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It has been reported that anemia is a prognostic predictor in patients with diastolic heart failure (DHF), however, the relationship between anemia and sudden death in those patients is still unclear. We prospectively studied 357 stable DHF patients and the proportion of anemic patients was 39% of the study population. During the mean follow-up period of 3.6+/-1.7 years, 30 (8.4%) patients died suddenly. Importantly, the Cox proportional-hazards regression analysis showed that lower hemoglobin level was significantly associated with the development of sudden death in the multivariate model (P

洞不全症候群を除く50症例を, 一過性心房細動 (一過性af) の誘発ができない20例と誘発のできる14例, 及び, 1ヵ月以上持続した慢性afに対して電気的除細動を施行した16例に分類し, 心房筋再分極の指標 (右房有効不応期ERP, 右房単相性活動電位持続時間MAP口90) , 伝導遅延の指標 (右房内局所最大伝導遅延率%CD) , wavelengthの指標 (MAPD90/%CD, ERP/%CD) , 右心房容積の指標 (心臓超音波検査による右房心内膜トレース/体表面積) を, それぞれ計測した.この結果, 一過性afの誘発には再分極相の短縮とそれによるwavelengthの短縮が関与し, 慢性afでは再分極相の短縮に加え, 増強した伝導遅延によりwavelengthはさらに短縮していた.また, 心房が拡大するとwavelengthは短縮した.この様に, ヒト心房筋において再分極相の短縮, 伝導遅延, 心房拡大はいずれもwavelengthを短縮し, afを発生, 持続させ易くすると考えられた.

Background: We reported an increased occurrence of cardiovascular diseases (CVDs) after the Great East Japan Earthquake by examining ambulance records, but it had to be confirmed by cardiologists. Methods and Results: We enrolled patients admitted to the cardiology department of the 10 hospitals in the disaster area from 4 weeks prior to 15 weeks after March 11 in the years 2008–2011 (n=14,078). The weekly occurrence of several CVDs, including heart failure (HF), pulmonary thromboembolism (PTE) and infectious endocarditis (IE), was sharply and significantly increased after the Earthquake. Conclusions: The Disaster caused significantly increases in the occurrence of HF, PTE and IE. (Circ J 2013; 77: 490–493)

Objectives Calcium overload induces spontaneous cyclic calcium release from the sarcoplasmic reticulum, leading to spontaneous myocardial oscillation. This study was designed to elucidate (1) the effect of the myocardial oscillation on changes in ventricular performance and (2) how these changes relate to the strength of the diastolic spontaneous myocardial oscillation and the spatial extent—that is, in how extensive an area of the epicardium it occurred. Methods the isovolumic pressure of the left ventricle and epicardial fura 2 fluorescence in isolated hamster hearts were simultaneously observed at various calcium concentrations ([Ca2+]o). Endothelial cells and pericytes of the capillaries, preferentially stained by fura 2, were passively oscillated by surrounding myocytes during diastole at concentrations greater than 1 mmol/1 of [Ca2+]o. The strength of the myocardial oscillation was evaluated as the root mean square (RMS) of fluctuation in the distance between endothelial cells or pericytes. The spatial extent of the myocardial oscillation was estimated as the appearance rate, defined as the ratio of the number of microscopic fields showing the capillary oscillation, to the total number of examined fields. Results Up to 4 mmol/l of [Ca2+]o, developed pressure and maximum rate of pressure rise significantly increased in a manner dependent on [Ca2+]o, but a further increase in [Ca2+]o significantly decreased these parameters. In the presence of ryanodine (2.5 μ mol/l), developed pressure and maximum rate of pressure rise monotonously increased in a manner dependent on [Ca2+]o. Although the oscillation was never observed at 1 mmol/l of [Ca2+]o (appearance rate = 0%), it occurred in some of the microscopic fields at 2 and 4 mmol/l (appearance rate = 19.5 and 56.3%, respectively) and occurred in all microscopic fields at concentrations greater than 4 mmol/l (appearance rate = 100%). Ryanodine, which completely eliminated the capillary oscillation, inhibited the increase of both RMS and end-diastolic pressure by an increase in [Ca2+]o. Conclusions Our data suggest that the myocardial oscillation impairs systolic and diastolic function in intact ventricle, and that these effects are associated with the spatial extent and the strength of the myocardial oscillation.

