scholarly journals Tibetan Medicine Duoxuekang Capsule Ameliorates High-Altitude Polycythemia Accompanied by Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Ke Chen ◽  
Ning Li ◽  
Fangfang Fan ◽  
ZangJia Geng ◽  
Kehui Zhao ◽  
...  
Keyword(s):  
Brain Injury ◽  
Western Blot ◽  
Signaling Pathway ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Hypobaric Hypoxia ◽  
Tibetan Medicine ◽  
Whole Blood Viscosity ◽  
The Brain ◽  
Tof Ms

Objective: Duoxuekang (DXK) capsule is an empirical prescription for Tibetan medicine in the treatment of hypobaric hypoxia (HH)-induced brain injury in the plateau. This study aimed to investigate the protective effects and underlying molecular mechanisms of DXK on HH-induced brain injury.Methods: UPLC–Q-TOF/MS was performed for chemical composition analysis of DXK. The anti-hypoxia and anti-fatigue effects of DXK were evaluated by the normobaric hypoxia test, sodium nitrite toxicosis test, and weight-loaded swimming test in mice. Simultaneously, SD rats were used for the chronic hypobaric hypoxia (CHH) test. RBC, HGB, HCT, and the whole blood viscosity were evaluated. The activities of SOD and MDA in the brain, and EPO and LDH levels in the kidney were detected using ELISA. H&E staining was employed to observe the pathological morphology in the hippocampus and cortex of rats. Furthermore, immunofluorescence and Western blot were carried out to detect the protein expressions of Mapk10, RASGRF1, RASA3, Ras, and IGF-IR in the brain of rats. Besides, BALB/c mice were used for acute hypobaric hypoxia (AHH) test, and Western blot was employed to detect the protein expression of p-ERK/ERK, p-JNK/JNK, and p-p38/p38 in the cerebral cortex of mice.Results: 23 different chemical compositions of DXK were identified by UPLC–Q-TOF/MS. The anti-hypoxia test verified that DXK can prolong the survival time of mice. The anti-fatigue test confirmed that DXK can prolong the swimming time of mice, decrease the level of LDH, and increase the hepatic glycogen level. Synchronously, DXK can decrease the levels of RBC, HGB, HCT, and the whole blood viscosity under the CHH condition. Besides, DXK can ameliorate CHH-induced brain injury, decrease the levels of EPO and LDH in the kidney, reduce MDA, and increase SOD in the hippocampus. Furthermore, DXK can converse HH-induced marked increase of Mapk10, RASGRF1, and RASA3, and decrease of Ras and IGF-IR. In addition, DXK can suppress the ratio of p-ERK/ERK, p-JNK/JNK, and p-p38/p38 under the HH condition.Conclusion: Together, the cerebral protection elicited by DXK was due to the decrease of hematological index, suppressing EPO, by affecting the MAPK signaling pathway in oxidative damage, and regulating the RAS signaling pathway.

Viscosity and Red Cell Deformity in Arterial Disease

1979 ◽  
Author(s):  
G Cella ◽  
H de Haas ◽  
M Rampling ◽  
V Kakkar
Keyword(s):  
Vascular Disease ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Arterial Disease ◽  
Plasma Viscosity ◽  
Control Group ◽  
Fibrinogen Concentration ◽  
Red Cell ◽  
Whole Blood Viscosity ◽  
Significant Difference

Haemorrheological factors have been shown to be affected in many kings of vascular disease. The present study was undertaken to correlate these factors in normal subjects and patients suffering from peripheral arterial disease. Twenty-two patients were investigated; they had moderate or severe intermittent claudication, extent of disease being confirmed by aorto-arteriography and ankle-systolic pressure studies. Twenty-five controls with no symptoms or signs of arterial disease were selected with comparable age and sex distribution. Whole blood viscosity was measured at shear rates of 230 secs-1 and 23 secs-lat 37°c using a Wells Brookfield cone plate microvisco meter. Plasma viscosity was also measured in an identical manner. Erythrocyte flexibility was measured by centrifuge technique and fibrinogen concentration as well as haematocrit by standard techniques. The fibrinogen concentration appeared to be the only significant parameter; the mean concentration in patients with peripheral vascular disease of 463 ± 73mg/l00ml in the control group ( < 0.05). Although whole blood viscosity was high in patients, when corrected to a common haematocrit, there was no significant difference between patients and controls. The same megative correlation was found for plasma viscosity. The red cell flexibility was found to be increased in patients as compared to the control group, but this effect appeared to be simply proportional to the fibrinogen concentration.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

scholarly journals Absence of association between whole blood viscosity and delirium after cardiac surgery: a case-controlled study

2016 ◽  
Vol 11 (1) ◽  
Author(s):  
Shokoufeh CheheiliSobbi ◽  
Mark van den Boogaard ◽  
Arjen J. C. Slooter ◽  
Henry A. van Swieten ◽  
Linda Ceelen ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Controlled Study ◽  
Whole Blood Viscosity

scholarly journals Whole blood viscosity parameters and cerebral blood flow.

