Search PubMed⌕ Search

Biomedical subjects

K Shimamoto

Publications and source records attributed to K Shimamoto.

At least 73 records · Page 4Linked to original sources
PubMed2000

The effects of an angiotensin-converting enzyme inhibitor and an angiotensin II receptor antagonist on insulin resistance in fructose-fed rats.

The aim of this study was to compare the effects of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II receptor (AT) antagonist on insulin resistance, especially on muscle fiber composition in fructose-induced insulin-resistant and hypertensive rats. Six-week-old male Sprague-Dawley rats were fed either normal rat chow (control) or a fructose-rich diet (FFR). For the last two weeks of a six-week period of either diet, the rats were treated with gum arabic solution as a vehicle (control or FFR), angiotensin-converting enzyme inhibitor (FFR+ACE), temocapril (1 mg/kg/ day) or an angiotensin II receptor antagonist (FFR+AT), CS-866 (0.3 mg/kg/day), by gavage, and then the euglycemic hyperinsulinemic glucose clamp technique was performed to evaluate insulin sensitivity. At the end of the glucose clamp, the soleus muscle was dissected for determination of the muscle fiber composition by ATPase methods. Blood pressure at the glucose clamp in the FFR group was significantly higher than that of the control group, and both temocapril and CS-866 significantly lowered the blood pressure of the FFR group. The average rate of glucose infusion during the glucose clamp, as a measure of insulin sensitivity (M value), was significantly lower in the FFR rats compared to the controls (15.4 +/- 0.4, 10.9 +/- 0.6 mg/kg/min, for control and FFR, respectively, P < .01). Both temocapril and CS-866 partially improved the M values compared to FFR (13.2 +/- 0.7, 12.8 +/- 0.5 mg/kg/min, for FFR+ACE, FFR+AT, respectively, P < .01 compared with FFR, P < .05 compared with control). The composite ratio of type I fibers of the soleus muscle was decreased significantly in the FFR rats compared with the controls (82% +/- 2%, 75% +/- 2%, for control and FFR, respectively, P < .01), and both temocapril and CS-866 restored a composite ratio of type I fibers to the same level as that of the controls (81% +/- 1%, 80% +/- 1% for FFR+ACE and FFR+AT, respectively). The M value was significantly correlated with the composition of type I and type II fibers. These results suggest that the fiber composition of skeletal muscle is correlated to insulin resistance, and that both ACE inhibitors and AT antagonists may modulate the muscle fiber composition in a hypertensive and insulin-resistant animal model, fructose-fed rats, to the same extent.

Angiotensin Receptor Antagonists↗
PubMed2000

Relationship between free radicals and adenosine in the mechanism of preconditioning: are they interrelated or independent triggers?

Both free radicals (FRs) and adenosine receptor activation contribute to triggering a mechanism of preconditioning (PC) against infarction. This study examined the possibility that there is some interaction between FRs and adenosine generation during PC. In the first series of experiments, the effects of an FR scavenger, N-2-mercaptopropionyl glycine (MPG), on the interstitial adenosine level during PC and on the infarct size-limiting effect of PC were assessed in the rabbit heart in situ. PC with 5-min ischemia/5-min reperfusion limited infarct size after 30-min coronary occlusion (expressed as a percentage of area at risk, %IS/AR) from 33.2 +/- 4.7% (S.E.) to 10.8 +/- 1.1% (p < 0.05). This cardioprotection was blocked by MPG (1.5 mg/kg/min i.v.) infused before and during PC (%IS/AR = 27.4 +/- 3.6). However, the same dose of MPG did not suppress elevation of the adenosine and inosine levels in the microdialysate from the myocardium during 5-min ischemia/reperfusion. In the second series of experiments, the effect of an FR-generating system (1 mM hypoxanthine and 20 mU/ml xanthine oxidase) on the purine production was compared to that of PC in isolated rabbit hearts. Whereas PC increased the adenosine level in the coronary effluent from 0.17 +/- 0.16 microM under baseline to 1.68 +/- 0.53 microM, infusion of the FR generators over a period of 5 min did not increase the adenosine release. However, infarct size was similarly reduced by PC and by 5-min transient infusion of FR generators, and the cardioprotection by the FR generators was abolished by 300 microM MPG. These results suggest that there is no interaction between free radicals and adenosine during the trigger phase of PC in the rabbit heart.

