The endothelial function of children with and without vascular disease, consisting of 41 controls, 24 with Kawasaki disease (KD), and 46 with diabetes mellitus (DM), was examined. Age at examination ranged from 3 to 23 years (mean, 12.0 +/- 4.7). The flow-mediated dilatation (FMD) and intima-media complex in the common carotid artery were measured. In controls age at examination was not associated with FMD or intima-media complex. FMD significantly decreased in children with KD and DM compared with the control group (control vs KD or DM: 11.7 +/- 14.7 vs 3.0 +/- 11.0 or 6.4 +/- 8.5%, respectively; p < 0.05). However, there was no significant difference for intima-media complex among the groups. Furthermore, FMD in KD patients with coronary arterial aneurysm was lower than that in KD patients without aneurysm (-0.5 +/- 9.2 vs 8.3 +/- 9.1%, p < 0.05). In DM patients, FMD in the high HbA1c group (HbA1c = 7%) was lower than that in the normal HbA1c group (HbA1c < 7%) (4.8 +/- 8.1 vs 11.4 +/- 7.8%, p < 0.05). In conclusion, FMD detected endothelial impairment in children with KD or type 1 DM regardless of overt vascular complications, and FMD impairment occurs prior to intima-media complex thickening. By measuring both FMD and intima-media complex, useful information for predicting vascular complications may be obtained.

Adolescent↗

PubMedDate not supplied

Membrane action of ethmozin on normoxic and hypoxic canine Purkinje fibers.

Transmembrane potentials were recorded from canine Purkinje fiber preparations before and after perfusion with ethmozin (0.05, 0.2, and 1.0 microgram/ml). Under normal oxygenation (95% O2 + 5% CO2; n = 9), ethmozin at 0.05 microgram/ml significantly (p less than 0.05) reduced maximal rate of depolarization (MRD), from 750 +/- 61 to 709 +/- 58 V/s, without affecting other parameters. MRD was further decreased to 647 +/- 53 and 540 +/- 78 V/s at 0.2 and 1.0 microgram/ml of this agent. Reduction of maximal diastolic potential, from -86.1 +/- 6.0 to -84.6 +/- 5.9 mV, occurred only at 1.0 microgram/ml, suggesting that the decrease in MRD is not voltage dependent. Ethmozin significantly shortened the action potential duration at 50 (APD50) and 90% (APD90) repolarization, from 231 +/- 16 and 306 +/- 18 to 199 +/- 26 and 279 +/- 14 ms, respectively. At 1.0 microgram/ml, these values were further reduced. The effective refractory period also showed a concentration-dependent shortening, but the ratio of the refractory period to APD90 was increased. The membrane responsiveness curve was shifted by ethmozin to more negative potentials. The h infinity (inactivation of the fast Na+ current) curve was shifted by 3.8 mV to more negative values by 1.0 microgram/ml ethmozin. "Slow response" produced by high K+ + isoproterenol (0.025 microgram/ml) was not affected by ethmozin (1.0 and 5.0 microgram/ml). Ethmozin exaggerated the electrophysiologic effects of hypoxia (95% N2 + 5% CO2; n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMedDate not supplied

Modification of cardiac subcellular remodeling due to pressure overload by captopril and losartan.

In view of the activation of renin-angiotensin system under conditions associated with pressure overload on the heart, we examined the effects of captopril, an angiotensin converting enzyme inhibitor, and losartan, an angiotensin II receptor antagonist, on cardiac function, myofibrillar ATPase and sarcoplasmic reticular (SR) Ca2+-pump (SERCA2) activities, as well as myosin and SERCA2 gene expression in hypertrophied hearts. Cardiac hypertrophy was induced in rats treated with or without captopril or losartan by banding the abdominal aorta for 8 weeks; sham operated animals served as control. Decrease in left ventricular developed pressure, +dP/dt and -dP/dt as well as increase in left ventricular end diastolic pressure and increased muscle mass due to pressure overload were prevented by captopril or losartan. Treatment of animals with captopril or losartan also attenuated the pressure overload-induced depression in myofibrillar Ca2+-stimulated ATPase, myosin ATPase, SR Ca2+-uptake and SR Ca2+-release activities. An increase in beta-myosin heavy chain mRNA and a decrease in alpha-myosin heavy chain mRNA as well as depressed SERCA2 protein and SERCA2 mRNA levels were prevented by captopril or losartan. These results suggest that both captopril and losartan improve myocardial function in cardiac hypertrophy by preventing changes in gene expression and subsequent subcellular remodeling due to pressure overload.

Angiotensin Receptor Antagonists↗

PubMedDate not supplied

Protective effect of pacing on reperfusion-induced ventricular arrhythmias in isolated rat hearts.

OBJECTIVES: To determine whether pacing would have a protective effect similar to preconditioning on reperfusion-induced ventricular arrhythmias and whether this protective effect would be induced by pacing-induced myocardial ischemia. DESIGN: Isolated rat hearts (n = 36) were perfused by the Langendorff technique and the working heart mode. Global ischemia was induced for 10 mins followed by reperfusion for 15 mins. The control group had no pacing, while in the other groups, the hearts were electrically paced three times at 300, 400 and 600 beats/min, respectively, for 5 mins with 1 min intervals between pacings. MAIN RESULTS: The incidence of reperfusion-induced ventricular fibrillation in controls was 100%, whereas that in the 300, 400 and 600 beats/min groups was reduced to 67% (not significant), 50% (P < 0.03) and 30% (P < 0.01), respectively. The mean duration of reperfusion-induced ventricular fibrillation was also significantly reduced in the 300, 400 and 600 beats/min groups compared with the control group. Coronary flow during pacing in the 400 and 600 beats/min groups, but not the 300 beats/min group, was reduced significantly compared with controls. In the 300 beats/min group, oxygen tension of the coronary effluent during pacing was decreased significantly, and proton production and lactate release of coronary effluent during pacing were increased significantly compared with the control group. CONCLUSIONS: Pacing exerted a protective effect similar to preconditioning against reperfusion-induced ventricular arrhythmias. Pacing-induced mild myocardial ischemia, in which coronary flow was maintained, may be involved in the mechanism of this protective effect.

Animals↗