1.
Calcium channel blockers and risk of breast cancer: a meta-analysis of 17 observational studies.
Li, W, Shi, Q, Wang, W, Liu, J, Li, Q, Hou, F
PloS one. 2014;(9):e105801
Abstract
PURPOSE Studies on the association between the use of calcium channel blockers (CCBs) and breast cancer risk have reported inconsistent results. We quantitatively assessed this association by conducting a meta-analysis based on the evidence from observational studies. METHODS We searched PubMed, MEDLINE, EMBASE and the Cochrane Library for relevant studies published up to and including December 31, 2013. We calculated pooled risk ratios (RRs) for cancer risk. RESULTS A total of 17 studies (9 cohort studies, 8 case-control studies) were selected for further study. These studies included 149,607 female subjects, of which 53,812 were CCBs users, who were followed for 2-16 years. The risks of breast cancer among patients receiving CCBs were significantly different for the pooled RRs (95% confidence interval) of cohort studies 1.08 (0.95, 1.20) and case-control studies 0.98 (0.86, 1.09). Differences were also noted for cancer risk, for CCBs use of <5 years 0.96 (0.78, 1.15), and for >5 years 1.01 (0.74, 1.28), as well as for ever used 1.08 (0.95, 1.20), and for current use 1.13 (0.83, 1.42). The RR for studies longer than 10 years was 1.71 (1.01, 2.42), and for studies evaluating nifedipine was 1.10 (0.87, 1.33) and diltiazem was 0.75 (0.40, 1.10). CONCLUSIONS The long-term use of CCBs appears to have a significant relationship with breast cancer. Well-designed clinical trials are needed to optimize the doses and types of these drugs needed to minimize their carcinogenic potential.
2.
The influence of hyperoxic ventilation during sodium nitroprusside-induced hypotension on skeletal muscle tissue oxygen tension.
Suttner, SW, Lang, K, Boldt, J, Kumle, B, Maleck, WH, Piper, SN
Anesthesiology. 2002;(5):1103-8
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Abstract
BACKGROUND Increasing inspired oxygen concentrations might provide a simple and effective intervention to increase oxygen tension in tissues during controlled hypotension. To test this hypothesis, the influence of hyperoxic ventilation (100% O2) on skeletal muscle oxygen partial pressure (Ptio2) in patients receiving sodium nitroprusside-induced controlled hypotension was studied. METHODS Forty-two patients undergoing radical prostatectomy were prospectively studied and randomly divided into three groups as follows: (1) Controlled hypotension induced by sodium nitroprusside (mean arterial blood pressure, 50 mmHg) and hyperoxic ventilation (CH-100%; n = 14); (2) controlled hypotension and ventilation with 50% O2 in nitrous oxide (CH-50%; n = 14); and (3) standard normotensive anesthesia with 50% O2 in nitrous oxide (control; n = 14). Ptio2 values were measured continuously in all patients using implantable polarographic microprobes. Arterial blood gases and lactate concentrations were analyzed in 30-min intervals. RESULTS Surgical blood loss and transfusion requirements were significantly reduced in both groups receiving hypotensive anesthesia. During surgery, arterial partial pressure of oxy-gen and arterial oxygen content were significantly higher in patients of the CH-100% group. Baseline values of Ptio2 were comparable between the groups (CH-50%: 25.0 +/- 0.7 mmHg; CH-100%: 25.2 +/- 0.2 mmHg; control: 24.5 +/- 0.2 mmHg). After a transient increase in Ptio2 in the CH-100% group during normotension, Ptio2 values returned to baseline and remained unchanged in the control group. Ptio2 decreased significantly during the hypotensive period in the CH-50% group. The lowest mean Ptio2 values were 15.0 +/- 4.1 mmHg in the CH-50% group, 24.2 +/- 4.9 mmHg in the CH-100% group, and 23.5 +/- 3.8 mmHg in the control group. There were no significant changes in lactate plasma concentrations in any group throughout the study period. CONCLUSIONS Hyperoxic ventilation improved skeletal muscle tissue oxygenation during sodium nitroprusside-induced hypotension. This improved local tissue oxygenation seems to be most likely due to an increase in convective oxygen transport and the attenuation of hyperoxemia-induced arteriolar vasoconstriction by sodium nitroprusside.