Sodium Restriction Counseling Reduces Cardiac Events in Patients With Heart Failure.

BACKGROUND: Many heart failure (HF) guidelines recommend sodium restriction for patients with HF, but the outcome of sodium restriction counseling (SRC) for HF patients is still unknown. We wanted to clarify whether SRC reduces cardiac events in patients with HF.Methods and Results:Overall, 800 patients (77±12 years) who were hospitalized for HF were enrolled. During HF hospitalization, patients received SRC; patients were required to have a salt intake of <6 g/day. After discharge, death or HF rehospitalization events were investigated. During a mean follow-up of 319±252 days, 83 patients died, and 153 patients were rehospitalized for HF. SRC significantly decreased all-cause death (odds ratio, 0.42; 95% confidence interval [CI], 0.23-0.76; P<0.01), especially cardiac death of hospitalized HF patients after discharge. In the multivariate analysis adjusted for age, sex, SRC, body mass index, hypertension, dyslipidemia, ß-blockers, and mineralocorticoid receptor antagonist intake, cardiac rehabilitation, and the type of HF, SRC remained a significant predictor of death. Kaplan-Meier analysis showed that SRC significantly reduced deaths and the combined outcome of HF rehospitalization and death. In patients with reduced left ventricular ejection fraction, SRC significantly decreased the mortality rate (odds ratio, 0.27; 95% CI, 0.10-0.71; P<0.01). CONCLUSIONS: SRC reduced the mortality rate after discharge of hospitalized HF patients.

Effects of Chewing Gum Base on Oral Hygiene and Mental Health: A Pilot Study.

The purpose of the present study was to clarify the long-term effects of frequent chewing of unflavored and odorless gum (hereafter, gum base) on oral hygiene and mental health. This single-arm study, which started with a 4-week control and ended with a 4-week intervention period, was conducted in two phases: one in 2017 and one in 2018. The participants comprised 36 dental hygiene students (17 in 2017, 19 in 2018). During the intervention period, all participants were required to chew a piece of gum base 7 times a day for 10 min each time. The unstimulated salivary flow rate and masticatory efficiency were measured and chewing number counted. Two questionnaires －the Profile of Mood States, second edition (POMS2) and the 30-item General Health Questionnaire (GHQ-30)－ were administered to assess mental health. In both phases, the unstimulated salivary flow rate showed a significant increase after the intervention period (p<0.05). In 2017, the GHQ-30 scores and masticatory efficiency showed a tendency toward a negative correlation after the intervention period (r=－0.4647, p=0.06). In 2018, a significant negative correlation was observed between chewing number and the POMS2 scores after the intervention period (r=－0.6296, p<0.01). These findings suggest that frequent chewing of gum base increases unstimulated salivary flow rate. However, no significant change was observed in the mental health.

Endothelial modulation of agonist-induced vasoconstriction in mesenteric microcirculation.

It is widely accepted that vascular endothelium regulates vasoconstriction via release of endothelium-derived relaxing factors (EDRF). The mesenteric circulation, which is the largest vascular bed, influences regulation of systemic blood pressure. However, the role of EDRF in the modulation of vascular tone in peripheral mesenteric circulation has not been extensively studied. Therefore, our recent studies investigated the role of the vascular endothelium in the regulation of methoxamine (alpha(1)-adrenoceptor agonist)-induced vasoconstriction and their age-related changes in rat mesenteric vascular beds. In mesenteric vascular beds with intact endothelium isolated from 8 week-old rats, the initial maximum vasoconstriction induced by continuous perfusion of methoxamine was time-dependently decreased during 3 hour-perfusion. Neither nitric oxide synthase inhibitor nor cyclooxygenase inhibitor altered this time-dependent reduction of methoxamine-induced vasoconstriction. Endothelium removal, K(+)-channel inhibitors and gap junction inhibitor significantly inhibited the time-dependent reduction of methoxamine-induced vasoconstriction. In the preparations with intact endothelium from 16 week-old rats, the time-dependent reduction of methoxamine-induced vasoconstriction disappeared. Furthermore, endothelium removal and treatment with cyclooxygenase inhibitor, thromboxane A(2) receptor antagonist or superoxide dismutase mimetic significantly reduced the methoxamine-induced vasoconstriction in the preparations from 16 week-old rats. These findings suggest that vascular endothelium acts to depress methoxamine-induced vasoconstriction by releasing endothelium-derived hyperpolarizing factor (EDHF), and dysfunction in this endothelial modulation develops with ageing.

Endothelium-derived hyperpolarizing factor (EDHF) mediates endothelium-dependent vasodilator effects of aqueous extracts from Eucommia ulmoides Oliv. leaves in rat mesenteric resistance arteries.

The vascular effects of an aqueous extract prepared from the leaves of Eucommia ulmoides Oliv. (ELE), a medicinal herb commonly used in antihypertensive herbal prescriptions in China, were investigated in rat mesenteric resistance arteries. The mesenteric vascular bed was perfused with Krebs solution and the perfusion pressure was measured with a pressure transducer. In preparations with an intact endothelium and precontracted with 7 microM methoxamine, perfusion of ELE (107102 mg/ml for 15 min) caused a concentration-dependent vasodilatation, which was abolished by chemical removal of the endothelium. The ELE-induced vasodilatation was inhibited by neither indomethacin (INDO, a cyclooxygenase inhibitor) nor NG-nitro-L-arginine-methyl ester (L-NAME, a nitric oxide inhibitor). The ELE-induced vasodilatation was significantly inhibited by tetraethylammonium (TEA, a K channel blocker) and 18alpha-glycyrrhetinic acid (18alpha-GA, a gap-junction inhibitor), and abolished by high K-containing Krebs' solution. Atropine (a muscarinic acetylcholine receptor antagonist) significantly inhibited the vasodilatation induced by ELE at high concentrations. These results suggest that the ELE-induced vasodilatation is endothelium-dependent but nitric oxide (NO)- and prostaglandin I2 (PGI2)-independent, and is mainly mediated by the endothelium-derived hyperpolarizing factor (EDHF) in the mesenteric resistance arteries. Furthermore, the ELE-induced EDHF-mediated response involves the activation of K-channels and gap junctions.