Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation

Brett C. Sheridan, Robert C. McIntyre, Daniel R. Meldrum, Joseph C. Cleveland, Jeanette Agrafojo, John H. Eisenach, David A. Fullerton

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

We tested the hypothesis that neutrophils contribute to endotoxin-induced impairment of endothelium-dependent and -independent cyclic guanosine monophosphate (cGMP)-mediated pulmonary vascular smooth muscle relaxation. Rats were studied 6 h after endotoxin (20 mg/kg, intraperitoneal) or saline (1 cc, intraperitoneal). Neutrophil-depleted rats were studied 4 days after administration of vinblastine (750 μg/kg, intravenous). Concentration-response curves were generated for acetylcholine and sodium nitroprusside in isolated pulmonary arterial rings (10-9 M to 10-6 M). The absolute neutrophil count of controls was 1050 ± 206 neutrophils/mL, and the absolute neutrophil count of vinblastine-treated rats was 100 ± 41 neutrophils/mL (p < .05 versus controls) and 25 ± 25 neutrophils/mL in vinblastine-treated rats receiving endotoxin (p < .05 versus control and endotoxin). Endotoxin-induced impairment of endothelium-dependent and -independent cGMP-mediated pulmonary vasorelaxation was significantly attenuated by prior treatment with vinblastine. We conclude that neutrophils contribute to the pathogenesis of endotoxin-induced impairment of cGMP-mediated pulmonary vascular smooth muscle relaxation.

Original languageEnglish (US)
Pages (from-to)35-38
Number of pages4
JournalShock
Volume6
Issue number1
StatePublished - Jul 1996
Externally publishedYes

Fingerprint

Vinblastine
Endotoxins
Vasodilation
Neutrophils
Lung
Cyclic GMP
Muscle Relaxation
Vascular Smooth Muscle
Endothelium
Nitroprusside
Acetylcholine

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

Sheridan, B. C., McIntyre, R. C., Meldrum, D. R., Cleveland, J. C., Agrafojo, J., Eisenach, J. H., & Fullerton, D. A. (1996). Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation. Shock, 6(1), 35-38.

Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation. / Sheridan, Brett C.; McIntyre, Robert C.; Meldrum, Daniel R.; Cleveland, Joseph C.; Agrafojo, Jeanette; Eisenach, John H.; Fullerton, David A.

In: Shock, Vol. 6, No. 1, 07.1996, p. 35-38.

Research output: Contribution to journalArticle

Sheridan, BC, McIntyre, RC, Meldrum, DR, Cleveland, JC, Agrafojo, J, Eisenach, JH & Fullerton, DA 1996, 'Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation', Shock, vol. 6, no. 1, pp. 35-38.
Sheridan BC, McIntyre RC, Meldrum DR, Cleveland JC, Agrafojo J, Eisenach JH et al. Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation. Shock. 1996 Jul;6(1):35-38.
Sheridan, Brett C. ; McIntyre, Robert C. ; Meldrum, Daniel R. ; Cleveland, Joseph C. ; Agrafojo, Jeanette ; Eisenach, John H. ; Fullerton, David A. / Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation. In: Shock. 1996 ; Vol. 6, No. 1. pp. 35-38.
@article{8a839b1ecc31421ea3f41c544c40dadd,
title = "Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation",
abstract = "We tested the hypothesis that neutrophils contribute to endotoxin-induced impairment of endothelium-dependent and -independent cyclic guanosine monophosphate (cGMP)-mediated pulmonary vascular smooth muscle relaxation. Rats were studied 6 h after endotoxin (20 mg/kg, intraperitoneal) or saline (1 cc, intraperitoneal). Neutrophil-depleted rats were studied 4 days after administration of vinblastine (750 μg/kg, intravenous). Concentration-response curves were generated for acetylcholine and sodium nitroprusside in isolated pulmonary arterial rings (10-9 M to 10-6 M). The absolute neutrophil count of controls was 1050 ± 206 neutrophils/mL, and the absolute neutrophil count of vinblastine-treated rats was 100 ± 41 neutrophils/mL (p < .05 versus controls) and 25 ± 25 neutrophils/mL in vinblastine-treated rats receiving endotoxin (p < .05 versus control and endotoxin). Endotoxin-induced impairment of endothelium-dependent and -independent cGMP-mediated pulmonary vasorelaxation was significantly attenuated by prior treatment with vinblastine. We conclude that neutrophils contribute to the pathogenesis of endotoxin-induced impairment of cGMP-mediated pulmonary vascular smooth muscle relaxation.",
author = "Sheridan, {Brett C.} and McIntyre, {Robert C.} and Meldrum, {Daniel R.} and Cleveland, {Joseph C.} and Jeanette Agrafojo and Eisenach, {John H.} and Fullerton, {David A.}",
year = "1996",
month = "7",
language = "English (US)",
volume = "6",
pages = "35--38",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Vinblastine attenuates endotoxin-induced impairment of CGMP-mediated pulmonary vasorelaxation

