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Objective: To investigate the prevalence and characteristics of depressed patients living in a Japanese leprosarium who have been isolated by national law and are now becoming very elderly., Methods: We surveyed the prevalence of depressed patients living in the National Tamazenshouen Sanatorium, a major leprosarium in Japan. We also investigated the characteristics of patients who had suffered a depressive episode during the last 5 years (2000-2004). The characteristics of residents who committed suicide were also studied., Results: At the time of the investigation, 48 out of 385 (12.5%) patients were depressed or had experienced a depressive episode. Forty-one residents had committed suicide since the leprosarium was established in 1907. Somatic symptoms and depressive moods were the predominant symptoms and were not limited to symptoms unique to leprosy. The period of isolation was not statistically correlated with the GDS-SF or PGC morale scale scores., Conclusion: The findings of this study emphasize the importance of consultation psychiatric for elderly leprosy residents and could be used as a reference for treatment in countries with ageing leprosy residents.

A 60-year-old man was diagnosed as adult T-cell leukemia with severe hypercalcemia because of production of parathyroid hormone-related protein. After admission, the patient had respiratory insufficiency with an infiltrative shadow in his lungs suggestive of pneumonia. However, neither improvement in respiratory function nor disappearance of the abnormal chest shadow was observed with administration of various antibiotics. An autopsy demonstrated the chest shadow had been caused by metastatic calcification associated with hypercalcemia due to production of parathyroid hormone-related protein. The possibility of metastatic calcification should be considered in patients with adult T-cell leukemia and hypercalcemia who have an abnormal chest shadow.

A 69-year-old female was admitted to our hospital because of leg edema, proteinuria (2.1 g/day), and gross hematuria. She had non-alcoholic liver cirrhosis of unknown etiology. Esophageal varices also were found. Examination of the renal biopsy specimen revealed mesangial proliferative glomerulonephritis with IgA deposits. Propranolol was administered orally to reduce portal hypertension, resulting in a progressive decrease in urinary microalbumin excretion. This case suggests that portal hypertension is involved in the pathogenesis of IgA nephropathy in liver cirrhosis.

Isolated rat hearts were subjected to retrograde perfusion to investigate the protective effects of adenosine and verapamil on the myocardium. In group 1, the perfusate was standard Krebs-Henseleit buffer solution. The perfusate was changed to Krebs-Henseleit buffer containing verapamil (100 nM) in group 2, adenosine (100 microM) in group 3 and both drugs in combination in group 4 for 30 min before ischemia and during 20 min of reperfusion. Group 2 displayed a recovery of creatine phosphate but not of ATP at the end of reperfusion. In group 4, the recovery of both ATP and creatine phosphate was significantly greater than in group 1. The coronary flow of group 4 was significantly higher than that of the other groups. Treatment with both verapamil and adenosine before and after global ischemia may protect the ischemic myocardium by improving high energy phosphate metabolism and coronary circulation.

Objective: The study was designed to demonstrate the time course of neutrophil chemotactic factor (NCF) release from blood-free isolated rat hearts and to clarify the characteristics of NCF in order to facilitate its identification., Methods: Coronary effluents were collected every minute from Langendorff perfused rat hearts during ligation of the left coronary artery for 40 min and reperfusion for 60 min. The neutrophil chemotactic activity in the effluents was assayed using modified Boyden's chambers with rat neutrophils isolated from peripheral blood as the indicator cells., Results: The NCF release started at 10 min of coronary artery occlusion. During the reperfusion period, NCF release peaked at 5 min (230% of preischaemic value). To clarify the characteristics of NCF, the changes in chemotactic activity were examined using various inhibitors and inactivators of possible NCF candidates (LTB4, PAF, 5-lipoxygenase, and thromboxane synthase). The heat stability of NCF was also examined to exclude heat labile molecules such as adenosine or complements appearing as NCF. Among the various substances examined, only PAF antagonists (CV-6209 and TCV-309 at concentrations of 10(-6) M and 10(-5) M respectively) abolished the chemotactic activity. However direct measurement of PAF in the effluents was unsuccessful., Conclusion: NCF is released from the heart early after ischaemic insult, with the highest peak occurring at 5 min of reperfusion. PAF related substances might be the primary NCF in the effluent but this remains to be determined.

