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Biomedical subjects

J Ikeda

Publications and source records attributed to J Ikeda.

At least 145 records · Page 8Linked to original sources
PubMed1987

The degree of increment in plasma catecholamines in patients with mitral stenosis by mild exercise.

Although sympathetic excitation during mild exercise may readily occur in patients with mitral stenosis (MS), the degree of increment in plasma catecholamines has not been fully investigated. We imposed mild ergometric exercise (50 watts, 300 kg/min for 5 minutes) on five patients with mild MS (mitral valve area greater than or equal to 1.0 cm2) and eight with severe MS (mitral valve area less than 1.0 cm2) while they were undergoing cardiac catheterization. In patients with severe MS, total plasma catecholamine levels during exercise were remarkably higher (2821 +/- 783 [SEM] pg/ml) than in those with mild MS (957 +/- 113 pg/ml, p less than 0.05) and in seven control subjects (612 +/- 75 pg/ml, p less than 0.05). This marked increment could not be predicted by heart rate response, which did not differ between severe and mild MS (166 +/- 5 vs 153 +/- 10 bpm). In contrast with catecholamine change, the cardiac index in severe MS showed a very small increment. Results suggest that mild daily exercise can remarkably increase plasma catecholamine levels in severe MS, and this may accelerate various complications of this disorder.

Adult↗
PubMed1986

Regulation of sperm flagellar movement by protein phosphorylation and dephosphorylation.

Flagellar motility of Triton models of sea urchin spermatozoa was reactivated by cyclic AMP-dependent protein kinase and a protein factor, termed motility activator, both of which were prepared from the detergent-extract of sea urchin spermatozoa. It was shown that phosphorylation of the motility activator by the protein kinase is necessary for the reactivation of flagellar motility [Ishiguro et al, J. Cell Biol. 92:777-782, 1982; Murofushi et al, in "Biological Functions of Microtubules and Related Structures," Academic Press, 1982]. Reactivating factor was also detected in a KCl-extract of the axoneme fraction devoid of the detergent-extractable materials. The activity of this factor was also cyclic AMP- and protein kinase-dependent. Furthermore, when freshly prepared Triton models were treated with phosphoprotein phosphatase prepared from bovine cardiac muscle, the flagellar motility was drastically suppressed. This inhibition of the motility was partially recovered by the addition of cyclic AMP and protein kinase to the phosphatase-treated models.

Adenosine Triphosphatases↗
PubMed1986

[Hydrocephalus in Paget's disease--a case report].

A case of Paget's disease in an elderly female who had a favourable evolution following ventriculoperitoneal (V-P) shunt is reported. On May 28, 1983, a 52-year-old female was transferred and admitted to us from the Dept. of Neurology because of headache in the occipital region and ataxic gait. On admission, neurological examinations revealed remarkably increased tendon reflexes, ataxic gait, and mild dementia. Headache was also observed, but urinary incontinence was not present. Skull X-ray showed "cotton wool appearance", which was characteristic of Paget's disease. On chemical analysis of blood and urine, serum Al-P and urinary OH-proline level were elevated, which established a diagnosis of Paget's disease. Triventricular dilatation was found on CT scan, and neck tomography showed basilar impression. After admission, the patient was treated with calcitonin, but it was interrupted because of side effects such as nausea and vomiting. Then she gradually took a turn for the worse, particularly dementia became severer. On July 25, 1983, V-P shunt was performed. After operation, "soft landing maneuver" was employed, namely the intraventricular pressure was checked and was gradually lowered with external CSF drainage system for 7 days. Thereafter the patient's head was elevated gradually from supine to sitting position through 7 days. Her hospital course after operation was that of gradual improvement. The purpose of this maneuver was to prevent sudden change of intraventricular pressure that causes aggravation of basilar impression and sudden respiratory arrest.

Cerebrospinal Fluid Shunts↗
PubMed1985

Reduction of plasma norepinephrine levels in response to brief coronary occlusion in experimental dogs.

Although an increased plasma norepinephrine (NE) level is sometimes observed during angina pectoris, it is difficult to say whether sympathetic overflow is its cause. The left anterior descending coronary artery was occluded by intracoronary balloon for 3 minutes in 12 closed-chest anesthetized dogs. During occlusion, heart rate did not change but aortic pressure slightly decreased. Occlusion caused a significant reduction in both NE levels in the aorta (177 +/- 17 to 134 +/- 16 pg/ml, p less than 0.01) and in the great cardiac vein (GCV) 296 +/- 44 to 249 +/- 44 pg/ml, p less than 0.01). After surgical vagotomy, the occlusion increased NE levels in the aorta (227 +/- 44 to 278 +/- 43 pg/ml, p less than 0.01) and in GCV (384 +/- 76 to 444 +/- 81 pg/ml, p less than 0.01), showing the release of vagal inhibition. These results may be applicable to patients with transient anterior myocardial ischemia; if plasma NE increases without marked hemodynamic changes, it is suggested that the sympathetic overflow is not a result but a possible cause of the ischemia.

