Modified Damus–Kaye–Stansel procedure using aortic flap technique for systemic ventricular outflow tract obstruction in functionally univentricular heart

Damus–Kaye–Stansel procedure is a useful method to relieve the systemic ventricular outflow tract obstruction in functionally univentricular heart. Regurgitation of pulmonary valve and recurrence of systemic ventricular outflow obstruction are the major concerns at the late phase of this procedure. Modification of original Damus–Kaye–Stansel procedure that can prevent the use of prosthetic materials is evaluated. The modified Damus–Kaye–Stansel procedure using aortic flap technique was performed in eight patients with functionally univentricular heart. Patients’ ages ranged from 3 to 28 months (mean 14 months). Follow-up period was 37 months as a mean (9–71 months), and the follow-up was complete. There was no operative mortality and no late death. In addition, there was no recurrence of systemic ventricular outflow tract obstruction throughout the follow-up period. Regurgitation of the pulmonary valve estimated by echocardiography at the latest follow-up was none to trivial in seven patients and mild in one. The modified Damus–Kaye–Stansel procedure using aortic flap technique is a safe, useful and reproducible technique to solve systemic ventricular outflow tract obstruction in functionally univentricular heart, and it can be an alternative for original technique or the so-called double-barrel modification.     

Urinary dysfunction and autonomic control in amyloid neuropathy

Abstract Uro-neurological assessment was performed in four patients with small-fiber neuropathy due to amyloidosis (2 transthyretin-type/2 immunoglobulin light-chain-type). Voiding difficulties were due to detrusor weakness and impaired bladder sensation. In two patients cholinesterase inhibition treatment caused urge incontinence, indicating detrusor denervation supersensitivity. The underlying mechanisms of urinary dysfunction seem to involve postganglionic cholinergic and afferent somatic nerves.     

Deconjugating activity for sulfoconjugated dopamine in homogenates of organs from dogs.

To clarify the possibility that sulfoconjugated dopamine (DA) may play a physiological role by being converted to active free DA, we examined the deconjugating activity in homogenates of organs from dogs. Each tissue homogenate was incubated with sulfoconjugated DA, and the deconjugating activity of the organs was compared. The kidney and liver exhibited the highest deconjugating activities. In contrast, the intestine and heart showed lower arylsulfatase activities, and almost no activity was found in the brain or skeletal muscle. Moreover, in the heart, the deconjugating activity for sulfoconjugated DA was higher in the atrium than the ventricle. These results indicate that sulfoconjugated DA is converted to active free DA in homogenates of organs from dogs and that the deconjugating activity varies between different parts of an organ. Sulfoconjugated DA must be looked upon as a possible precursor or reservoir for the production of active free DA.     

Behavioural and ECoG spectrum changes induced by intracerebral infusion of interferons and interleukin 2 in rats are antagonized by naloxone.

Rat interferon, alpha-interferon, interleukin 2 and recombinant interleukin-2 injected into the third cerebral ventricle produced typical behavioural sedation and/or sleep and ECoG synchronization in rats while beta-interferon produced no behavioural sleep or ECoG synchronization. A slight sedation was observed after the largest dose of beta-interferon only. During sleep induced by lymphokines, a dose-dependent increase in total voltage power as well as in the 0.5-3, 4-7 and 12-16 Hz frequent bands was observed. Much smaller doses were required to produce similar behavioural and ECoG spectrum effects after infusion of interferons and interleukin-2 into the locus coeruleus. No significant behavioural and ECoG changes were obtained after infusion of the same doses of interferons and interleukin-2 into other areas of the brain (caudate nucleus, dorsal hippocampus, substantia nigra pars compacta, ventromedial hypothalamus). The behavioural and ECoG effects of alpha-interferon, rat interferon and interleukin-2 were blocked in animals pretreated with naloxone. These results are consistent with the hypothesis that the behavioural and ECoG effects of these lymphokines are mediated at locus coeruleus level by stimulation of opiate receptors.     

‘Ischemic tolerance’ phenomenon detected in various brain regions

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the ‘ischemic tolerance’ phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of ‘ischemic tolerance’.     

Successful mitral valve repair for active infective endocarditis accompanied by anorexia nervosa

Infective endocarditis of the mitral area accompanied by anorexia nervosa is extremely rare. A 34-year-old Japanese woman presented with high fever and a heart murmur that had developed over the previous 2-month period. Echocardiography revealed mitral regurgitation and vegetation attached to the anterior mitral leaflet, which had markedly prolapsed to the left atrium. We removed the vegetation with a small part of the anterior mitral leaflet and successfully repaired the mitral valve. The patient showed good recovery, and the mitral regurgitation and left ventricular chamber size had satisfactorily decreased at 2 months after the operation.     

Two cases of thyroid metastases from renal cell carcinoma]

The identification and diagnosis of thyroid metastases from renal cell carcinoma are rare in living patients in spite of more frequent incidence during autopsy. We reported two cases of thyroid metastases from renal cell carcinoma. In both cases, histological examination revealed metastasis from renal cell carcinoma and negative immunohistological stain for thyroglobulin ruled out primary thyroid carcinoma.     

Effect of verapamil on ventilatory and circulatory responses to hypoxia and hypercapnia in normal subjects.

Recent investigations have shown that the calcium channel blocker verapamil attenuated the hypoxic ventilatory chemosensitivity of carotid body in animals. To determine whether this is also the case in humans, transient physiological chemodenervation by O2 breaths (withdrawal test) during sustained hypoxia (N = 7), and ventilatory and circulatory responses to progressive hypoxia and hypercapnia (N = 8) were examined after oral administration of verapamil. During sustained hypoxia after verpamil, there was a significant reduction of withdrawal response from 5th to 25th min value (p < 0.01), but not after placebo. On the other hand, no significant difference in ventilatory responses to progressive hypoxia and hypercapnia was observed after verapamil. Verapamil run reveals similar features with placebo run in circulatory parameters except blood pressure response, which tended to be suppressed by verapamil. We conclude that verapamil attenuates peripheral chemoreceptor activity with time during sustained mild hypoxia in normal adult humans and this may be explained by delayed depletion in intracellular Ca2+ for chemotransduction of the peripheral chemoreceptors.