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Biomedical subjects

K Minami

Publications and source records attributed to K Minami.

At least 127 records · Page 7Linked to original sources
PubMed1998

Novel 31-amino-acid-length endothelins cause constriction of vascular smooth muscle.

We have reported that human chymase specifically cleaves big endothelins (ETs) at the Try31-Gly32 bond, and produces novel trachea-constricting 31-amino-acid-length ETs, ETs(1-31). In this study, we investigated the effect of synthetic ETs(1-31) on the contractile activity toward porcine coronary arteries and rat aortae. Although ETs(1-31) exhibited less potent vasoconstrictile activity in these tissues than 21-amino-acid-length ETs(1-21), or a similar extent, ET-1(1-31) caused significantly slower-developing and longer-lasting contraction than ETs(1-21). The ETA receptor antagonist, BQ485, completely inhibited the activity of ET-1(1-31). The ETB receptor antagonist, BQ788, also inhibited the activity of ET-1(1-31) toward rat aortae more efficiently than that ET-1(1-21). Therefore, trachea-constricting peptides ETs(1-31) play roles as vasoconstrictors in a different manner from ETs(1-21).

Animals↗
PubMed1998

Sites of volatile anesthetic action on kainate (Glutamate receptor 6) receptors.

Molecular mechanisms of anesthetic action on neurotransmitter receptors are poorly understood. The major excitatory neurotransmitter in the central nervous system is glutamate, and recent studies found that volatile anesthetics inhibit the function of the alpha-amino-3-hydroxyisoxazolepropionic acid subtype of glutamate receptors (e.g. glutamate receptor 3 (GluR3)), but enhance kainate (GluR6) receptor function. We used this dissimilar pharmacology to identify sites of anesthetic action on the kainate GluR6 receptor by constructing chimeric GluR3/GluR6 receptors. Results with chimeric receptors implicated a transmembrane region (TM4) of GluR6 in the action of halothane. Site-directed mutagenesis subsequently showed that a specific amino acid, glycine 819 in TM4, is important for enhancement of receptor function by halothane (0. 2-2 mM). Mutations of Gly-819 also markedly decreased the response to isoflurane (0.2-2 mM), enflurane (0.2-2 mM), and 1-chloro-1,2, 2-trifluorocyclobutane (0.2-2 mM). The nonanesthetics 1, 2-dichlorohexafluorocyclobutane and 2,3-dichlorooctafluorobutane had no effect on the functions of either wild-type GluR6 or receptors mutated at Gly-819. Ethanol and pentobarbital inhibited the function of both wild-type and mutant receptors. These results suggest that a specific amino acid, Gly-819, is critical for the action of volatile anesthetics, but not of ethanol or pentobarbital, on the GluR6 receptor.

Amino Acid Sequence↗
PubMed1998

Aortic valve surgery following previous coronary artery bypass grafting. Impact of calcification and leaflet movement.

We reviewed the reports of 27 patients who had an aortic valve replacement after previous coronary artery bypass grafting. The aortic valve disease -- mainly aortic stenosis -- showed a rapid rate of progression. In the time interval between coronary artery bypass grafting and aortic valve replacement of 4.6+/-2.2 years the peak-to-peak pressure gradient of the aortic valve rose from 20.2+/-14.3 to 63.0+/-22.7 mmHg. As there is a great interest to identify the patients with a high risk of a rapid progression because of a high mortality of an aortic valve replacement as the second cardiac operation following a coronary artery bypass grafting we also reviewed the cardiac catheterisation films and found a high incidence of calcification and impaired aortic valve motion (81.5% of the patients had already calcified aortic valves and 81.5% had a impaired valve motion) at the time of coronary artery bypass grafting. We concluded that if a patient has to be operated for coronary artery disease an aortic valve replacement should be considered not only according to hemodynamic criteria but also when the aortic valve is calcified or its leaflets' motion is impaired.

Aged↗
PubMed1998

Stimulatory effect of lymphocyte-derived factor on catecholamine efflux from cultured bovine adrenal medullary cells.