Angina Pectoris↗
PubMed1985

Phosphoprotein phosphatase inhibits flagellar movement of Triton models of sea urchin spermatozoa.

Phosphoprotein phosphatase prepared from bovine cardiac muscle was used to study the roles of axonemal phosphoproteins in the flagellar motility of sea urchin spermatozoa. When isolated axonemes were incubated with cyclic AMP-dependent protein kinase, gamma-[32P]ATP and cyclic AMP, more than 15 polypeptides were phosphorylated. Most were dephosphorylated by treatment with phosphoprotein phosphatase. When Triton models of sea urchin spermatozoa were treated with phosphoprotein phosphatase followed by an addition of ATP, the flagellar motility of the models was drastically reduced in comparison with that of the untreated models. The motility of the phosphatase-treated Triton models was partially restored by an addition of cyclic AMP and cyclic AMP-dependent protein kinase. These data give strong support to the idea that the motility of eukaryotic flagella is controlled by a protein phosphorylation-dephosphorylation system.

Adenosine Triphosphatases↗
PubMed1985

Extremely long-acting antihypertensive effects of KF-4317, a alpha- and beta 1-adrenoceptor blocker.

The hypotensive effects of 4-(2-hydroxy-3-[(1-methyl-3-phenylpropyl)amino]propoxy)benzeneacetamide hydrochloride (KF-4317, a novel alpha- and beta 1-adrenoceptor blocker) were evaluated in spontaneously hypertensive rats and renal hypertensive dogs as well as in normotensive dogs, cats and rabbits, using various routes of administration. Single oral, intraduodenal and intravenous administrations of KF-4317 induced definite hypotensive effects. When intraduodenally given to anesthetized rabbits, KF-4317 elicited a much more prolonged effect on the blood pressure than labetalol, while neither atenolol nor propranolol showed hypotensive effects. Pretreatment with phentolamine abolished its depressor effect, but not its bradycardic effect, indicating that the former effect is mediated by alpha-blockade. When orally given to the conscious hypertensive rats and dogs, it exerted an extremely long-acting effect with a property of very gradual onset of action. Furthermore, KF-4317 neither showed any sign indicative of orthostatic hypotension in an experimental model nor exhibited any intrinsic sympathomimetic activity, though a very weak local anesthetic effect was observed. From these results, it could be concluded that KF-4317 possesses some pharmacological properties similar to labetalol, but in contrast to labetalol it is beta 1-selective, and it may be useful in the treatment of patients with hypertension.

Adrenergic alpha-Antagonists↗
PubMed1985

[Internal carotid aneurysmal formation following spontaneous regression of the dural arteriovenous malformation in the posterior fossa--a case report].

The patient was first admitted on August 19, 1975 with 5 years' headache and tinnitus. Physical examination revealed bruit over the left mastoid area. Left angiography, performed in August, 1975, revealed a dural arteriovenous malformation, which was supplied by enlarged left middle meningeal artery, occipital artery, meningohypophyseal artery and superior cerebellar artery and was draining into the left sigmoid sinus. At the first operation, the left external carotid artery was ligated at the neck, and then coagulation of dural vessels was performed through left temporo-occipital craniotomy. Tinnitus and bruit were disappeared after operation. Postoperative right angiogram showed no residual dural AVM, however, ligation of the right external carotid artery was required to reduce symptomes. In June, 1979 the left brachial arteriography was performed, and revealed a dural AVM around the left sigmoid sinus supplied by anastomotic vessels between external carotid artery and cervical artery arising from the vertebral artery. Because of subarachnoid hemorrhage, repeated angiography in April, 1982, revealed progressively enlarging dural AVM, although no aneurysm was seen in the left internal carotid arterial system. The patient readmitted on October, 28, 1983 with severe headache and confusion. CT scan showed slightly high density in the left basal cistern. Angiogram showed no dural AVM and a saccular aneurysm arising from the left internal carotid artery at C2 portion, which was successfully clipped by surgery. Only two cases of spontaneous regression of dural AVM in the posterior fossa were reported previously, and the authors added a case, which showed a newly developed aneurysm after spontaneous regression of the posterior fossa dural AVM.

Carotid Artery Diseases↗