Mitral complex lesions following vagal stimulation in rabbits: relationship between the direction of mitral regurgitation jet and the site of mitral complex lesions.

BACKGROUND AND AIM OF THE STUDY: Cervical vagal stimulation in rabbits frequently causes bigeminy due to premature ventricular contractions, which is followed by systolic murmur and mitral regurgitation (MR). Peculiar lesions of the mitral valves, mitral annulus and papillary muscles frequently develop within a week. The study aim was to identify the relationship between the direction of MR jet and the site of mitral complex lesions in this experimental model of MR. METHODS: Color Doppler echocardiography was performed on anesthetized rabbits to examine MR, with simultaneous electrocardiographic monitoring. The animals in which the MR jet following cervical vagal stimulation streamed forward or backward alone in the left atrium were dissected on the day of vagal stimulation (n = 11) or one week later (n = 14), and their mitral complex lesions examined. RESULTS: Among 11 animals dissected on the day of vagal stimulation, six of seven in which the MR jet streamed backward in the left atrium showed marked bleeding only in the anterior mitral leaflet, and three of four in which the MR jet streamed forward showed marked bleeding only in the posterior mitral leaflet. Among 14 animals dissected one week later, eight of 10 in which the MR jet streamed backward showed marked lesions only in the anterior mitral leaflet or anterior papillary muscle, and three of four in which the MR jet streamed forward, showed marked lesions only in the posterior leaflet or posterior papillary muscle. CONCLUSION: A close relationship was detected between the direction of MR jet and the site of mitral complex lesion, suggesting that mitral valve prolapse might be, at least in part, the cause of MR.

Construction of molecular wires based on a gold(I) bis-sigma-acetylide building block incorporated into ruthenium(II) polypyridyl complexes.

An Ru(II)-Au(I)-Ru(II) triad has been synthesized from [Ru(bpy)2(3-ethynylphenanthroline)]2+ with Au(tht)Cl and characterized by spectroscopic means such as NMR and ESI-MS; the Ru(II)-Au(I)-Ru(II) triad shows an intense emission at 620 nm upon excitation at 360 nm, which suggests an efficient energy transfer from the Au site to Ru sites via extended pi-conjugation through the ethynyl units.

[An elderly hypertensive patient with ocular bruits and angiographically confirmed stenosis of intracranical internal carotid arteries].

The patient was 47 years old on his first visit in 1969 and has been treated at our outpatient clinic until now, at the age of 79. The initial blood pressure was 164/98 mmHg without abnormalities on electrocardiogram or urinalysis. He was followed-up for 8 years with non-pharmacologic treatment, which was eventually changed to antihypertensive drug treatment. At the age of 71 he was admitted because blood pressure increased to 210/110 mmHg, with marked fluctuation. At admission bilateral ocular (right < left) and carotid bruits (right < left) were detected. At the age of 75 he had cerebellar infarction with reversible neuro-logic deficits. At the age of 76 he was again addmitted because the labile hypertension was difficult to control. Cerebral angiography which was performed to clarify the relationship between labile hypertension and cerebral ischemia revealed significant bilateral stenosis at the portion of the cavernous sinus in the internal carotid arteries. The stenosis was more remarkable on the left side than the right side. Based on the angiographic findings we considered the ocular bruits to be not a murmur of augmentation flow but a stenotic murmur.