Postprandial Hypotension due to a Lack of Sympathetic Compensation in Patients with Diabetes Mellitus.

Postprandial hypotension is an important hemodynamic abnormality in diabetes mellitus, but few reports are available on the relationship between autonomic dysfunction and postprandial hypotension. Ten diabetic patients and 10 healthy volunteers were recruited for this study. Postural blood pressure and heart rate changes were measured before lunch, and then the hemodynamic responses to a standardized meal were investigated. Holter electrocardiogram (ECG) monitoring was conducted for assessing spectral powers and time-domain parameters of RR variations. Postural changes from the supine to the upright position decreased the systolic blood pressure of the diabetics from 133(+-)16 to 107(+-)20 mmHg (p<0.01), but did not decrease the systolic blood pressure of the controls. The heart rate remained constant in the diabetics but was increased in the controls. Food ingestion decreased systolic blood pressure in the diabetics, with a maximum reduction of 25(+-)5 mmHg. This decrease was not associated with any changes in the ratio of low frequency to high frequency, and yet the heart rate remained almost constant. Indexes involving parasympathetic tone were not affected. Food ingestion did not affect blood pressure in the control group. These findings suggest that lack of compensatory sympathetic activation is a factor contributing to postprandial hypotension in diabetics, and that parasympathetic drive does not make a significant contribution to this condition

Prognostic significance of right bundle branch block in patients with acute inferior myocardial infarction

There is little information available concerning the influence of right bundle branch block (RBBB) on the prognosis of patients with inferior myocardial infarction (MI). In this study we evaluated the influence of RBBB on the short-term prognosis of patients with inferior MI. Our study subjects were 1,265 hospitalized patients with Q wave MI. Patients were divided into 4 groups based on the presence or absence of RBBB and on the location of the infarction. RBBB was classified into 4 categories according to the timing of its appearance and its duration as new permanent, transient, old and age indeterminate. In-hospital death and pulmonary congestion were observed more frequently in patients with RBBB than in those without RBBB. Moreover, in inferior MI as in anterior MI, in-hospital death and pulmonary congestion occurred more frequently in new permanent RBBB patients than in patients with other types of RBBB. Multivariate regression analysis reveals that new permanent RBBB was a strong independent predictor for an adverse short-term prognosis in patients with inferior MI, as well as in patients with anterior MI. New permanent RBBB during inferior MI is a strong independent predictor for increased in-hospital mortality, regardless of the infarction location.</p

Effect of clonidine on the release of serotonin from the rat hippocampus as measured by microdialysis

The purpose of the present study is to clarify the effect of clonidine on the release of serotonin from the rat hippocampus in vivo. For this purpose, endogenous serotonin release was measured by brain microdialysis. Potassium-evoked serotonin release from the hippocampus of freely moving rats was significantly inhibited when clonidine (10-5 M) was added to the perfusion solution, while the 5-hydroxyindoleacetic acid output remained unchanged. In catecholaminergically denervated rats, clonidine (10-5 M) also inhibited the potassium-evoked serotonin release from the hippocampus and the 5-hydroxyindoleacetic acid output was unaffected by clonidine. These results suggest that the inhibitory effect of clonidine on serotonin release from the hippocampus might reflect the activation of [alpha]2-adrenoceptors which are localized on the serotonergic nerve terminals.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30049/1/0000417.pd

Opioid receptor regulation of 5-hydroxytryptamine release from the rat hippocampus measured by in vivo microdialysis

The modulation of serotonin (5-HT) release by opioid receptors in the hippocampus of the awake, unrestrained rat was evaluated by use of in vivo microdialysis. The hippocampus was perfused with Ringer's solution (2 [mu]l/min), and extracellular levels of 5-HT and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were estimated by assaying their concentration in the dialysate by HPLC-ECD. Addition of potassium (K+, 60 and 120 mM) to the perfusate evoked a concentration-dependent release of 5-HT, but did not alter extracellular 5-HIAA levels. Co-perfusion of morphine (0.1 to 10 [mu]M) with K+ (120 mM) produced a concentration-dependent reduction of 5-HT release. Naltrexone (0.03 to 3 mg/kg, i.p.), a relatively selective [mu]-opioid receptor antagonist, blocked in a dose-dependent manner the morphine (10 [mu]M)-induced inhibition of 5-HT release. Naltrexone alone did not alter significantly either extracellular 5-HT levels or the release of 5-HT evoked by K+. Neither co-perfusion with [-Pen2, -Pen5]-enkephalin (DPDPE, 1 to 10 [mu]M), an agonist selective for [delta]-opioid receptors, nor with U-69593 (10 [mu]M), an agonist selective for [kappa]-opioid receptors, modified the K+ (120 mM)-evoked release of 5-HT. These findings indicate that [mu]-opioid receptors modulate the physiological release of 5-HT from serotonergic neurons in the rat hippocampus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30746/1/0000396.pd