Some patients with acquired long QT syndrome (LQTS) represent an incomplete form of congenital LQTS in which a mutation or polymorphism in one of the LQTS genes is clinically inapparent until the patient is exposed to a particular drug or other predisposing factor. A 15-year-old man in the

In isolated cardiac muscle, spontaneous Ca2+ release from the sarcoplasmic reticulum (SR) occurs and is propagated as a wave by a regenerative Ca2+-induced Ca2+ release mechanism. We have already reported that this wave is followed by a refractory period. The aim of this study is to investigate whether such a refractory period could also inactivate Ca2+ release from the SR triggered by an action potential. Myocytes were enzymatically isolated from guinea pig ventricles and loaded with acetoxymethylester form of fura-2 (fura-2 AM). The membrane potential was recorded with a conventional microelectrode technique, and spatio-temporal changes in fura-2 fluorescence were recorded using a digital TV system. After perfusion with potassium-free Tyrode solution, interactions between fluorescence transients due to propagating waves and action potential-induced fluorescence transients were observed. In this study, the action potentialinduced fluorescence transients could be detected in the next video frame after the propagation of the waves and showed gradual restitution of the transients. In addition, the sum of the fluorescence transients triggered by an action potential and the fluorescence transients due to the waves did not show significant change whenever the preceding waves were propagating. These results show that the interaction between the action potential-induced Ca2+ release and the calcium wave-induced Ca2+ release from the SR have the following characteristics: (1) For the action potentialinduced Ca2+ release, no absolute refractory period was observed 33 msec after the calcium wave. This suggests that the calcium waves can be reset by the action potential. (2) Regardless of whether the two release mechanisms are different, both share a common compartment of Ca2+ storage.

Diabetes mellitus (DM) is a major risk factor for heart failure, independent of coronary artery disease or hypertension (HT). Therefore, our study was designed to examine the mechanisms of DM-induced left ventricular (LV) diastolic dysfunction. In this study, we made five different 10-week treatment groups of Dahl salt-sensitive rats as follows: Control; a low-salt (0.5% NaCl) diet, HT; a high-salt (5% NaCl) diet, DM; a low-salt diet with streptozotocin (STZ) injection (30 mg kg(-1) i.p.), HT+DM; a high-salt diet with STZ injection, and the Olmesartan group; a high-salt diet with STZ treated with an angiotensin receptor blocker, olmesartan (1 mg kg(-1) day(-1)). Cardiac diastolic dysfunction with a preserved systolic function was noted in the HT group, and was most prominently noted in the HT+DM group, characterized by enhanced cardiac fibrosis, whereas the extent of HT and myocardial hypertrophy was comparable between the two groups. Myocardial expressions of collagen III, transforming growth factor-beta2, angiotensin-converting enzyme (ACE), angiotensin II type-1 receptor and myocardial oxidative stress (evaluated by 4-hydroxy-2-nonenal-modified protein) were mostly enhanced in the HT+DM group. Importantly, there was a positive correlation between the extent of diastolic dysfunction and that of myocardial ACE expression. All these cardiac abnormalities induced by DM and HT were ameliorated in the olmesartan group. These results indicate that DM accelerates diastolic dysfunction in hypertensive heart disease through activation of the renin-angiotensin system, with subsequent inflammatory and oxidative stresses and myocardial fibrosis, suggesting that an inhibition of the system is effective for the treatment of diastolic dysfunction in this combined disorder.