Adenosine↗
PubMed2000

Infarct size limitation by bradykinin receptor activation is mediated by the mitochondrial but not by the sarcolemmal K(ATP) channel.

Earlier studies have shown that activation of bradykinin B2 receptor triggers protein kinase C (PKC)-mediated cardioprotective mechanism in ischemic preconditioning (PC). In the present study, we examined whether the effector in this B2-receptor triggered pathway of PC is the ATP sensitive potassium (K(ATP)) channel in the mitochondria (mito-K(ATP) channel) or K(ATP) channel in the sarcolemma (sarc-K(ATP) channel). Isolated rabbit hearts were perfused with modified Krebs-Henseleit buffer in a Langendorff mode, and regional myocardial ischemia was induced by occluding a left coronary artery for 30 min and then reperfusing for 2 hours. Infarct size was determined by triphenyltetrazolium chloride staining and expressed as a percentage of area at risk (% IS/AR). Infusion of bradykinin (500 nmol/L) for 15 min prior to ischemia significantly reduced % IS/AR from 37.4 +/- 2.9 (SE) of the untreated controls to 12.0 +/- 3.3%. This protective effect of bradykinin was completely abolished by coinfusion of 5-hydroxydecanoate (5-HD, 50 micromol/L), a selective mito-K(ATP) channel blocker (% IS/AR = 44.2 +/- 6.4). In contrast, a high dose of HMR1098 (20 micromol/L), which is a newly developed sarc-K(ATP) channel selective blocker with IC50 of 0.6 micromol/L, failed to modify the infarct size limitation by preischemic infusion of bradykinin (% IS/AR = 11.7 +/- 3.4). Neither 5-HD nor HMR1098 alone modified infarct size (% IS/AR = 37.8 +/- 3.8 and 35.1 +/- 6.2, respectively). These results suggest that opening of the mito-K(ATP) channel but not the sarc-K(ATP) channel is involved in infarct size limitation by a mechanism triggered by bradykinin B2 receptor activation.

Analysis of Variance↗
PubMed2000

Phytochromes confer the photoperiodic control of flowering in rice (a short-day plant).

The photoperiodic sensitivity 5 (se5) mutant of rice, a short-day plant, has a very early flowering phenotype and is completely deficient in photoperiodic response. We have cloned the SE5 gene by candidate cloning and demonstrated that it encodes a putative heme oxygenase. Lack of responses of coleoptile elongation by light pulses and photoreversible phytochromes in crude extracts of se5 indicate that SE5 may function in phytochrome chromophore biosynthesis. Ectopic expression of SE5 cDNA by the CaMV 35S promoter restored the photoperiodic response in the se5 mutant. Our results indicate that phytochromes confer the photoperiodic control of flowering in rice. Comparison of se5 with hy1, a counterpart mutant of Arabidopsis, suggests distinct roles of phytochromes in the photoperiodic control of flowering in these two species.

Amino Acid Sequence↗
PubMed2000

Over-expression of a single Ca2+-dependent protein kinase confers both cold and salt/drought tolerance on rice plants.

A rice gene encoding a calcium-dependent protein kinase (CDPK), OsCDPK7, was induced by cold and salt stresses. To elucidate the physiological function of OsCDPK7, we generated transgenic rice plants with altered levels of the protein. The extent of tolerance to cold and salt/drought stresses of these plants correlated well with the level of OsCDPK7 expression. Therefore, OsCDPK7 was shown to be a positive regulator commonly involved in the tolerance to both stresses in rice. Over-expression of OsCDPK7 enhanced induction of some stress-responsive genes in response to salinity/drought, but not to cold. Thus, it was suggested that the downstream pathways leading to the cold and salt/drought tolerance are different from each other. It seems likely that at least two distinct pathways commonly use a single CDPK, maintaining the signalling specificity through unknown post-translational regulation mechanisms. These results demonstrate that simple manipulation of CDPK activity has great potential with regard to plant improvement.

Adaptation, Physiological↗
PubMed2000

dull: rice mutants with tissue-specific effects on the splicing of the waxy pre-mRNA.