Stroke ◽  
1982 ◽  
Vol 13 (3) ◽  
pp. 296-301 ◽  
Author(s):  
J Grotta ◽  
R Ackerman ◽  
J Correia ◽  
G Fallick ◽  
J Chang
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Whole Blood Viscosity

The influence of lipoproteins on whole-blood viscosity at multiple shear rates

Metabolism ◽  
2005 ◽  
Vol 54 (6) ◽  
pp. 764-768 ◽  
Author(s):  
Arnold Slyper ◽  
Anh Le ◽  
Jason Jurva ◽  
David Gutterman
Keyword(s):  
Blood Viscosity ◽  
Whole Blood ◽  
Whole Blood Viscosity ◽  
Shear Rates

Standardization and automation of the measurement of whole blood viscosity

2016 ◽  
Vol 9 (4) ◽  
pp. 593-601
Author(s):  
J.H.A. Heuvelmans ◽  
P.A.M.M. Aarts ◽  
H. Goslinga
Keyword(s):  
Blood Viscosity ◽  
Whole Blood ◽  
Whole Blood Viscosity

scholarly journals Hydroxyurea Improves Oxygen Transport Effectiveness in Sickle Cell Anemia Patients

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2716-2716
Author(s):  
Vivien A. Sheehan ◽  
Sheryl Nelson ◽  
Caroline Yappan ◽  
Bogdan R. Dinu ◽  
Danielle Guffey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sickle Cell ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Patient Characteristics ◽  
Whole Blood Viscosity ◽  
Shear Rates ◽  
High Shear Rates ◽  
Altered Blood ◽  
Low Shear

Abstract Background: Sickle cell disease (SCD) patients have altered blood rheology due to erythrocyte abnormalities, including increased aggregation and reduced deformability, which together affect microcirculatory blood flow and tissue perfusion. At equal hematocrit, sickle cell blood viscosity is increased compared to normal individuals. The hematocrit to viscosity ratio (HVR) is a measure of red blood cell (RBC) oxygen carrying capacity, and is reduced in SCD with clinical consequences related to altered blood flow and reduced tissue oxygenation. Erythrocyte transfusions reduce HVR at low shear rates that mimic venous circulation, and do not change HVR at high shear rates that mimic arterial blood flow. Hydroxyurea is a safe and effective therapy for SCD; however, its effects on sickle cell rheology and HVR have not been fully investigated. Evaluating the effects of hydroxyurea on viscosity is especially critical, before its use is extended widely to patients with cerebrovascular disease or genotypes with higher hematocrit and higher viscosity such as Hemoglobin SC (HbSC). Methods: To determine the effects of hydroxyurea on viscosity and HVR, we designed a prospective study to measure whole blood viscosity at 45 s-1 (low shear) and 225 s-1(high shear) rates in pediatric patients with SCD using a Brookfield cone and plate viscometer under oxygenated conditions. Venous blood samples (1-3mL) were collected in EDTA and analyzed no more than 4 hours after phlebotomy; samples were run in duplicate by persons blinded to the patient’s sickle genotype and treatment status. Laboratory values were obtained using an ADVIA hematology analyzer. Samples were analyzed from three non-overlapping cohorts of patients with SCD and HbAA individuals for comparison: untreated HbSS patients (n= 43), HbSS patients treated with hydroxyurea at maximum tolerated dose (n=98), untreated HbSC patients (n=53) and HbAA patients (n=19). Laboratory parameters that differed significantly among the SCD groups were analyzed by simple linear regression. Results: Patient characteristics and viscosity measurements are shown in the Table. Within the SCD population, the viscosity was lowest among the untreated HbSS patients, presumably due to their low hematocrit, while viscosity was higher in HbSS patients on hydroxyurea and HbSC patients. When the HVR was calculated for each group, no significant difference was identified between untreated HbSS and untreated HbSC patients. However, hydroxyurea treatment significantly increased HVR at both 45s-1 and 225 s-1 (p<0.001), indicating that the slightly increased viscosity in this cohort was more than compensated by a higher hematocrit. Correlations were tested for hemoglobin (Hb), mean corpuscular volume (MCV), white blood cell count (WBC), absolute neutrophil count (ANC), absolute reticulocyte count (ARC), % fetal hemoglobin (HbF), and average red cell density in g/dL with HVR, at both shear rates. The hydroxyurea-associated HVR increase at both shear rates was independent of %HbF or MCV, but the increased HVR at 225 s-1was associated with lower WBC (p<0.001), lower ANC (p=0.002), and lower red cell density (p=.009). Conclusions: We provide prospective data on whole blood viscosity measurements in a large cohort of children with SCD. Hydroxyurea increases the hematocrit in HbSS patients more than the viscosity, and thus improves HVR. These findings imply that hydroxyurea improves RBC oxygen transport at both high and low shear rates, which should confer clinical benefits, and these effects are independent of HbF induction. Concerns about hydroxyurea increasing whole blood viscosity and reducing tissue oxygenation in children with cerebrovascular disease or HbSC patients may not be warranted, if the same beneficial HVR effects are achieved. Abstract 2717. Table 1. Patient characteristics. Viscosity was typically measured in duplicate and averaged for each patient. HVR at 45 s-1 and 225s-1 was calculated as hematocrit/viscosity. Results are presented as mean ± 2SD. HbAAn=19 HbSS, untreatedn=43 HbSS, on Hydroxyurean=98 HbSCn=53 Age (years) 15.4 ± 3.8 10.4 ± 5.1 10.7 ± 3.4 10.5 ± 4.3 Hemoglobin (gm/dL) 13.5 ± 1.7 8.5 ± 1.0 9.9 ± 1.4 11.0 ± 1.2 Hematocrit (%) 40.9 ± 5.3 25.5 ± 3.1 28.4 ± 3.7 31.3 ± 3.2 Viscosity (cP) at 45s-1 5.3 ± 0.9 4.6 ± 1.2 4.3 ± 0.9 5.5 ±0.9 HVR at 45s-1 7.5 ± 0.9 5.8 ± 1.1 6.75 ± 1.0 5.77 ± 0.7 Viscosity (cP) at 225s-1 3.8 ± 0.5 3.3 ± 0.5 3.4 ± 0.5 4.1 ± 0.5 HVR at 225s-1 10.3 ± 0.7 7.7 ± 0.8 8.53 ± 0.8 7.72 ± 0.6 Disclosures Off Label Use: Hydroxyurea is not FDA approved for use in pediatric sickle cell patients.

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