Diastolic heart failure (DHF) is a major cardiovascular disorder with poor prognosis; however, its molecular mechanism still remains to be fully elucidated. We have previously demonstrated the important roles of Rho-kinase pathway in the molecular mechanisms of cardiovascular fibrosis/hypertrophy and oxidative stress, but not examined in the development of heart failure. Therefore, we examined in this study whether Rho-kinase pathway is also involved in the pathogenesis of DHF in Dahl salt-sensitive rats, an established animal model of DHF. They were maintained with or without fasudil, a Rho-kinase inhibitor (30 or 100 mg/kg/day, PO) for 10 weeks. Untreated DHF group exhibited overt heart failure associated with diastolic dysfunction but with preserved systolic function, characterized by increased myocardial stiffness, cardiomyocyte hypertrophy, and enhanced cardiac fibrosis and superoxide production. Fasudil treatment significantly ameliorated those DHF-related myocardial changes. Western blot analysis showed that cardiac Rho-kinase activity was significantly increased in the untreated DHF group and was dose-dependently inhibited by fasudil. Importantly, there was a significant correlation between the extent of myocardial stiffness and that of cardiac Rho-kinase activity. These results indicate that Rho-kinase pathway plays an important role in the pathogenesis of DHF and thus could be an important therapeutic target for the disorder.

Background: Diastolic heart failure (DHF) is a major cardiovascular disorder with poor prognosis; however, its molecular mechanism remains to be fully elucidated. We have previously demonstrated that activation of Rho-kinase pathway is substantially involved in the pathogenesis of oxidative stress and cardiac remodeling. In this study, we thus examined whether Rho-kinase pathway is also involved in the pathogenesis of DHF. Methods: We maintained male Dahl salt-sensitive rats for 10 weeks, starting from 7 weeks of age, with either 0.5% NaCl (control) or 8% NaCl (DHF) with or without oral treatment with fasudil, a selective Rho-kinase inhibitor (30 and 100 mg/kg/day) (n=13–31). We serially measured hemodynamic variables and cardiac function by echocardiography, followed by histological analysis. Results: At week 17, the untreated DHF group exhibited overt heart failure (e.g. lung edema) associated with diastolic dysfunction but with preserved systolic function, characterized by increased myocardial stiffness, cardiomyocyte hypertrophy, and enhanced cardiac fibrosis and superoxide production (all P Conclusions: These results indicate that activation of Rho-kinase pathway plays an important role in the pathogenesis of DHF through cardiomyocyte hypertrophy and interstitial fibrosis, suggesting the therapeutic importance of Rho-kinase for the treatment of DHF in humans.

Background The repolarization properties of the crista terminalis (CT) cells have not been elucidated in patients with sinus node disease (SND). In the present study a new technique of recording the monophasic action potential (MAP) at the CT was used to examine the repolarization of the right atrium (RA) in SND patients. Methods and Results Symptomatic SND (n=13) patients and age-, sex-matched control patients (n=13) were tested. The MAP duration (MAPD) at a basic cycle length of 600 ms was recorded at the CT in the superior vena cava - RA junction and at the middle - anterior RA with the effective refractory period (ERP) at the high RA. In 6 controls and 4 SND patients, the effect of adenosine triphosphate on the MAPD was examined. The MAPD at the CT exceeded that at the middle - anterior RA in both groups. The MAPD at the CT in the SND group was significantly prolonged compared with the control group (CT: 358±39 ms vs 289±43 ms). Between the SND and control groups, the MAPD at the middle - anterior RA (278±36 ms vs 265±39 ms) and ERP (294±42 ms vs 266±41 ms) did not differ. Both the corrected-sinus node recovery time and sinoatrial conduction time were better correlated with the MAPD at the CT than the MAPD at the middle - anterior RA and ERP. Adenosine triphosphate shortened the MAPD, which was augmented at the CT in the SND patients. Conclusion A novel method of estimating the MAP at the CT revealed the characteristics of atrial repolarization in SND patients. (Circ J 2005; 69: 1361 - 1367)