In the endosperm of japonica rice, du-1 and du-2 mutations cause the reduction of amylose contents. It was previously shown that the Wx(b) allele of rice, which is predominantly distributed in japonica rice, has a mutation in the 5' splice site of intron 1 resulting in the creation of two weak 5' splice sites within exon 1. In du-1 and du-2 mutants, spliced Wx(b) transcripts were highly reduced, whereas the processing of transcripts derived from three other genes highly expressed in endosperm was not apparently influenced. Results of competitive RT-PCR analysis indicate that transcripts spliced at the two newly created 5' splice sites were equally affected in these two mutants. Genetic and molecular analyses of the effects of du-1 and du-2 on Wx(a) pre-mRNA with normal splice sites indicate that these two mutations do not affect the processing of Wx(a) pre-mRNA after splicing, suggesting that du-1 and du-2 are mutations of genes required for the efficient splicing of mutated Wx(b) pre-mRNA. Furthermore, du-1 and du-2 showed differential effects in endosperm and pollen. Although both mutations caused similar effects on the splicing of Wx(a) transcripts in endosperm, du-1 caused higher reduction of Wx(b) mRNA in pollen than in endosperm, while du-2 had a lesser effect in pollen than in endosperm. Based on these results, we propose that the du-1 and du-2 loci of rice encode tissue-specifically regulated splicing factors that are involved in alternative splicing of pre-mRNA in rice.

Alternative Splicing↗
PubMed2000

Studies on hemodynamic instability in paroxysmal supraventricular tachycardia: noninvasive evaluations by head-up tilt testing and power spectrum analysis on electrocardiographic RR variation.

Hemodynamic instability is a crucial determinant of the best therapeutic option in paroxysmal supraventricular tachycardia (PSVT). However, it is still unclear if hemodynamic instability is tachycardia dependent or independent. We performed frequency-domain analysis of electrocardiographic RR variations during induced PSVT and head-up tilt tests after successful ablation to investigate the role of autonomic vasomotor function in hemodynamic instability during PSVT. Thirty-six patients with (syncope group, n = 18) and without (nonsyncope group, n = 18) syncope and/or presyncope during PSVT were enrolled in this study. Serial blood pressure, heart rate, and variations in heart rate during induced PSVT and head-up tilt tests were examined. Initial blood pressure fall and heart rate changes during induced PSVT were greater in the syncope group than in the nonsyncope group. A significant positive linear relationship was found between these two. Delayed blood pressure fall was observed in the syncope group, independent of heart rate changes. Syncope in PSVT could be predicted from the results of head-up tilt tests with 82% accuracy. Heart rate responses after isoproterenol infusion were significantly greater in the syncope group than in the nonsyncope group. The changes in low frequency to high frequency (LF:HF) values during induced PSVT and head-up tilt tests were significantly greater in the syncope group than in the nonsyncope group, and an exponential correlation was found between LF:HF changes in both tests. We conclude that PSVT rate and vasomotor reaction are related with hemodynamic instability during PSVT and head-up tilt testing is a useful method for determining if patients will have syncope during PSVT.

Adolescent↗
PubMed2000

Post-transcriptional gene silencing in cultured rice cells.

Post-transcriptional gene silencing (PTGS) has been shown to occur in many transgenic dicotyledonous plants. Although transgene silencing has been documented in transgenic monocots, PTGS has been only recently described in monocotyledonous plants. To study PTGS in rice, we generated 25 transgenic rice cell lines in which the 35S-gus gene was stably integrated. In one transgenic cell line, lack of gus expression was shown to be caused by PTGS based on the results of run-on transcription assays. Furthermore, to examine whether reintroduction of the same plasmid DNA into cells in which the gus gene was highly expressed causes the suppression of the gus expression, the gus plasmid was introduced into protoplasts isolated from a high gus-expressing line. Results of the kinetic analysis of the GUS activities in transfected protoplasts indicated that the gus expression in transfected protoplasts was suppressed by the gus plasmid but not by the luc plasmid harboring the 35S-luciferase gene, suggesting that suppression of the gus expression by introduced plasmid DNA was homology-dependent. These results suggest that the transgenic protoplasts may be a useful experimental system to study PTGS in rice and other species.