Iodine-labelled fatty acids have been proposed as new tracers of cardiac metabolisms. However, it is not clear how these tracers would reflect the intracellular metabolism. Therefore, we measured the uptake and release of iodine 125-labelled phenylpentadecanoic acid (IPPA), its beta-methyl substitute (BMIPP) and 201Tl in cultured myocytes of mouse embryos, and compared these values to intracellular adenosine triphosphate (ATP) content after metabolic inhibitions of oxidative phosphorylation by sodium cyanide (CN), glycolysis by 2-deoxyglucose (2-DG) or fatty acid beta-oxidation by lactate. The uptake and release of BMIPP was not changed by any inhibitors suggesting BMIPP would not be metabolized in the myocytes. The uptake of IPPA was significantly reduced by 2DG and 60-80% of IPPA was metabolized to hydrophilic catabolites. The correlation of BMIPP and IPPA uptake to intracellular ATP content were high (r = 0.89, p < 0.05; r = 0.86, p < 0.1), but there was poor correlation of 201Tl to ATP values (r = 0.53, n.s.). These results suggested that iodine-labelled fatty acids could be used as better tracers of myocardial metabolism than 201Tl.

This study was designed to clarify the state of beta-adrenergic signal transduction and the disordered level of its transduction in hypertensive hearts, using myocardium from spontaneously hypertensive rats (SHR) as a generic model of essential hypertension. Beta-adrenergic receptor binding sites and dissociation constants in the extracted membranes of adult (70-100 days of age) SHR heart were not significantly different from those of Wistar-Kyoto (WKY) rats, the non-hypertensive control. The adenylate cyclase activities stimulated by isoproterenol with GTP, NaF and forskolin were significantly higher in SHR compared to those in WKY. To determine whether differences in signal transduction are natural or are a result of hypertension, we evaluated chronotropic responses in cultured cells of fetal hearts which had not been exposed to hypertension. Fetal cardiac muscle cells of SHR were more sensitive than WKY to isoproterenol stimulation over a wide concentration range. However, there were no statistically significant differences between these two strains with respect to the density of binding sites. These results suggest that in the transduction of adrenergic signals, alterations distal to the beta-receptors are present in the adult hearts of hypertensive rats, and, that the adrenergic signal transduction is already exaggerated in the pre-hypertensive fetal stage.

Changes in contractility and intracellular free Ca([Ca++]i) were measured in spontaneously beating cultured heart cells following exposure to indo-1 acetoxymethyl ester (indo-1AM) and fura-2 acetoxymethyl ester (fura-2AM). Although a 10 microM concentration of indo-1AM slightly decreased the beating rate, 5 and 10 microM concentrations of fura-2AM produced arrest of contraction within 10 min. However, contractility returned to normal after washing. With indo-1, the diastolic and peak systolic levels of [Ca++]i were 282 +/- 23 and 1107 +/- 122 nM, respectively, and 84 +/- 8 and 582 +/- 93 nM, respectively, with fura-2. The difference between the indo-1 and fura-2 generated responses are statistically significant (p less than 0.01). These results demonstrate that indo-1 and fura-2 can affect [Ca++]i, but the influence of indo-1 is less than that of fura-2 in the heart cells.