Large Vasopressin in SIADH

A 76-year-old man with small cell lung cancer associated with the syndrome of inappropriate secretion of ADH (SIADH) visited our hospital. The serum Na level was normal on the first visit, but 2 weeks later it decreased to 114 mEq/L with an extremely high plasma vasopressin (VP) level of 1520 pg/ml. Serum Na was normalized after the reduction of the tumor size by chemotherapy, but the plasma VP level remained between 150 to 600 pg/ml. On gel filtration of plasma VP two peaks of immunoreactive VP were eluted at the positions of a larger molecule than authentic VP and authentic VP, and VP in urine gave only one peak compared to that of authentic VP. The dilution curve of plasma VP was almost parallel and that of urine was completely parallel to the standard curve. These findings suggest that a larger VP with low physiological activity was predominantly secreted in the present patient and manifested relatively mild symptoms despite the extremely high plasma VP level

Inhibitory effects of clonidine on serotonergic neuronal activity as measured by cerebrospinal fluid serotonin and its metabolite in anesthetized rats

Clonidine-induced changes in the serotonergic neuronal activity of the central nervous system were estimated by measuring the concentrations of serotonin (5-HT) and its major metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), in the cerebrospinal fluid (CSF) of anesthetized rats. Clonidine (30 and 300 [mu]g/kg, i.v.) led to 74% and 60% reductions in the concentration of 5-HT in the CSF 60 min after administration. CSF 5-HIAA concentrations were also decreased to 77% and 66%, respectively. Clonidine-induced (30 [mu]g/kg, i.v.) decreases in CSF 5-HT and 5-HIAA concentrations were attenuated by pretreatment with idazoxan (5 mg/kg, i.p.). Idazoxan by itself did not alter the CSF 5-HT and 5-HIAA concentrations. Decreased CSF 5-HT and 5-HIAA concentrations after i.v. administration of clonidine (30 [mu]g/kg) were abolished by noradrenergic denervation after pretreatment with 6-hydroxydopamine (200 [mu]g/rat, i.c.v.). These results suggest the possibility that clonidine acts to inhibit the serotonergic neuronal activity, which is mediated via the [alpha]2-adrenoceptors. It indicates, moreover, that noradrenergic nervous systems are involved in the clonidine-induced inhibition of serotonergic neuronal activity. Therefore, noradrenergic neurons play a significant role in mediating the actions of clonidine on serotonergic neuronal activity in the rat brain.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31094/1/0000771.pd

人間ドック受診者における高脂血症者の臨床データ解析

OBJECTIVE: To assess the clinical data of hyperlipidemia patients of urban male workers at the annual health examination, and to ascertain a suitable dietary education program to reduce plasma cholesterol and triglyceride levels in Japanese male patients. METHOD: Subjects were 273 males (mean age 47 years), who visited a medical examination center in Tokyo between April 2002 and March 2003 for an annual health examination. The subjects were diagnosed according to the guidelines of Japan Atherosclerosis Society for Diagnosis. The subjects fall into 6 hyperlipidemia groups: TC≧220mg/dl, LDLC≧140mg/dl, HDLC<40mg/dl, TG≧150mg/dl, TC≧220mg/dl & LDLC≧140mg/dl, TC≧220mg/dl & TG≧150mg/dl. RESULT: High cholesterol group (TC≧220mg/dl) were 48.7%, High triglyceride group (TG≧150mg/dl) were 36.3%, High LDL cholesterol group (LDLC≧140mg/dl) were 10.6%, Low HDL cholesterol group (HDLC<40mg/dl) were 4.4%. 38.1% belonged to the High cholesterol group and High LDL cholesterol group as well, 16.1% belonged to the High cholesterol group and High triglyceride group as well. Good correlations were found between TC and LDLC (r=0.87), TC and HDLC (r=0.39) and negative correlations were between TG and LDLC (r=-0.42), TG and HDLC (r=-0.39). CONCLUSION: This study pointed towards the acquisition of a dietary education program to reduce plasma cholesterol and triglyceride levels in Japanese male patients