Cells, Cultured↗
PubMed2000

Spatially and temporally regulated expression of rice MADS box genes with similarity to Arabidopsis class A, B and C genes.

The floral morphology of grass species is distinct from that of typical dicot plants. In order to achieve a better understanding of the molecular basis for this diversion, we isolated RAP1A, RAP1B and RAG, putative rice orthologs for the Arabidopsis class A gene APETALA1 (AP1) and class C gene AGAMOUS (AG). The expression patterns of RAP1A, RAG and OsMADS2, a rice ortholog of the class B gene, were analyzed by in situ hybridization. RAP1A mRNA was expressed in the apical region of the floral meristem at an early stage of spikelet development, and then its expression was localized in developing lemma, palea and lodicules. The OsMADS2 transcript was first observed in the region where stamen primordia are formed. Soon after, OsMADS2 mRNA appeared in the lodicule primordia as well as the stamen primordia, and this RNA accumulation pattern persisted until late stages of floral development. The expression of RAG was observed in stamens and pistils of wild-type young spikelets. These RNA accumulation patterns are mostly similar to those of Arabidopsis class A, B, C genes, supporting the notion that the ABC model may be extended to rice.

Amino Acid Sequence↗
PubMed2000

Antisense waxy genes with highly active promoters effectively suppress waxy gene expression in transgenic rice.

To regulate Waxy (Wx) gene expression by introducing antisense genes, we connected the 2.3 kb Wx cDNA having 450 bp of the Wx first intron in reverse orientation to rice Wx and maize alcohol dehydrogenase1 (Adh1) promoters and used these constructs to transform rice plants. Of 10 independent transgenic lines analysed, four lines showed various degrees of reduction in amylose and WAXY (WX) protein levels in the endosperm. In two transgenic lines, complete absence of amylose was observed which made the seeds opaque white like glutinous rice (amylose-deficient waxy (wx) mutant). In one of the transgenic lines, A1 line, the presence of the antisense Wx gene cosegregated with reduction of amylose content in the endosperm. In the same line, a reduction in the level of endogenous Wx mRNA was observed in immature endosperm. Interestingly, this reduction was observed only with mature spliced transcripts but not with unspliced transcripts. Reduced amylose synthesis was also observed in pollen grains of four transgenic lines. These results suggest that integrated antisense Wx gene caused a reduction in amylose synthesis in endosperms and pollen grains of transgenic rice carrying the antisense Wx cDNA. These results indicate that manipulation of starch and other carbohydrates in rice grain is possible using antisense genes.

Amylose↗
PubMed2000

Relationship between blood pressure level and mortality rate: an 18-year study conducted in two rural communities in Japan.

BACKGROUND: There have been very few studies on life prognosis of cardiovascular disease according to blood pressure stratification in the Japanese. Therefore, in Japan, although treatment of hypertension is possible, albeit at times difficult, due to the availability of various antihypertensive medications, the appropriate time at which treatment should be started remains a problem. OBJECTIVE: To investigate the long-term prognosis of cardiovascular disease in the Japanese general population according to blood pressure stratification in the Japanese. DESIGN: A community-based prospective cohort study of 1996 men and women between the ages of 40 and 64 years at the baseline examination was conducted over an 18-year period. Information on death was obtained from local public health nurses and death certificates. The causes of death were clarified by questionnaires sent to doctors in the hospital in which the deceased was hospitalized, and the causes of death were analysed in each blood pressure category at baseline examination. RESULTS: Mortality from cardiovascular disease increased with increases in the level of blood pressure and was significantly higher in > or = 140 mmHg group in systolic blood pressure and > or = 90 mmHg group in diastolic blood pressure, adjusted for age, sex and other cardiovascular risk factors in the Japanese general population. However, mortality risk from cardiovascular disease did not have a J-shaped relationship with systolic and diastolic blood pressure. CONCLUSION: We conclude that the optimum time for starting treatment in Japanese people is when blood pressure is 140/90 mmHg or less.

Adult↗
PubMed2000

The contribution of skeletal muscle tumor necrosis factor-alpha to insulin resistance and hypertension in fructose-fed rats.