AU - Sheridan, Brett C.

AU - McIntyre, Robert C.

AU - Meldrum, Daniel R.

AU - Cleveland, Joseph C.

AU - Agrafojo, Jeanette

AU - Eisenach, John H.

AU - Fullerton, David A.

PY - 1996/7

Y1 - 1996/7

N2 - We tested the hypothesis that neutrophils contribute to endotoxin-induced impairment of endothelium-dependent and -independent cyclic guanosine monophosphate (cGMP)-mediated pulmonary vascular smooth muscle relaxation. Rats were studied 6 h after endotoxin (20 mg/kg, intraperitoneal) or saline (1 cc, intraperitoneal). Neutrophil-depleted rats were studied 4 days after administration of vinblastine (750 μg/kg, intravenous). Concentration-response curves were generated for acetylcholine and sodium nitroprusside in isolated pulmonary arterial rings (10-9 M to 10-6 M). The absolute neutrophil count of controls was 1050 ± 206 neutrophils/mL, and the absolute neutrophil count of vinblastine-treated rats was 100 ± 41 neutrophils/mL (p < .05 versus controls) and 25 ± 25 neutrophils/mL in vinblastine-treated rats receiving endotoxin (p < .05 versus control and endotoxin). Endotoxin-induced impairment of endothelium-dependent and -independent cGMP-mediated pulmonary vasorelaxation was significantly attenuated by prior treatment with vinblastine. We conclude that neutrophils contribute to the pathogenesis of endotoxin-induced impairment of cGMP-mediated pulmonary vascular smooth muscle relaxation.

AB - We tested the hypothesis that neutrophils contribute to endotoxin-induced impairment of endothelium-dependent and -independent cyclic guanosine monophosphate (cGMP)-mediated pulmonary vascular smooth muscle relaxation. Rats were studied 6 h after endotoxin (20 mg/kg, intraperitoneal) or saline (1 cc, intraperitoneal). Neutrophil-depleted rats were studied 4 days after administration of vinblastine (750 μg/kg, intravenous). Concentration-response curves were generated for acetylcholine and sodium nitroprusside in isolated pulmonary arterial rings (10-9 M to 10-6 M). The absolute neutrophil count of controls was 1050 ± 206 neutrophils/mL, and the absolute neutrophil count of vinblastine-treated rats was 100 ± 41 neutrophils/mL (p < .05 versus controls) and 25 ± 25 neutrophils/mL in vinblastine-treated rats receiving endotoxin (p < .05 versus control and endotoxin). Endotoxin-induced impairment of endothelium-dependent and -independent cGMP-mediated pulmonary vasorelaxation was significantly attenuated by prior treatment with vinblastine. We conclude that neutrophils contribute to the pathogenesis of endotoxin-induced impairment of cGMP-mediated pulmonary vascular smooth muscle relaxation.

UR - http://www.scopus.com/inward/record.url?scp=0030184951&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030184951&partnerID=8YFLogxK

M3 - Article

VL - 6

SP - 35

EP - 38

JO - Shock

JF - Shock

SN - 1073-2322

IS - 1

ER -