Peristomal skin disorders in patients with intestinal and urinary ostomies: influence of adhesive forces of various hydrocolloid wafer skin barriers.

PURPOSE: This study examines the adhesiveness of hydrocolloid wafers and its relationship to physical damage of the underlying skin. DESIGN: Observational study. SUBJECTS AND SETTING: All subjects received ostomy care at the Tokyo Ostomy Center and outpatient departments of 4 hospitals in Tokyo, Japan. One hundred ninety-four of 917 patients receiving care over a 23-year span agreed to participate in the research. Subjects met 2 inclusion criteria: (1) ostomy management was performed using a combination of skin barriers and an adhesive ostomy pouch; and (2) the patient's medical file and color photographs were available, allowing analysis of the peristomal skin over time. INSTRUMENT: Photographs were taken with an Olympus (OM2) camera equipped with an Olympus macro lens and a ring flash. METHODS: We analyzed the impact of the adhesive force of various hydrocolloid wafers on the underlying skin. Photographs were digitized and systematically examined the peristomal skin exposed to regular use of skin barriers. The observation period varied among individual patients, ranging from 1 week to 30 years after surgery. RESULTS: The incidence of dermatologic changes (active, inactive, and area cutanea changes) was lower in patients who used skin barriers with adhesive force of not more than 2 Newtons(N) than among those using higher forces (>2 N). Specifically, there was a significant difference in change of the area cutanea. The incidence of papules and erosion was unrelated to the adhesive force of skin barriers. CONCLUSIONS: These results suggest that the peristomal skin is irritated by repeated peeling, resulting in physical damage to the horny layer of the skin. The presence of papules and erosion was not associated with the adhesive force of skin barriers. This finding suggests that these changes are associated with an inflammatory process, possibly caused by chemical substances within the skin barrier.

Rescue of pulmonary hypertension with an oral sulfonamide antibiotic sulfisoxazole by endothelin receptor antagonistic actions.

Pulmonary hypertension (PH) is a disease of unknown etiology that ultimately causes right ventricle heart failure with a lethal outcome. An increase in circulating endothelin (ET)-1 levels may contribute to disease progression. This study aimed to examine the possible effects of an orally active ET receptor antagonist, sulfisoxazole (SFX), for the rescue of PH, right ventricular hypertrophy, and eventual right ventricular failure. PH rats (single injection of monocrotaline [MCT]) were treated with an ET antagonist, SFX, an orally active sulfonamide antibody. Effects of SFX on PH rats were assessed in terms of survival rate, pulmonary artery blood pressure (PABP), autonomic nerve activity, and atrial natriuretic peptide (ANP) concentration in right ventricular myocytes and plasma. SFX did not change systemic blood pressure, however, it significantly suppressed the elevation of PABP. SFX maintained the derangement of autonomic nerve control, blunted an increase in ANP in myocytes and plasma, and significantly improved survival in right heart failure and/or related organs dysfunction in PH rats. The ET antagonistic action of the antimicrobial agent, SFX, was experimentally confirmed for treatment of PH in rats.

Three different bradycardic agents, zatebradine, diltiazem and propranolol, distinctly modify heart rate variability and QT-interval variability.

Zatebradine, diltiazem and propranolol are all antiarrhythmic agents, and all induce bradycardia, but each is known to have a different initial molecular mechanism: zatebradine is a channel blocker of the hyperpolarization-activated inward current (I(f)); diltiazem is a blocker of the L-type Ca(2+) channel (I(CaL)), and propranolol is a beta-blocker. To further investigate the mechanisms underlying their clinical effects, we studied their effects on heart rate variability (HRV) and QT-interval variability (QTV). To this end, guinea pigs were treated with either zatebradine (1.5 mg/kg, i.p.), diltiazem (40 mg/kg, i.p.) or propranolol (20 mg/kg, i.p.). A dose of each agent that decreased HR by 20-22% was used in this study. HRV and QTV were analyzed by a fast Fourier and/or a wavelet transform algorithm. Zatebradine, an I(f) channel blocker, had no significant effect on HRV and QTV. Diltiazem, a non-dihydropyridine I(CaL) blocker, increased high frequency (HF) power and decreased the power ratio of the low frequency (LF) range to the HF range (L/H) in HRV, and increased QTV. Propranolol, a non-selective beta-antagonist, decreased LF power and L/H ratios in HRV, and appreciably reduced QTV. These differences in pharmacological action may help us better understand the antiarrhythmic and/or proarrhythmic actions of these agents when they are used clinically for reducing HR.

Synaptic degradation of cardiac autonomic nerves in streptozotocin-induced diabetic rats.

BACKGROUND: Cardiac autonomic neuropathy (CAN) is a common complication in type I diabetes mellitus (DM). Nevertheless, the relationship between functional and structural disturbances of cardiac autonomic nerves remains unclear. METHODS AND RESULTS: To clarify this relationship, we studied heart rate variability (HRV) and ultrastructural changes of cardiac autonomic nerves in streptozotocin (STZ)-induced DM in rats. STZ was injected (65mg/kg intravenous) into the tail vein of male Wistar rats to destroy ß cells in the pancreatic islets. After STZ injection, fasting blood sugar (FBS) increased from baseline values of 75±3mg/dl up to 328±12mg/dl within 1week and it reached up to 353±24mg/dl within 17weeks. HR in these rats was decreased within 20days and low HR was maintained for the observation period. TP and HF power started decreasing 20days after STZ injection, and this decrease progressed throughout the observation period. The L/H power ratio was decreased 80days after STZ. Electron microscopic findings indicated a depletion of neurotransmitter vesicles and degradation of parasympathetic nerve endings but not of sympathetic ones in the SA node region of the heart in the early stages of DM. In the late stages of DM, the same region showed degradation of both sympathetic and parasympathetic nerve endings. CONCLUSION: Synaptic degradation in parasympathetic nerves immediately after the onset of DM, and in sympathetic nerves much later in the development of DM is consistent with functional derangements in cardiac autonomic nerve activities assessed by HRV analysis.

Cardiac autonomic nerve abnormalities in chronic heart failure are associated with presynaptic vagal nerve degeneration.

BACKGROUND: Understanding of the functional and structural disturbances of cardiac autonomic nerves in ventricular hypertrophy and eventual chronic heart failure (CHF) remains unclear. METHODS AND RESULTS: ECG signals were obtained by a radio transmitter from male Wistar rats that received monocrotaline (MCT) via subcutaneous injection. Heart rate (HR) and HR variability (HRV) were analyzed. The RR interval, total power (TP), low frequency (LF) power, high frequency (HF) power, and LF/HF (L/H) power ratio were measured. Ultrastructural changes in cardiac autonomic nerves at the sinoatrial (SA) node region were studied using an electron microscope. TP and HF powers in MCT-induced right ventricular hypertrophy (RVH) and eventual CHF were significantly decreased, and HR was significantly increased at week 5 or later after the MCT injection. The electron microscopic findings indicated the depletion of neurotransmitter vesicles and degradation of parasympathetic but not sympathetic nerve endings in the SA node region of the heart. CONCLUSION: MCT-induced RVH and CHF rats showed presynaptic vagal nerve degradation prior to sympathetic nerve derangement in the heart.