[Evaluation of preoperative cardiac function for orthopedic surgery by chest CT and coronary arteriogram].

BACKGROUND: In patients with spinal cord diseases, it is difficult to obtain stress electrocardiogram and to evaluate preoperative cardiac risk. We evaluate these patients by chest CT and if the patients have calcified coronary artery, we recommend further testing by coronary arteriogram. METHODS: We evaluated the patients who had undergone coronary arteriogram from January 2008 through December 2009. RESULTS: In 27 out of 158 cases (17.1%) operations were postponed or cancelled. In 12 out of 112 patients with no subjective symptom but with coronary calcification operations were also postponed or cancelled. CONCLUSIONS: Preoperative chest CT and coronary arteriogram are useful for evaluation of preoperative cardiac function.

The Na+-Ca2+ exchanger contributes to beta-adrenoceptor mediated positive inotropy in mouse heart.

The L-type Ca2+ current (I(Ca,L)) plays an important role in the regulation of cardiac contractility. However, there is little data with regard to the significance of the I(Ca,L)-independent mechanism of beta-adrenoceptor mediated positive inotropy. The effects of isoproterenol (ISO) on I(Ca,L) and contractility in the presence of Ca2+ channel blockers (nifedipine, verapamil) were examined in adult mouse ventricular myocytes. ISO increased contractility over the level before the administration of Ca2+ channel blocker, although it had a very limited effect on I(Ca,L). The positive inotropy of ISO disappeared after administration of Ni2+, an inhibitor of the Na+-Ca2+ exchanger. The addition of ISO after nifedipine pretreatment also increased the [Ca2+]i transient over the control level and the application of Ni2+ or KB-R7943, a selective Na+-Ca2+ exchange inhibitor (reverse mode), abolished the increase in [Ca2+]i transient. Therefore, an I(Ca,L)-independent mechanism plays a significant role in beta-adrenoceptor mediated positive inotropy. The Na+-Ca2+ exchanger is necessary for the development of this action.

Negative inotropic effects of angiotensin II, endothelin-1 and phenylephrine in indo-1 loaded adult mouse ventricular myocytes.

Angiotensin II (Ang II). endothelin-1 (ET-1) and phenylephrine are receptor agonists that share the signal transduction acting through acceleration of phosphoinositide hydrolysis in the heart. Because the regulation of myocardial contractility induced by these receptor agonists shows a wide range of species-dependent variation among experimental animals, we carried out experiments to elucidate the mechanism of contractile regulation induced by these agents in mice which are employed currently more as transgenic models. Effects of Ang II, ET-1 and phenylephrine on cell shortening and Ca2+ transients were investigated in single ventricular myocytes loaded with indo-1/AM. Ang II (10(-8), 10(-7) M), ET-1 (10(-10), 10(-9) M) and phenylephrine (10(-6), 10(-5) M in the presence of the beta-adrenoceptor antagonist timolol) decreased the cell shortening [Ang II: 58.4+/-9.03 (n = 8), 50.3+/-11.90% (n = 6); ET-1: 48.4+/-8.27, 31.2+/-6.45% (n = 5); phenylephrine: 45.7+/-11.60, 28.7+/-5.89% (n = 5)]. By contrast, the amplitude of Ca2+ transients was not significantly influenced by these agonists. The selective protein kinase C inhibitor chelerythrine at 10(-6) M significantly inhibited the decrease in cell shortening induced by these receptor agonists. These results indicate that Ang II, ET-1 and phenylephrine elicit a negative inotropic effect with insignificant alteration of Ca2+ transients, which may be mainly mediated by activation of protein kinase C in mouse ventricular cardiomyocytes.