Study of propofol in bovine aortic endothelium

I. Inhibitory effect on bradykinin-induced intracellular calcium immobilization

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4 Citations (Scopus)

Abstract

Background: Propofol has been found to affect the intracellular calcium concentration with clinical manifestations of hypotension and bradycardia. The purpose of this study is to examine the effect of propofol on intracellular calcium immobilization in bovine aortic endothelium under the stimulation of bradykinin. Methods: In order to validate the effect of propofol on the alteration of intracellular calcium concentration, we used the cultured bovine endothelial cells (Gm 7372a) to measure the calcium immobilization within the cells pre-incubated with or without propofol of clinical concentration. Using Fluo-3 staining and a fluorescence spectrophotometer (confocal microscope), intracellular calcium immobilization was demonstrated by the appearance of "hot spots" within the cytoplasm and perinuclear regions after addition of bradykinin to the cells. The changes of fluorescence density measured within these areas versus the effect of time were analyzed and compared with the cells in control group. Results: After addition of bradykinin, intracellular calcium hot spots increased dramatically within seconds and reached a maximal level within 20 seconds. The concentrations of calcium gradually decreased to a constant level after about 3 min following the addition of bradykinin to the cells. With pretreatment of propofol at 0.01 mM and 37°C for 30 min, the immobilization of intracellular calcium from the intracellular stores were significantly inhibited that was demonstrated by the decreased appearance of hot spots when compared with control. Conclusions: Our data demonstrated that under the stimulation of bradykinin, propofol at 0.01 mM, could inhibit intracellular calcium release from the intracellular stores in bovine aortic endothelial cells. This phenomenon might explain the possible mechanism for the clinical manifestations of hypotension and/or bradycardia associated with propofol.

Original languageEnglish
Pages (from-to)181-186
Number of pages6
JournalActa Anaesthesiologica Sinica
Volume38
Issue number4
Publication statusPublished - 2000

Fingerprint

Bradykinin
Propofol
Immobilization
Endothelium
Calcium
Bradycardia
Hypotension
Endothelial Cells
Fluorescence
Cytoplasm
Staining and Labeling
Control Groups

Keywords

  • Bradykinin
  • Calcium
  • Endothelium
  • Propofol

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

@article{8c7eba3ddce2429cab81c5b72e31993c,
title = "Study of propofol in bovine aortic endothelium: I. Inhibitory effect on bradykinin-induced intracellular calcium immobilization",
abstract = "Background: Propofol has been found to affect the intracellular calcium concentration with clinical manifestations of hypotension and bradycardia. The purpose of this study is to examine the effect of propofol on intracellular calcium immobilization in bovine aortic endothelium under the stimulation of bradykinin. Methods: In order to validate the effect of propofol on the alteration of intracellular calcium concentration, we used the cultured bovine endothelial cells (Gm 7372a) to measure the calcium immobilization within the cells pre-incubated with or without propofol of clinical concentration. Using Fluo-3 staining and a fluorescence spectrophotometer (confocal microscope), intracellular calcium immobilization was demonstrated by the appearance of {"}hot spots{"} within the cytoplasm and perinuclear regions after addition of bradykinin to the cells. The changes of fluorescence density measured within these areas versus the effect of time were analyzed and compared with the cells in control group. Results: After addition of bradykinin, intracellular calcium hot spots increased dramatically within seconds and reached a maximal level within 20 seconds. The concentrations of calcium gradually decreased to a constant level after about 3 min following the addition of bradykinin to the cells. With pretreatment of propofol at 0.01 mM and 37°C for 30 min, the immobilization of intracellular calcium from the intracellular stores were significantly inhibited that was demonstrated by the decreased appearance of hot spots when compared with control. Conclusions: Our data demonstrated that under the stimulation of bradykinin, propofol at 0.01 mM, could inhibit intracellular calcium release from the intracellular stores in bovine aortic endothelial cells. This phenomenon might explain the possible mechanism for the clinical manifestations of hypotension and/or bradycardia associated with propofol.",
keywords = "Bradykinin, Calcium, Endothelium, Propofol",
author = "Yu-Ting Tai and Wu, {C. C.} and Gong-Jhe Wu and Huai-Chia Chang and Tyng-Guey Chen and Ruei-Ming Chen and Ta-Liang Chen",
year = "2000",
language = "English",
volume = "38",
pages = "181--186",
journal = "Asian Journal of Anesthesiology",
issn = "2468-824X",
publisher = "Elsevier Taiwan LLC",
number = "4",

}

TY - JOUR

T1 - Study of propofol in bovine aortic endothelium

T2 - I. Inhibitory effect on bradykinin-induced intracellular calcium immobilization

AU - Tai, Yu-Ting

AU - Wu, C. C.

