Search PubMed⌕ Search

Biomedical subjects

H Mukai

Publications and source records attributed to H Mukai.

At least 217 records · Page 12Linked to original sources
PubMed1988

Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia.

Fifty patients with supraventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies and cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR-CBT) in nine patients, AV reentrant tachycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra-atrial reentrant tachycardia (SNRT or IART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in five patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVR-CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%), 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR-CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.

Adult↗
PubMed1988

Effects of neuromedin B, gastrin-releasing peptide-10 and their fragment peptides on secretion of gastrointestinal and pancreatic hormones in dogs.

The effects of neuromedin B (NMB), gastrin-releasing peptide (GRP)-10 and their C-terminal fragment peptides on the pancreatic and gastrointestinal hormone release were studied in dogs. Intravenous bolus injections of NMB and GRP-10 (4.5 nmol/kg) into conscious dogs elicited a sharp and statistically significant rise in plasma gastrin and insulin levels, but only GRP-10 brought on a significant rise in the plasma glucagon and enteroglucagon levels. The degree of stimulation of gastrin and insulin secretion by NMB and GRP-10 was dose-dependent. With a dose of 4.5 nmol/kg, the minimum size of C-terminal fragment peptides of NMB and GRP-10 to stimulate gastrin secretion was NMB and GRP-10, respectively. Both NMB and GRP-10 (0.1-100 nmol/l) stimulated insulin release from the isolated canine pancreas. The glucagon release was stimulated by 10 and 100 nmol/l GRP-10 and was not stimulated by the same doses of NMB. The somatostatin release was not influenced by either peptide. It is concluded that 1) NMB and GRP-10 can stimulate gastrin and pancreatic hormone secretion, and the latter effect may be mainly due to a direct action on the islet cells; 2) the stimulatory effect of GRP-10 is stronger than that of NMB. The difference in the minimal active fragment between NMB and GRP-10 suggests that the amino acid of position 3 - NMB (Leu) and GRP-10 (His) - may play an important role in their biological activity.

Amino Acid Sequence↗
PubMed1987

Stimulation of dog gastropancreatic hormone release by neuromedin B and its analogues.

The effects on gastrin, insulin, and glucagon release of neuromedin B (NMB), the C-fragment decapeptide of gastrin-releasing peptide-10 (GRP-10), seven analogues replacing amino acid positions 3, 6, and 9, and two C-terminal desamide analogues were examined in conscious dogs using intravenous bolus injection of these peptides study the structure-activity relationship of two bombesin-related peptides identified in mammals. The replacement from valine of position 6 of GRP-10 to threonine effectively reduced the stimulatory potency of these hormone secretions. Removal of the C-terminal amide of NMB and GRP-10 resulted in an almost complete loss of their stimulatory effect on gastrin secretion. [Leu3]GRP-10 elicited the most potent stimulatory activity on three hormone secretions among the analogues including NMB and GRP-10. These results indicate that valine in position 6 of GRP-10 and C-terminal amide of two peptides play an important role in the bioactivities of bombesin family peptides.

Amino Acid Sequence↗
PubMed1986

Receptor-mediated model relating anticonvulsant effect to brain levels of camazepam in the presence of its active metabolites.

In a displacement test using 3H-diazepam as a radioligand, the in vitro affinities of metabolites of camazepam (CZ) for the benzodiazepine receptors were 1-50 times more potent than that of CZ. In contrast, only three metabolites (temazepam, oxazepam, and hydroxy CZ), as well as CZ itself, exhibited an in vivo affinity parallel to their ability to protect against pentylenetetrazole--induced clonic convulsion in rats. In addition, CZ and these active metabolites displaced the radioligand from their receptor sites in a concentration-dependent saturable manner, indicating the competitive bimolecular interaction of these molecules with their receptors. The percent anticonvulsant effect was a nonlinear, single-valued function of the in vivo percent displacement of specific 3H-diazepam binding, independent of these displacers after i.v. dosing; this relationship could be approximated by the Hill equation. On the basis of these findings, a receptor-mediated model, including the Langmuir equation to describe the receptor binding-brain concentration relationship and the Hill equation to accommodate the anticonvulsant effect-receptor binding relationship, was constructed. This model was found to adequately relate the time course values of anticonvulsant effect and of brain levels of CZ and its active metabolites after oral administration. These results demonstrate that CZ and its active metabolites exert anticonvulsant effect by competitive binding to the benzodiazepine receptors.

Animals↗
PubMed1986

Sequential changes of extracellular matrix and proliferation of Ito cells with enhanced expression of desmin and actin in focal hepatic injury.

Immunohistochemical investigations were carried out on the properties of the cells and extracellular matrix (ECM) in focal hepatic injuries. A liquid nitrogen-cooled syringe needle was thrust into the rat liver. Necrotic areas became permeated with plasma within 24-hour period. Areas became strongly positive for fibronectin and were infiltrated with inflammatory cells positive for lysozyme. By the third day, Ito cells were proliferated in the peripheral portions of the damaged areas. These Ito cells showed enhanced immunostaining for desmin and actin but were negative for lysozyme. Interstitial fibers which were immunochemically positive for Types I and IV collagens, laminin, and fibronectin, began to increase from Day 3. They appeared on the rim of the hepatocytes adjacent to the damaged areas and extended into the injured regions with the Ito cells. An increase in basal laminas associated with capillaries and bile ducts also increased with a 1-day delay. The damaged areas were replaced by granulation tissue by Day 5. A rapid diminution then occurred in the granulation tissue, and normal hepatic tissue was restored in 7-10 days. These observations demonstrate that ECM changed in a sequential manner and then finally disappeared from the damaged site within 10 days. Although various cells, including parenchymal cells, macrophages, endothelial cells, and cholangiolar cells contributed to the healing of the damaged area, Ito cells, which exhibit unique phenotypic changes, presumably had a major role in the process.

Actins↗