Myocardial infarction (MI) is one of the major etiologies of chronic heart failure (CHF) in Japan.The prognoses of CHF patients after MI (n=283) were investigated by comparing them with those of CHF patients with nonischemic cardiomyopathy (NICM, n=310) from the CHF registry (CHART; n=1,154). The Kaplan-Meier (KM) analyses revealed that the 3-year all-cause mortality was significantly higher in the MI cohort compared with the NICM cohort (29.0% vs 12.4%, p0.0005). Age/gender/treatment-adjusted KM analysis revealed significant differences only in the cohorts with preserved left ventricular ejection fraction (LVEF), defined as LVEF45%, or in less symptomatic patients (New York Heart Association I or II). Multivariate Cox regression analysis showed that beta-blocker (BB) was associated with a significant reduction in mortality from cardiac causes, and either angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ACEI/ARB) was significantly related to the improvement of survival in the MI cohort (adjusted hazard ratio: 0.222 and 0.497, p0.05), even though these medicines were used significantly less often in the MI cohort.Underlying MI has a significant impact on the survival of Japanese CHF patients, especially those with preserved LVEF or with fewer symptoms. The appropriate expansion of ACEI/ARB or BB therapy might be necessary to improve their survival.

Background High mortality and a high readmission rate characterize diastolic heart failure (DHF), but evidence-based therapeutic strategies have not been established for DHF. Methods The aim of a multicenter, randomized open trial (the Diastolic Heart Failure Assessment Study in Tohoku District, DIAST) is to evaluate the safety and prognostic efficacy of the multiple action non-selective β-blocker carvedilol in 160 patients with DHF (left-ventricular ejection fraction ≥50%). The target dose of carvedilol is 10 mg twice a day and the mean follow-up is estimated to be 2 years. The primary endpoints are to evaluate (1) all-cause mortality or hospitalization, (2) cardiovascular mortality or hospitalization and (3) worsening heart failure. The secondary endpoints are to assess (1) cardiovascular events, (2) the individual components of the above combined endpoints, (3) the duration of hospitalization, (4) the functional class and exercise capacity and (5) the safety and tolerability. All patients' data are processed using an original registration system on an internet homepage. Several substudies to assess neurohumoral factors, heart rate variability, oxidative stress and sleep apnea will clarify the pathophysiology of DHF. Conclusions The DIAST will contribute to establish therapeutic guidelines for DHF. (Circ J 2004; 68: 660 - 664)

The heart of the decapod crustacean is activated by regular impulse bursts from the cardiac ganglion. The cardiac pump function depends on ganglionic burst frequency, burst duration, and burst impulse frequency. Here, we activated isolated lobster cardiac ostial muscle (Orbicularis ostii muscle, OOM) by stimulus trains in vitro in order to characterize the response of the contractile apparatus to [Ca2+]i. We employed stimulus trains that generate a steady state between the [Ca2+]i and force in order to estimate the Ca2+ sensitivity of myofilaments. Force and [Ca2+]i transients were simultaneously recorded using a silicon strain gauge and the fluorescence of iontophoretically microinjected fura-2 salt. We examined the effects of tetanus duration (TD), the interval between trains, and 6 microM cyclopiazonic acid, an inhibitor of the SR Ca2+ pump, on the steady-state force-[Ca2+]i relationship. The instantaneous force-[Ca2+]i relationships appeared sigmoidal (EC50 and Hill coefficient, 98.8+/-32.7 nM and 2.47+/-0.20, mean +/- SD, respectively), as did the curves superimposed after 500 ms following the start of stimulation, indicating that the force-[Ca2+]i relationship had reached a steady state at that time. Also, the maximum activated force (Fmax) was estimated using the steady-state force-[Ca2+]i relationship. Prolonged stimulus trains, decreasing the interval between recurrent trains from 5 to 2.5 s, and cyclopiazonic acid each increased the measured EC50 without changing Fmax. The EC50 correlated strongly with averaged [Ca2+]i over time. We conclude that the steady-state force-[Ca2+]i relationships in the OOM indicate cooperation between force generation and Ca2+ binding by the myofilaments. Our data also suggest the existence of a novel Ca2+-dependent mechanism which reduces Ca2+ sensitivity and accelerates relaxation of lobster cardiac muscle myofilaments.