OBJECTIVE: The aim of this study was to determine the role of tumor necrosis factor-alpha (TNF-alpha) in skeletal muscle tissue in insulin resistance and hypertension and the effect of anti-hypertensive medicine on skeletal muscle TNF-alpha in fructose-induced insulin-resistant and hypertensive rats (fructose-fed rats: FFR). DESIGN AND METHODS: Six-week-old male Sprague-Dawley rats were fed either normal rat chow or fructose-rich chow. For the last 2 weeks of a 6-week period of either diet, the rats were treated with a vehicle (control or FFR); temocapril, an angiotensin converting enzyme inhibitor (ACEI); or CS-866, an angiotensin II type 1 receptor blocker (ARB). The euglycemic hyperinsulinemic glucose clamp technique was performed to evaluate insulin sensitivity (M value). TNF-alpha levels in soleus and extensor digitorum longus (EDL) muscles and epididymal fat pads were measured. We also measured the TNF-alpha concentration in an incubated medium secreted from soleus muscle strips with or without angiotensin II. RESULTS: TNF-alpha levels were significantly higher in the soleus and EDL muscles, but not in the epididymal fat, in the FFRs compared with the control rats. Temocapril and CS-866 lowered systolic blood pressure, improved insulin resistance, and reduced TNF-alpha in both skeletal muscles. There were significant negative correlations between M values and TNF-alpha levels in both soleus and EDL muscles. Also, the soleus muscle strip incubation with 10(-7) mol/l angiotensin II increased TNF-alpha secreted into the incubation medium compared to the incubation without angiotensin II. These results suggest that skeletal muscle TNF-alpha is linked to insulin resistance and hypertension and that angiotensin II may be one of the factors that regulate skeletal muscle TNF-alpha.

Adipose Tissue↗
PubMed2000

Roles of tyrosine kinase and protein kinase C in infarct size limitation by repetitive ischemic preconditioning in the rat.

In this study, we examined the possibility that infarct-size limitation by repetitive preconditioning (PC) is achieved by activation of both protein kinase C (PKC) and tyrosine kinase. In addition, we assessed whether such kinase activation is triggered by angiotensin II type 1 (AT1) and alpha1-adrenergic receptors and whether sarcolemmal and mitochondrial adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channels play roles as effectors of cardioprotection in the rat. Under pentobarbital anesthesia, myocardial infarction was induced by 20-min coronary occlusion and 3-h reperfusion in the rat. Infarct size was determined by tetrazolium and expressed as a percentage of area at risk (%IS/AR). PC with one cycle of 5-min ischemia/5-min reperfusion before 20-min ischemia significantly reduced %IS/AR from the control value of 49.4 +/- 2.0 to 35.4 +/- 2.8, and repetitive PC with two cycles of 5-min ischemia/5-min reperfusion further limited %IS/AR to 3.2 +/-0.9. Infarct-size limitation by single-cycle PC was completely abolished by a PKC inhibitor, staurosporine (100 microg/kg; %IS/ AR, 45.7 +/- 5.0). In contrast, the cardioprotection by repetitive PC was only partially blocked by staurosporine (%IS/AR, 19.8 +/- 2.4), another PKC inhibitor, polymyxin B (5 mg/kg; %IS/AR, 16.2 +/- 3.1), or a tyrosine kinase inhibitor, genistein (5 mg/kg; %IS/AR, 21.8 +/- 1.4). However, a combined injection of genistein and staurosporine additively inhibited protection of repetitive PC (%IS/AR, 36.4 +/- 1.7). Staurosporine, polymyxin B, or genistein alone did not modify %IS/AR in nonpreconditioned rat hearts. Infarct-size limitation by repetitive PC was not attenuated by pretreatment with a selective AT1-receptor blocker (CV11974, 10 mg/kg), prazosin (0.6 mg/kg; %IS/AR, 6.4 +/- 3.2 and 1.6 +/- 0.5, respectively). A selective blocker of mitochondrial K(ATP) channels, 5-hydroxydecanoate (3 mg/kg), completely abolished the cardioprotective effect (%IS/AR, 50.8 +/-3.5), but HMR1883 (3 mg/kg), a selective blocker of sarcolemmal K(ATP) channels, failed to inhibit the preconditioning effect (%IS/AR, 4.4 +/- 0.7). These findings suggest that repetition of PC provokes activation of both PKC and tyrosine kinase, leading to enhanced antiinfarct tolerance by opening of mitochondrial but not sarcolemmal K(ATP) channels. It is unlikely that activation of either AT1 or alpha1-adrenergic receptor alone is crucial to trigger preconditioning. Key Words: Tyrosine kinase-Genistein-Angiotensin II-alpha1-Adrenergic receptor-Sarcolemmal K(ATP) channel-Mitochondrial K(ATP) channel.