AU - Wu, Gong-Jhe

AU - Chang, Huai-Chia

AU - Chen, Tyng-Guey

AU - Chen, Ruei-Ming

AU - Chen, Ta-Liang

PY - 2000

Y1 - 2000

N2 - Background: Propofol has been found to affect the intracellular calcium concentration with clinical manifestations of hypotension and bradycardia. The purpose of this study is to examine the effect of propofol on intracellular calcium immobilization in bovine aortic endothelium under the stimulation of bradykinin. Methods: In order to validate the effect of propofol on the alteration of intracellular calcium concentration, we used the cultured bovine endothelial cells (Gm 7372a) to measure the calcium immobilization within the cells pre-incubated with or without propofol of clinical concentration. Using Fluo-3 staining and a fluorescence spectrophotometer (confocal microscope), intracellular calcium immobilization was demonstrated by the appearance of "hot spots" within the cytoplasm and perinuclear regions after addition of bradykinin to the cells. The changes of fluorescence density measured within these areas versus the effect of time were analyzed and compared with the cells in control group. Results: After addition of bradykinin, intracellular calcium hot spots increased dramatically within seconds and reached a maximal level within 20 seconds. The concentrations of calcium gradually decreased to a constant level after about 3 min following the addition of bradykinin to the cells. With pretreatment of propofol at 0.01 mM and 37°C for 30 min, the immobilization of intracellular calcium from the intracellular stores were significantly inhibited that was demonstrated by the decreased appearance of hot spots when compared with control. Conclusions: Our data demonstrated that under the stimulation of bradykinin, propofol at 0.01 mM, could inhibit intracellular calcium release from the intracellular stores in bovine aortic endothelial cells. This phenomenon might explain the possible mechanism for the clinical manifestations of hypotension and/or bradycardia associated with propofol.

AB - Background: Propofol has been found to affect the intracellular calcium concentration with clinical manifestations of hypotension and bradycardia. The purpose of this study is to examine the effect of propofol on intracellular calcium immobilization in bovine aortic endothelium under the stimulation of bradykinin. Methods: In order to validate the effect of propofol on the alteration of intracellular calcium concentration, we used the cultured bovine endothelial cells (Gm 7372a) to measure the calcium immobilization within the cells pre-incubated with or without propofol of clinical concentration. Using Fluo-3 staining and a fluorescence spectrophotometer (confocal microscope), intracellular calcium immobilization was demonstrated by the appearance of "hot spots" within the cytoplasm and perinuclear regions after addition of bradykinin to the cells. The changes of fluorescence density measured within these areas versus the effect of time were analyzed and compared with the cells in control group. Results: After addition of bradykinin, intracellular calcium hot spots increased dramatically within seconds and reached a maximal level within 20 seconds. The concentrations of calcium gradually decreased to a constant level after about 3 min following the addition of bradykinin to the cells. With pretreatment of propofol at 0.01 mM and 37°C for 30 min, the immobilization of intracellular calcium from the intracellular stores were significantly inhibited that was demonstrated by the decreased appearance of hot spots when compared with control. Conclusions: Our data demonstrated that under the stimulation of bradykinin, propofol at 0.01 mM, could inhibit intracellular calcium release from the intracellular stores in bovine aortic endothelial cells. This phenomenon might explain the possible mechanism for the clinical manifestations of hypotension and/or bradycardia associated with propofol.

KW - Bradykinin

KW - Calcium

KW - Endothelium

KW - Propofol

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M3 - Article

VL - 38

SP - 181

EP - 186

JO - Asian Journal of Anesthesiology

JF - Asian Journal of Anesthesiology

SN - 2468-824X

IS - 4

ER -