-chest anesthetized dogs, the effects of intracoronary recombinant human TNF-alpha (rTNF-alpha; 100 ng/kg for 60 min) on myocardial microvascular transport of a small hydrophilic indicator was examined by the single-injection, residue-detection method. Intracoronary infusion of rTNF-alpha increased myocardial microvascular transport after 120 min. This increase was preceded by a sustained decline in cardiac output and was associated with the appearance of areas with myocardial necrosis in the regional left ventricular wall. The myocardial plasma flow rate and maximum plasma flow rate in response to a 30-s coronary occlusion were not influenced by rTNF-alpha, although a decrease in the myocardial plasma flow rate was observed after 180 min. Circulating neutrophil counts were increased by rTNF-alpha, but the increase in myocardial capillary permeability could not be ascribed to regional neutrophil infiltration. We conclude that picomolar levels of rTNF-alpha can influence the movement of small hydrophilic molecules across the myocardial microvascular barrier in vivo and induce a prolonged decrease in cardiac performance. These effects may be important elements in myocardial pathophysiology.
KW - Animals
KW - Cell Count
KW - Coronary Circulation
KW - Dogs
KW - Female
KW - Hemodynamics
KW - Hyperemia
KW - Male
KW - Microcirculation
KW - Myocardium
KW - Neutrophils
KW - Recombinant Proteins
KW - Tumor Necrosis Factor-alpha
M3 - Journal article
C2 - 8304524
VL - 266
SP - H60-7
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
SN - 0363-6143
IS - 1 Pt 2
ER -
ID: 32476641