Analysis of Variance↗
PubMed2000

Prognostic value of impaired myocardial fatty acid uptake in patients with acute myocardial infarction.

Impaired cardiac fatty acid uptake, assessed by the radiolabelled fatty acid analogue beta-methyl-p-iodophenyl pentadecanoic acid (I-123-BMIPP), is observed in the myocardium following acute ischaemic events, but the long-term prognostic implication has not been established. This study aimed to determine the prognostic value of cardiac BMIPP uptake in patients with acute myocardial infarction. Following the assessment of thallium-201 and I-123-BMIPP uptake, 101 post-infarct patients were prospectively followed up with primary end points of cardiac death, heart failure and non-fatal infarction. During a mean follow-up of 28 months, three cardiac deaths, three non-fatal infarctions, 23 revascularizations and four recurrences of angina pectoris were observed. Multivariate analysis identified reduced uptake of BMIPP and perfusion, no beta-blocking treatment and greater thallium-BMIPP mismatch (i.e. larger BMIPP defect than thallium defect) as significant predictors for overall cardiac events. Prior myocardial infarction, reduced left ventricular ejection fraction and greater thallium-BMIPP mismatch were selected as independent predictors of harder cardiac events. Female patients, those with greater BMIPP defect or greater thallium-BMIPP mismatch showed worse clinical outcomes. The inclusion of BMIPP data improved the prognostic values of conventional significant predictors. In conclusion, impaired myocardial I-123-BMIPP uptake and perfusion-BMIPP mismatch are related to a high probability of fatal and non-fatal cardiac events, suggesting the aetiological relevance and prognostic value of impaired cardiac fatty acid metabolism in viable, but jeopardized, myocardium following acute myocardial infarction.

Adult↗
PubMed2000

Does primary stenting preserve cardiac function in myocardial infarction? A case-control study. NORTH-981 investigators. Network of revascularisation therapy in Hokkaido.

OBJECTIVE: To investigate whether coronary stenting limits myocardial injury and preserves left ventricular function. DESIGN AND SETTING: Prospective multicentre case-control study of primary percutaneous transluminal coronary angioplasty (PTCA) with and without stenting, performed in seven cardiovascular centres. SUBJECTS AND METHODS: 45 consecutive patients with acute myocardial infarction who were treated with successful primary stenting (Stent group) and did not have restenosis were paired with 45 matched control subjects with acute myocardial infarction treated by successful primary PTCA without stenting, also with no restenosis (POBA group). RESULTS: In comparison with the POBA group, the Stent group-especially those patients with a left anterior descending coronary artery lesion-had a smaller hypokinesis area (mean (SD): 15. 1 (20.0) v 34.4 (24.3) chords), reduced hypokinesis area/risk area (25.2 (31.9)% v 58.8 (40.1)%), and a larger ejection fraction (63.3 (10.2)% v 51.7 (11.7)%) evaluated by quantitative left ventriculography using the centerline method. In the Stent group, the correlation between risk area and hypokinesis area was significantly shifted downward. Multiple logistic regression analysis on infarct size limitation (hypokinesis area/risk area < 50%) identified preinfarction angina in all subjects and preinfarction angina and stenting in patients with left anterior descending coronary artery lesions as explanatory factors. CONCLUSIONS: Primary PTCA using a coronary stent is effective in preventing myocardial injury and restoring left ventricular function in patients with anterior acute myocardial infarction.

Adult↗
PubMed2000

Hypoparathyroidism potentiates cardiovascular complications through disturbed calcium metabolism: possible risk of vitamin D(3) analog administration in dialysis patients with end-stage renal disease.