The current reperfusion strategy in Japan for acute myocardial infarction (AMI) is that the majority of early arrival patients are treated with primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI, intravenous thrombolysis (IV-T), intracoronary thrombolysis (IC-T) and rescue PCI has not been compared in the clinical situation. In the present study, 3,258 cases of AMI in 1992-2000 from the data base of the Miyagi Study Group for AMI were analyzed. These patients were hospitalized within 6 h of the onset of symptoms. IV-T and IC-T were initially performed in 120 and 441 patients, respectively, and 41 and 199 rescue PCI procedures, respectively, were needed. Primary PCI was performed in 1,822 cases, and no reperfusion therapy was done in 875 patients. The crude 30-day in-hospital mortality was 12.7% for IV-T, 3.7% for IC-T, 4.8% for primary PCI, 7.9% for rescue PCI, and 14.1% in patients who did not undergo reperfusion therapy. The covariate-adjusted odds ratio (95% confidence interval) was 0.38 (0.28-0.52) for primary PCI, 0.30 (0.15-0.60) for IC-T, 1.04 (0.51-2.10) for IV-T and 0.77 (0.46-1.30) for rescue PCI. The present data verify that primary PCI is superior to other reperfusion strategies in the real clinical situation and justifies the current unique strategy of reperfusion therapy for AMI used in Japan. (Circ J 2003; 67: 209 - 214)

To examine the adverse reactions to TS-1 for patients with recurrent head and neck cancer, five patients with locoregional recurrences and two with distant metastasis were enrolled in the present study and took TS-1 as outpatients. All patients underwent irradiation with or without surgery before administration of TS-1. One patient was given 100 mg of TS-1 daily, and six patients were given 120 mg of TS-1 daily. Thirteen courses consisted of the regimen of four weeks of TS-1 administration followed by two weeks of intermission, nine courses consisted of the regimen of two weeks of administration followed by one week of intermission, and seven courses consisted of the regimen of two weeks of administration followed by two weeks of intermission. Anemia, leukopenia, neutropenia, and liver dysfunction were often observed as adverse reactions to TS-1 administration. Grade 3 bilirubinemia was observed in only one course, but other adverse reactions consisted of grade 1 or grade 2. Almost all adverse reactions returned to normal after the cessation of drug administration. Based on these results, we conclude that TS-1 is a safe drug for the treatment of outpatients with recurrent head and neck cancer.

The significance of heart-rate turbulence (HRT) in patients with chronic heart failure (CHF) was evaluated to examine whether it is sensitive to the risk of ventricular tachycardia (VT). HRT is reported to predict the prognosis after myocardial infarction (MI), but its prognostic value in patients with CHF remains unknown. HRT was measured in 50 CHF patients (left ventricular ejection fraction50% and/or left ventricular end-diastolic diameter55 mm, 34 cardiomyopathy, 16 post-MI) and 21 patients without obvious heart diseases (control). HRT slope and HRT onset were measured by the original definitions using digitized Holter ECG recordings. Cardiac pump function was assessed by echocardiography. The value of the HRT slope was significantly lower in CHF than in control (3.7 +/- 1.7 vs 16.4 +/- 5.3, mean +/- SD, p0.01). The value of the HRT onset in patients with CHF was significantly higher than that in control patients (-1.1 +/- 1.9 vs -3.6 +/- 1.7, mean +/- SD, p0.05). The HRT slope and onset in CHF patients with VT were nearly identical to those without VT. The HRT slope appears to be a powerful prognostic marker that shows significant differences between CHF subgroups when divided by clinical events; that is, CHF death and CHF hospitalization. However, it has limited value for predicting fatal ventricular arrhythmias.

