Data on microcirculatory parameters of GTS- 21 treated rats assessed by intravital microscopy

Abstract

This article contains animal experimental data associated with the research article entitled "GTS-21 reduces microvascular permeability during experimental endotoxemia" (Schmidt et al., 2017) [1] (supplementary datasets of baseline intravital microscopic measurements, baseline TNF-α levels and vital parameters of the evaluated experimental groups are provided). Beneficial anti-inflammatory effects of cholinergic mediators on microvascular inflammation have been demonstrated by intravital microscopic investigations (Schmidt et al., 2015) [2], therefore we evaluated the effect of the cholinergic mediator GTS-21 on microcirculatory alterations during endotoxemia [1]. The data regarding microcirculatory effects of GTS-21 treatment ((3-(2,4-Dimethoxybenzylidene)-anabaseine dihydrochloride; 1 mg/kg; i.v.) in non-endotoxemic animals are presented in this article.

Fig. 1

Data on microcirculatory parameters of GTS-21 treated non-endotoxemic animals compared with the crystalloid treated control group 180 min after the baseline IVM. A: No significant difference in macromolecular leakage was observed between the non-endotoxemic GTS-21 control group and the control group 180 min after baseline IVM (scatter plots with medians and interquartile range (Q1–Q3) are displayed; ns: not significant). B: No significant difference in the number of adherent leukocytes was observed between the non-endotoxemic GTS-21 control group and the control group 180 min after baseline IVM (adherent leukocytes are expressed as cells/100 µm venule length; scatter plots with medians and interquartile range (Q1–Q3) are displayed; ns: not significant). C: Venular wall shear rate was significantly increased in postcapillary venules in the non-endotoxemic GTS-21 control group compared to the control group 180 min after baseline IVM (venular wall shear rate is expressed as ^s−1; * non-endotoxemic GTS 21 control vs. control; p<0.05; scatter plots with medians and interquartile range (Q1–Q3) are displayed). D: No significant difference in TNF-α levels was observed between the non-endotoxemic GTS-21 group and the control group 180 min after baseline IVM (TNF-α levels are expressed as pg/ml; scatter plots with medians and interquartile range (Q1–Q3) are displayed; ns: not significant).

Fig. 2

Vital parameters during the 240 min experiment in the experimental groups. A: heart frequency (HF, (min⁻¹)), B: mean arterial pressure (MAP, mmHg)), C: temperature (°C), 2D: pH, E: hematocrit (HCt, (%)); bar diagrams with medians and interquartile range (Q1–Q3) are displayed.

Fig. 3

Microcirculatory parameters and TNF α levels at the baseline IVM. No significant differences were observed between all experimental groups (n=10/group) at the baseline IVM before randomization (scatter plots with medians and interquartile range (Q1–Q3) are displayed; ns: not significant). A: Macromolecular leakage of fluorescein isothiocyanate-labeled bovine albumin expressed as the ratio of perivenular to venular fluorescence intensity in arbitrary units. B: Number of adherent leukocytes expressed as cells/100 µm venule length. C: Venular wall shear rate based on mean red blood cell velocities expressed as s⁻¹. D: TNF-α levels expressed as pg/ml.

Fig. 4

Exemplary fluorescent IVM images of postcapillary venules with the approximate median perivenular macromolecular leakage values of the respective experimental groups at the baseline IVM visualizing the results of Fig. 3A.