Ambient Fine Particulate Matter Exposure and Blood Pressure: Evidence from a Large Chinese Multiple Follow-Up Study.

Objective: This study aimed to investigate the association of ambient PM2.5 exposure with blood pressure (BP) at the population level in China. Methods: A total of 14,080 participants who had at least two valid blood pressure records were selected from the China Health and Retirement Longitudinal Survey during 2011-2015. Their long-term PM2.5 exposure was assessed at the geographical level, on the basis of a regular 0.1° × 0.1° grid over China. A mixed-effects regression model was used to assess associations. Results: Each decrease of 10 µg/m3 in the 1 year-mean PM2.5 concentration (FPM1Y) was associated with a decrease of 1.24 [95% confidence interval (CI): 0.84-1.64] mmHg systolic BP (SBP) and 0.50 (95% CI: 0.25-0.75) mmHg diastolic BP (DBP), respectively. A robust association was observed between the long-term decrease in PM2.5 and decreased BP in the middle-aged and older population. Using a generalized additive mixed model, we further found that SBP increased nonlinearly overall with FPM1Y but in an approximately linear range when the FPM1Y concentration was < 70 µg/m3; In contrast, DBP increased approximately linearly without a clear threshold. Conclusion: Efficient control of PM2.5 air pollution may promote vascular health in China. Our study provides robust scientific support for making the related air pollution control policies.

Inhibition of endoplasmic reticulum stress alleviates secondary injury after traumatic brain injury.

Apoptosis after traumatic brain injury has been shown to be a major factor influencing prognosis and outcome. Endoplasmic reticulum stress may be involved in mitochondrial mediated neuronal apoptosis. Therefore, endoplasmic reticulum stress has become an important mechanism of secondary injury after traumatic brain injury. In this study, a rat model of traumatic brain injury was established by lateral fluid percussion injury. Fluorescence assays were used to measure reactive oxygen species content in the cerebral cortex. Western blot assays were used to determine expression of endoplasmic reticulum stress-related proteins. Hematoxylin-eosin staining was used to detect pathological changes in the cerebral cortex. Transmission electron microscopy was used to measure ultrastructural changes in the endoplasmic reticulum and mitochondria. Our results showed activation of the endoplasmic reticulum stress-related unfolded protein response. Meanwhile, both the endoplasmic reticulum stress response and mitochondrial apoptotic pathway were activated at different stages post-traumatic brain injury. Furthermore, pretreatment with the endoplasmic reticulum stress inhibitor, salubrinal (1 mg/kg), by intraperitoneal injection 30 minutes before injury significantly inhibited the endoplasmic reticulum stress response and reduced apoptosis. Moreover, salubrinal promoted recovery of mitochondrial function and inhibited activation of the mitochondrial apoptotic pathway post-traumatic brain injury. These results suggest that endoplasmic reticulum stress might be a key factor for secondary brain injury post-traumatic brain injury.

Protective effects of ginsenoside Rb1 on septic rats and its mechanism.

This study aims to observe the protective effects of ginsenoside Rb1 on liver and lung in rats with septic shock and reveal its mechanism. Rats were randomly divided into three groups: sham, cecal ligation and puncture (CLP), and CLP with ginsenoside Rb1. Then, the survival rate, arterial blood pressure, TLR4 mRNA, and TNF-α levels were determined. The liver and lung tissues were stained with hematoxylin-eosin (HE). The overall survival rate of the Rb1 group was significantly higher than that of the CLP group. Mean arterial blood pressure went down in both the CLP and Rb1 groups after CLP, and there was a significant difference both in the sham and Rb1 groups when compared with the CLP group. The Rb1 treatment group had markedly lower TLR4 mRNA expression and TNF-α levels than the CLP group. In the CLP group, pathology showed swelling, degeneration, necrosis, and neutrophil infiltration in the liver and alveolar epithelial cells. However, in the Rb1 group, there was mild degeneration and slight neutrophil infiltration, but no obvious necrosis. Rb1 may improve the survival rate, ameliorate arterial blood pressure, and protect the liver and lung in septic shock rats by downregulating the expression of TLR4 mRNA and inhibiting the production of TNF-α.

[Effects of adrenergic beta-1 antagonists on hemodynamics of severe septic patients].

OBJECTIVE: To explore the effects of adrenergic beta-1 antagonists on hemodynamics of severe septic patients. METHODS: A total of 16 severe septic patients underwent mechanical ventilation from June 2012 to December 2012 at Fourth Affiliated Hospital of Nanchang University. There were 14 males and 2 females with a mean age of (58 ± 6) years (range: 48 - 67 years). Among them, there were multiple trauma (n = 4), acute severe pancreatitis (n = 6) and recent tumorectomy for gastrointestinal cancer (n = 6). The adrenergic beta-1 antagonist esmolol was injected through central venous catheter to reduce heart rate by 20% from baseline. Various indices (heart rate, systolic blood pressure, diastolic blood pressure, cardiac output, cardiac index, central venous pressure, pulmonary artery wedge pressure, pulmonary vascular resistance index, systemic vascular resistance index and stroke volume index) were monitored by a multifunctional and hemodynamic monitor connected to pulmonary artery catheter. And other indices of arterial pressure of carbon dioxide (PaCO2), lactate (Lac) concentration, superior vena cava oxygen saturation (ScvO2), superior vena cava carbon dioxide pressure (PcvO2) and central venous-to-arterial carbon dioxide tension difference (Pcv-aCO2) were measured by a blood-gas-analyzer before 10 minutes and after 3 hours of dosing. RESULTS: Heart rate and cardiac index decreased significantly at 3 hours post-dosing compared with that at pre-dosing ((91 ± 13) vs (114 ± 15) beats per minute, (3.4 ± 0.7) vs (4.2 ± 0.8) L×min(-1)×m(-2), P < 0.05), but systolic blood pressure, diastolic blood pressure, central venous pressure, pulmonary wedge pressure, pulmonary vascular resistance index, systemic vascular resistance index and stroke index showed no significant changes ((100 ± 13) vs (108 ± 14) mm Hg (1 mm Hg = 0.133 kPa), (62 ± 7) vs (64 ± 6) mm Hg, (11.8 ± 2.5) vs (12.1 ± 2.4) mm Hg, (13 ± 5) vs (14 ± 4) mm Hg, (201 ± 72) vs (179 ± 95) dyn×s/(cm(5)×m(2)), (1360 ± 520) vs (1366 ± 538) dyn×s/(cm(5)×m(2)), (40 ± 9) vs (38 ± 6) ml/(beat×m(2)), all P > 0.05). ScvO2, Lac and Pcv-aCO2 also showed no significant change ((72.8 ± 5.3)% vs (70.1 ± 4.0)%, (2.11 ± 0.13) vs (2.31 ± 0.23) mmol/L, (3.9 ± 1.0) vs (4.5 ± 0.8) mm Hg, all P > 0.05). CONCLUSION: Adrenergic beta-1 antagonist may reduce cardiac output in proportion to the percentage decreases in heart rate in severe septic patients without adverse effects upon cardiac function and systemic perfusion.