The case-fatality rate from acute myocardial infarction (AMI) appears to have been declining in recent decades, so the present study reviewed the trend in in-hospital case-fatalities from AMI in Miyagi Prefecture, Japan, 1980-1999. The causes of death and the effects of gender and age on the trend were also analyzed. From the AMI registration database of the Miyagi Study Group for AMI, 12,961 cases of AMI were analyzed. The 30-day in-hospital case-fatality was calculated from the data for 1980-1999: data for causes of death were available for 1980-1997, and the data concerning primary percutaneous transluminal coronary angioplasty (PTCA) for AMI were available for 1997-1999. The in-hospital case-fatality rate declined from 17.0% in the early 80s to 7.3% in the late 90s (approximately 57% reduction). The in-hospital case-fatality rate was higher in female patients. Rhythm failure substantially decreased in the late 1980s. Pump failure is decreasing, but is still the biggest problem. The in-hospital case-fatality rate was significantly lower in patients received PTCA. The declining trend in the in-hospital case-fatality rate suggests the benefits of current therapeutic procedures, including primary PTCA, for AMI. Pump failure is an important target for further decreasing the trend.

A dysfunction of the sarcoplasmic reticulum (SR) causes an increase in the myogenic tone of rat skeletal muscle small arteries (A SK ), but not that of mesenteric small arteries (A MS ). We hypothesized that the difference depends on the activity of voltage-dependent Ca 2+ channels in these vessels. To test this, we measured the membrane potential of these vessels and examined ryanodine-induced constrictions by manipulating the activity of voltage-dependent Ca 2+ channels. The isolated vessels were cannulated to control the transmural pressure. To assess the vascular tone, the inner diameter was measured with a video-digitizing system. The membrane potential of A SK was more depolarized between 20 to 100 mm Hg of transmural pressure. A MS was not constricted by the Ca 2+ channel agonist Bay K 8644 (1 nM-1 μM) alone, but substantially constricted in the presence of ryanodine (1 μM). Ryanodine also augmented the KCl (20 mM)-induced constriction. In A sk , the Ca 2+ channel blocker nisoldipine fully dilated the ryanodine-induced constriction; however, the ryanodine-induced constriction was less susceptible to nisoldipine than was the myogenic and phenylephrine-induced constriction caused mainly by increased Ca 2+ influx. In conclusion, the contribution of the SR function to Ca 2+ metabolism depends on the activity of dihydropyridine-sensitive Ca 2+ channels. The dysfunction of SR by ryanodine may impair the Ca 2+ extrusion rather than increase Ca 2+ influx in rat small arteries.