To compare the extractability of creatine phosphate with that of ATP by alcohol extraction, both compounds were extracted from normal perfused rat heart tissues by using various stepwise concentrations of ethanol and 0.4 M HClO4. Powdered samples (6-15 mg wet wt) from the freeze-clamped tissues were homogenized in 2 ml of the ethanol solutions. After centrifugation, the supernatant was removed; each centrifuged sediment was rehomogenized with 2 ml of 0.4 M HClO4 and centrifuged. The supernatant was neutralized with 0.4 m KHCO3. The same powdered samples were directly homogenized with 2 ml of 0.4 M HClO4 and treated in the same manner. Only a small amount of ATP in the tissues was extracted by an 85% or higher concentration of ethanol. Further, about 13% of the tissue ATP was not extractable by the subsequent perchloric acid extraction. In contrast to ATP, creatine phosphate in the tissues was partially extracted by 95% ethanol and nearly all of the tissue creatine phosphate was extracted by 70% ethanol. The total creatine phosphate obtained by 70% ethanol and by subsequent perchloric acid extraction was significantly higher than that obtained by direct perchloric acid extraction. From these results, it was concluded that the extractability of creatine phosphate in the tissue by alcohol extraction is clearly different from that of ATP. Additionally, the stepwise extraction is recommended as a useful method for the extraction of energy metabolites in perfused rat heart tissue.

The effects of carvedilol (an alpha.beta-blocker) on lipid metabolism were assessed in addition to its hypotensive effect. The subjects were 18 men and 18 women, 20 with hypertension and 16 normotensives with other conditions requiring carvedilol treatment. They were aged from 31 to 79 years and were given a daily dose of 5-20 mg carvedilol (average, 9.7 mg/day) for 12 weeks. Significant falls were seen in blood pressure and heart rate after 12 weeks in the hypertensive subjects (mean +/- SE) (systolic: from 164 +/- 2 to 141 +/- 2 mm Hg, P less than 0.001; diastolic: from 98 +/- 1 to 85 +/- 2 mm Hg, P less than 0.001; heart rate: from 71 to 65 beats/min, P less than 0.001). Smaller changes in blood pressure and heart rate were seen in the normotensive subjects, with the fall in systolic pressure being significant (from 143 +/- 3 to 135 +/- 2 mm Hg, P less than 0.01). There were no significant changes in the overall serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, and phospholipid levels. In the subgroup with a pretreatment serum triglyceride level of greater than 150 mg/dl, a significant fall of 52.1 mg/dl was seen (P less than 0.05). Lipoprotein analysis showed a significant fall in alpha-lipoprotein levels (P less than 0.05). The atherogenic index did not change significantly, and it was concluded that carvedilol was an effective antihypertensive agent that produced no adverse effects and possibly had beneficial effects on lipid metabolism.

Hypothermic synchronized retroperfusion (HSRP) was applied in closed-chest dogs after acute coronary occlusion to determine whether this intervention can significantly retard the otherwise rapidly developing irreversible ischemic injury. The left anterior descending coronary artery (LAD) was occluded for 3 hours in 22 dogs and for 6 hours in 16 dogs. Starting 30 minutes after occlusion, HSRP was applied during maintained coronary occlusion in 21 dogs. The remaining dogs served as untreated controls. Arterial blood was cooled to 20 degrees C and retroperfused in diastole into the regional coronary veins. Hemodynamics, contrast cineangiography and two-dimensional echocardiography were measured sequentially. Glycogen-depleted ischemic areas and necrotic zones were delineated in transverse slices of the left ventricle. Untreated controls dogs further deteriorated; in contrast, HSRP between 30 minutes and 3- and 6-hour LAD occlusion significantly reduced the rate-pressure product (21.3 +/- 4.0% or 26.8 +/- 8.2%) and left ventricular end-diastolic pressure (39.5 +/- 9.5% or 51.4 +/- 7.7%) and increased ejection fraction (28 +/- 17% and 33 +/- 2.0%). HSRP caused no arrhythmias and led to much less necrosis of ischemic myocardium in the treated 3- or 6-hour occlusion series (7.4 +/- 2.7% or 28.9 +/- 12.6%) than in respective untreated controls (47.1 +/- 8.9% and 72.3 +/- 5.9%). Moderately hypothermic closed-chest phased retroperfusion appears to protect reversibly injured ischemic myocardium and improve cardiac function. Such treatment may be particularly suitable in the earliest stages of evolving myocardial infarction, when maintenance of myocardial viability is essential for preservation of jeopardized myocardium while awaiting coronary bypass revascularization or nonsurgical thrombolytic reperfusion.

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.