Gender differences in masticatory function in elderly adults with natural dentition

Odontology - The purpose of this study was to clarify the presence or absence of gender differences in masticatory function in elderly adults with completely natural dentition. Fifty-six elderly...     

Does intravenous landiolol, a β1-adrenergic blocker, affect stroke volume variation?

Purpose

There are no reports about the effect of bradycardia on stroke volume variation (SVV), and we hypothesized that induced bradycardia alters the value of SVV. Landiolol, an ultra-short-acting adrenergic β₁-receptor blocking agent, was reported to induce bradycardia without decreasing blood pressure. The initial aim of this prospective study was to investigate changes in SVV values by induced bradycardia in patients with good cardiac function.

Methods

At 30 min after anesthesia induction, if heart rate (HR) was >80 bpm, the patient was chosen as a subject. Ten ASA physical status I–II patients aged 38–75 years who were scheduled for elective abdominal surgery were included in this study. Baseline values were recorded, and then administration of landiolol was started at 125 μg/kg/min for 1 min and then continued at 40 μg/kg/min. SVV and other parameters were recorded at baseline and 3 min after continuous landiolol injection.

Results

Landiolol significantly decreased systolic arterial pressure, and diastolic arterial pressure, contrary to our expectations, and also HR, SVV, cardiac output, stroke volume index, and pressure of end-tidal CO₂, whereas systemic vascular resistance values increased significantly.

Conclusions

SVV decreased after continuous administration of a β₁-adrenergic blocker, probably because of a decrease in the difference of maximum stroke volume (SV) and minimum SV, or the downward shift of the Frank–Starling curve that occurred after landiolol administration. We believe that SVV values might be overestimated or misinterpreted when HR is decreased by landiolol and might not necessarily indicate that the patient is hypervolemic or normovolemic.     

Critical neuroprotective roles of heme oxygenase‐1 induction against axonal injury‐induced retinal ganglion cell death

Although axonal damage induces significant retinal ganglion cell (RGC) death, small numbers of RGCs are able to survive up to 7 days after optic nerve crush (NC) injury. To develop new treatments, we set out to identify patterns of change in the gene expression of axonal damage‐resistant RGCs. To compensate for the low density of RGCs in the retina, we performed retrograde labeling of these cells with 4Di‐10ASP in adult mice and 7 days after NC purified the RGCs with fluorescence‐activated cell sorting. Gene expression in the cells was determined with a microarray, and the expression of Ho‐1 was determined with quantitative PCR (qPCR). Changes in protein expression were assessed with immunohistochemistry and immunoblotting. Additionally, the density of Fluoro‐gold‐labeled RGCs was counted in retinas from mice pretreated with CoPP, a potent HO‐1 inducer. The microarray and qPCR analyses showed increased expression of Ho‐1 in the post‐NC RGCs. Immunohistochemistry also showed that HO‐1‐positive cells were present in the ganglion cell layer (GCL), and cell counting showed that the proportion of HO‐1‐positive cells in the GCL rose significantly after NC. Seven days after NC, the number of RGCs in the CoPP‐treated mice was significantly higher than in the control mice. Combined pretreatment with SnPP, an HO‐1 inhibitor, suppressed the neuroprotective effect of CoPP. These results reflect changes in HO‐1 activity to RGCs that are a key part of RGC survival. Upregulation of HO‐1 signaling may therefore be a novel therapeutic strategy for glaucoma. © 2014 Wiley Periodicals, Inc.