Materials and methods: Eighty-four patients were randomly divided into two groups receiving either study drug infusion. Anxiety
score, level of sedation using the Bispectral Index and Observer’s Assessment of Alertness and Sedation, hemodynamic stability, and
overall patient’s feedback on anxiolysis were assessed.
Results: Both groups showed a significant drop in mean anxiety score at 10 and 30 min after starting surgery. Difference in median
anxiety scores showed a significant reduction in anxiety score at the end of the surgery in the dexmedetomidine group compared to the
propofol group. Dexmedetomidine and propofol showed a significant drop in mean arterial pressure in the first 30 min and first 10 min
respectively. Both drugs demonstrated a significant drop in heart rate in the first 20 min from baseline after starting the drug infusion.
Patients in the dexmedetomidine group (76.20%) expressed statistically excellent feedback on anxiolysis compared to patients in the
propofol group (45.20%).
Conclusion: Dexmedetomidine infusion was found to significantly reduce anxiety levels at the end of surgery compared to propofol
during regional anesthesia.
METHODS: Observational study. Nonglaucomatous patients on NIPD underwent systemic and ocular assessment including mean arterial pressure (MAP), body weight, serum osmolarity, visual acuity, IOP measurement, and ASOCT within 2 hours both before and after NIPD. The Zhongshan Angle Assessment Program (ZAAP) was used to measure ASOCT parameters including anterior chamber depth, anterior chamber width, anterior chamber area, anterior chamber volume, lens vault, angle opening distance, trabecular-iris space area, and angle recess area. T tests and Pearson correlation tests were performed with P<0.05 considered statistically significant.
RESULTS: A total of 46 eyes from 46 patients were included in the analysis. There were statistically significant reductions in IOP (-1.8±0.6 mm Hg, P=0.003), MAP (-11.9±3.1 mm Hg, P<0.001), body weight (-0.7±2.8 kg, P<0.001), and serum osmolarity (-3.4±2.0 mOsm/L, P=0.002) after NIPD. All the ASOCT parameters did not have any statistically significant changes after NIPD. There were no statistically significant correlations between the changes in IOP, MAP, body weight, and serum osmolarity (all P>0.05).
CONCLUSIONS: NIPD results in reductions in IOP, MAP, body weight, and serum osmolarity in nonglaucomatous patients.
Methods: The current study was carried on 49 hypertensive rats divided into seven groups, including i) control; ii) L-NAME (10 mg/kg); iii) sodium nitroprusside (SNP) (50 μg/kg) plus L-NAME; iv and v) aqueous fraction of ZJ (150 mg/kg and 300 mg/kg) plus L-NAME; vi) and vii) ethyl acetate fractions of ZJ (150 mg/kg and 300 mg/kg) plus L-NAME. The rats were orally treated with both fractions for four weeks and received intravenous L-NAME on the 28th day. The mean arterial pressure (MAP), systolic blood pressure (SBP) and heart rate (HR) of the rats were recorded then maximal changes (Δ) of MAP, SBP and HR were calculated and compared with changes of control and L-NAME.
Results: According to the obtained results of the present study, it was shown that the administration of L-NAME significantly increased ΔMAP, ΔSBP and ΔHR, and these effects were significantly attenuated by administration of SNP. The pre-treatment with both doses (150 mg/kg and 300 mg/kg) of aqueous and ethyl acetate fractions could significantly reduce cardiovascular responses induced by L-NAME that comparable with SNP. However, a lower dose of aqueous fractions and higher dose of ethyl acetate fractions were reported with stronger effects.
Conclusion: The results of the current study showed that both the aqueous and ethyl acetate fractions of ZJ through the effect on nitric oxide system can prevent the development of HTN induced by L-NAME.
PURPOSE: The purpose of this study was to investigate the clinical characteristics, including 24-hour ocular perfusion pressure and risk of progression in patients with baseline central VF defect, as compared with those with peripheral VF defect in NTG.
DESIGN: This was a prospective, longitudinal study.
METHODS: A total of 65 NTG patients who completed 5 years of follow-up were included in this study. All the enrolled patients underwent baseline 24-hour intraocular pressure and blood pressure monitoring via 2-hourly measurements in their habitual position and had ≥5 reliable VF tests during the 5-year follow-up. Patients were assigned to two groups on the basis of VF defect locations at baseline, the central 10 degrees, and the peripheral 10- to 24-degree area. Modified Anderson criteria were used to assess global VF progression over 5 years. Kaplan-Meier analyses were used to compare the elapsed time of confirmed VF progression in the two groups. Hazard ratios for the association between clinical risk factors and VF progression were obtained by using Cox proportional hazards models.
RESULTS: There were no significant differences between the patients with baseline central and peripheral VF defects in terms of demography, clinical, ocular and systemic hemodynamic factors. Eyes with baseline defects involving the central fields progressed faster (difference: βcentral=-0.78 dB/y, 95% confidence interval=-0.22 to -1.33, P=0.007) and have 3.56 times higher hazard of progressing (95% confidence interval=1.17-10.82, P=0.025) than those with only peripheral defects.
CONCLUSION: NTG patients with baseline central VF involvement are at increased risk of progression compared with those with peripheral VF defect.
METHODS: Sodium nitrite (50mg/L) was given to angiotensin II-infused hypertensive C57BL/6J (eight to ten weeks old) mice for two weeks in the drinking water. Arterial systolic blood pressure was measured using the tail-cuff method. Vascular responsiveness of isolated aortae and renal arteries was studied in wire myographs. The level of nitrite in the plasma and the cyclic guanosine monophosphate (cGMP) content in the arterial wall were determined using commercially available kits. The production of reactive oxygen species (ROS) and the presence of proteins (nitrotyrosine, NOx-2 and NOx-4) involved in ROS generation were evaluated with dihydroethidium (DHE) fluorescence and by Western blotting, respectively.
RESULTS: Chronic administration of sodium nitrite for two weeks to mice with angiotensin II-induced hypertension decreased systolic arterial blood pressure, reversed endothelial dysfunction, increased plasma nitrite level as well as vascular cGMP content. In addition, sodium nitrite treatment also decreased the elevated nitrotyrosine and NOx-4 protein level in angiotensin II-infused hypertensive mice.
CONCLUSIONS: The present study demonstrates that chronic treatment of hypertensive mice with sodium nitrite improves impaired endothelium function in conduit and resistance vessels in addition to its antihypertensive effect, partly through inhibition of ROS production.