Spontaneous asynchronous contractile activity caused by spontaneous release of calcium ions (Ca2+) from the sarcoplasmic reticulum (SR) is thought to be the cause of deterioration of ventricular function under conditions of calcium overload. We examined whether dantrolene sodium, which can inhibit Ca2+ release from the skeletal SR, improves the systolic and diastolic function of calcium-overloaded hearts. In isolated hamster left ventricles, the concentration of Ca2+ in the perfusate ([Ca2+] o) was increased from 1 mmol/L to 7 mmol/L in 1-mmol/L steps in the absence (control, n=6) and presence of dantrolene sodium (11.8 μmol/L, n=5). Left ventricular developed pressure and its maximum rate of rise (max dP/dt) increased with an increase in [Ca2+]o up to 4 mmol/L, and decreased with a further increase in [Ca2+]o. In the presence of dantrolene sodium, developed pressure and max dP/dt increased up to 5 mmol/L [Ca2+]o. Thus, dantrolene sodium improves Ca2+ tolerance. In isolated ventricles perfused with 1 mmol/L [Ca2+] o, dantrolene sodium decreased developed pressure by 33.7±7.4% and max dP/dt by 37.4±5.6% (mean±SEM, n=8) at 1 mmol/L [Ca2+]o. In contrast, at 5 mmol/L [Ca2+]o. ('calcium-overloaded state'), dantrolene sodium increased developed pressure by 6.8±2.6% and max dP/dt by 14.4±5.7%, and decreased the end-diastolic pressure by 5.3±1.9% (n=8) . Dantrolene sodium partially suppressed the spontaneous contractile activities observed microscopi-cally on the epicardium of ventricles perfused with 5 mmol/L [Ca2+] o. Dantrolene sodium improved the Ca2+ tolerance of left ventricles and exerted positive inotropic effects and decreased diastolic stiffness in calcium-overloaded hamster left ventricles by suppressing spontaneous contractile activity. (Jpn Circ J 1997; 61: 855 - 863)

Leaf mold of tomato was found on cv. Momotaro-fight in 2003 in Ehime Prefecture. The symptoms were marginal indefinite yellowing on the upper leaf surface, and downy, gray to brown sporulation on the lower surface underneath the spots. The symptoms and morphology were the same as seen with Passalora fulva. The fungal isolates were identified as races 2.4, 2.4.11, 4, and 4.11 by inoculation tests. Races 4 and 4.11 have never before been found in Japan.

Although changes in intracellular Ca2+ concentration ([Ca2+]i) are spatially heterogeneous during spontaneous contraction in mammalian cardiac muscle, it has not yet been observed how [Ca2+]i changes spatially within cardiac myocytes during delayed (DADs) and early (EADs) afterdepolarizations. The aim of this study is to characterize the spatial features of the increase in [Ca2+]i during such afterdepolarizations and to understand the ionic mechanisms responsible for them. Myocytes were enzymatically isolated from guinea pig ventricles and loaded with fura 2-acetoxymethylester, the Ca2+ fluorescence indicator dye. Membrane potential was recorded with a conventional microelectrode technique, and spatiotemporal changes in fura 2 fluorescence and cell length were recorded using a digital television system. After superfusion with potassium-free Tyrode solution, DADs and EADs were induced. During DADs, fluorescence transients were heterogeneous within myocytes (n = 11). Furthermore, they often propagated within myocytes as if they were "waves." In contrast, during EADs, fluorescence transients showed no waves within myocytes but rather showed synchronous changes throughout the myocytes (n = 15). The results of this study suggest that the spatial features of the increase in [Ca2+]i differ between the DADs and EADs. We concluded from these differing features that the ionic mechanisms responsible for the two triggered activities are different.

The purpose of this study is to clarify the kinds of cells that fluoresce in isolated perfused heart intracoronarily loaded with fura 2-AM or indo 1-AM. The hearts from hamsters perfused by the Langendorff method were loaded with fura 2-AM or indo 1-AM intracoronarily. The epicardium was excited by ultraviolet light at a wavelength of 340 or 380 nm (fura 2) or 360 nm (indo 1). Epifluorescent images from arrested hearts prepared with St Thomas' cardioplegic solution were observed through an inverted microscope and taken by a still camera. Endothelial cells and pericytes of the capillaries showed intense fluorescence. In the intercapillary spaces, a less intense but still apparent fluorescence emitted by myocytes could also be detected. On the other hand, fluorescence from smooth muscle cells and fibroblasts could not be identified. Therefore, epifluorescence in the isolated perfused heart loaded with fura 2-AM or indo 1-AM was mainly generated within endothelial cells, pericytes, and myocytes. To evaluate calcium fluorescence in isolated hearts quantitatively, the fluorescence of endothelial cells and pericytes of the capillaries must be taken into consideration.