BACKGROUND/AIM: Progressive cardiovascular calcification in dialysis patients with end-stage renal disease (ESRD) is a serious complication; however, the precise mechanism remains uncertain. We tested whether metabolic calcium abnormalities and hypoparathyroidism might have a correlation with cardiovascular complications in ESRD patients. METHODS: A series of 48 ESRD patients with cardiovascular diseases and/or congestive heart failure, aged 36-82 (61 +/- 12) years, 23 male and 25 female, were enrolled in this study. Serum total calcium (Ca, mmol/l), inorganic phosphate (mmol/l), and intact parathyroid hormone (iPTH, pg/ml) levels were determined in all cases. RESULTS: Organic heart disease was confirmed in 28 patients (58.3%), including 15 with coronary artery disease: 8 with aortic aneurysm, 8 with stenotic valvular heart disease, 9 with excessive mitral annular calcification, 3 with dialysis cardiomyopathy, and 7 with obstructive arterial disease. Serum iPTH measurement revealed hypoparathyroidism (iPTH <60) in 20 of 48 (41.7%) and hyperthyroidism (iPTH >/=200) in 13 of 48 (27.1%) subjects. The 20 patients with low iPTH had a higher prevalence of valvular heart disease, a higher total Ca level corrected for serum albumin (2.70 +/- 0.30 in low iPTH vs. 2.47 +/- 0.30 in normal iPTH, 2.35 +/- 0.20 in high iPTH, p = 0.003) and a higher tendency of vitamin D(3) analog use (65% in low iPTH vs. 33% in normal iPTH and 46% in high iPTH, p = 0.078). Moreover, corrected serum Ca exhibited a negative logarithmic correlation with serum iPTH: corrected Ca = -0.284x log (iPTH) + 3.021 (r = 0.637, p = 0.0001). Multiple logistic regression analysis revealed diabetes and hypoparathyroidism (iPTH <60) as risk factors for cardiovascular complications in ESRD. CONCLUSION: These results suggest that hypercalcemia and hypoparathyroidism in conjunction with vitamin D(3) use might play an important role in cardiovascular complications of chronic dialysis patients.

Adult↗
PubMed2000

Technetium-99m sestamibi/tetrofosmin myocardial perfusion scanning in cardiac and noncardiac sarcoidosis.

Left ventricular (LV) and right ventricular (RV) involvement in sarcoidosis must be firmly confirmed to determine patients' prognosis. We examined whether myocardial perfusion images using technetium-99m single photon emission computed tomography (SPECT) have a diagnostic benefit in the evaluation of biventricular involvement. Sixteen patients with sarcoidosis, aged 21-78 (54 +/- 12) years old, 5 males and 11 females, complicated with cardiac disease (cardiac sarcoidosis, n = 6) including tachyarrhythmias of ventricular origin (n = 5), atrioventricular block (n = 4), and congestive heart failure (NYHA > or = II, n = 1), were enrolled in this study. Myocardial SPECT using technetium-99m sestamibi or tetrofosmin was performed and semiquantitatively scored for comparison with 25 control subjects. Perfusion abnormalities were more frequently recognized in sarcoidosis (LV 5/16, 31% and RV 14/16, 88% vs. LV 0/25, 0% and RV 8/25, 32% in controls). LV involvement had a close correlation with atrioventricular block and with congestive heart failure, and multiple sites of RV involvement correlated with ventricular tachyarrhythmia of RV origin. Total number of defect segments were highest in cardiac sarcoidosis (18/30, 60% vs. 19/60, 32% in noncardiac sarcoidosis, and 11/150, 7% in controls, p = 0.0001), and semiquantitatively evaluated total LV and RV scores (ranging from 0 to 18) were higher than those of controls (15.1 +/- 1.8 vs. 11.4 +/- 3.0 in noncardiac sarcoidosis, and 9.0 +/- 5.0 in cardiac sarcoidosis) and exhibited a significant positive linear correlation with the RV ejection fraction (y = 19.8 + 1.83x, r = 0.786, p = 0.001). Biventricular SPECT using technetium-99m is clinically useful for the noninvasive evaluation of both ventricular involvements in sarcoidosis.

Adult↗