The effects of lymphocytes and their conditioned medium on catecholamine efflux and uptake were examined in cultured bovine adrenal medullary cells. Co-culture of adrenal medullary cells with lymphocytes for 3 days caused an increase in appearance of catecholamines in the culture medium. Treatment of adrenal medullary cells with a conditioned medium prepared from lymphocytes also enhanced the appearance of catecholamines in culture medium in time- (8-48 h) and concentration-dependent manners. Heat treatment of the conditioned medium at 60 and 100 degrees C for 10 min reduced its stimulatory effect to 59 and 20% of control, respectively. After gel filtration on a Sephadex G-25 column or dialysis (<8 kDa molecular mass cutoff), the stimulatory activity of the conditioned medium was found in a high molecular fraction. The conditioned medium had little effect on the activity of lactate dehydrogenase in the medium of cultured adrenal medullary cells and on desipramine-sensitive [3H]norepinephrine uptake by the cells. These findings suggest that lymphocytes release a heat-sensitive factor(s) (molecular mass of more than 8 kDa) which increases efflux of catecholamines from cultured adrenal medullary cells.

Adrenal Medulla↗
PubMed1998

Frequency-dependent changes in contribution of SR Ca2+ to Ca2+ transients in failing human myocardium assessed with ryanodine.

We tested the influence of blocking sarcoplasmic reticulum (SR) function with ryanodine (1 microM) on stimulation rate-dependent changes of intracellular Ca2+ transients and twitch force in failing human myocardium. Isometrically contracting, electrically stimulated muscle strips from ventricles of 10 end-stage failing human hearts were used. Muscles were loaded with the intracellular Ca2+ indicator aequorin. At stimulation rates from 0.5-3 Hz, intracellular Ca2+ transients and twitch force were simultaneously recorded before and after ryanodine exposure (37 degrees C). Ryanodine significantly reduced twitch force at 1 Hz by 46 +/- 9% and aequorin light by 57 +/- 10% in failing human myocardium (P < 0.05). The blunted or inverse aequorin light- and force-frequency relation became positive after ryanodine: in failing human myocardium, twitch force and aequorin light before ryanodine did not increase with increasing frequency and force decreased significantly at 3 Hz (P < 0.05). After ryanodine, twitch force (P < 0.05) and aequorin light increased with increasing stimulation frequency and were maximum at 2 Hz. The data indicate that inhibition of SR function significantly reduces twitch force and Ca2+ transients in failing human myocardium, but converts the blunted or inverse Ca(2+)- and force-frequency relation into a positive one. We infer that Ca2+ responsible for approximately 50% of twitch force is derived from the SR and approximately 50% from sarcolemmal Ca2+ influx in failing human myocardium. This sarcolemmal component increases at higher stimulation frequencies.

Calcium↗
PubMed1998

[A case report of aortoesophageal fistula due to thoracoabdominal aortic aneurysm].

Aortoesophageal fistulas due to thoracic aneurysms are usually fatal, with few reported survivors. A 57-year-old man with aortoesophageal fistula due to thoracoabdominal aortic aneurysm underwent the graft replacement of thoracoabdominal aorta. In the postoperative course, prosthetic graft infection had occurred in the result of residual esophageal fistula. On the 32nd postoperative day (POD), a subtotal esophagectomy was performed and the esophagus was reconstructed by gastrointestinal interposition technique via a retrosternal route. Following the second operative procedure, inflammatory reactions had been improved with systemic administration of antibiotics and continuous irrigation of the infected cavity. On 77th POD, he was discharged.

Aortic Aneurysm, Abdominal↗
PubMed1998

Aortic valve replacement after previous coronary artery bypass grafting in a patient with antiphospholipid syndrome.

We report a 55-year-old female patient with antiphospholipid syndrome secondary to systemic lupus erythematosus. The patient had undergone coronary artery bypass grafting for myocardial infarction due to left main trunk stenosis at the age of 52. Subsequently, she developed aortic insufficiency and underwent aortic valve replacement without any hemodynamic or hemostatic problems. Both coronary and valve disease should be considered in patients with antiphospholipid syndrome secondary to systemic lupus erythematosus.

Antiphospholipid Syndrome↗
PubMed1998

[A case report of gastric perforation after coronary artery bypass grafting with right gastroepiploic artery].

A 71-year-old man, who had received coronary angioplasty to right coronary artery 1 year before, was admitted because of unstable angina. An urgent CABG was performed using the left internal thoracic artery and the right gastroepiploic artery. Coronary anastomosis was performed under ventricular fibrillation due to porcelain aorta. Seven days after surgery, abdominal pain was suddenly experienced. A chest X-P showed subphrenic free air. So an emergent laparotomy was performed, and a 2 x 2 cm gastric perforation was found on the anterior wall of the greater gastric curvature. Partial gastrectomy was performed. However, he unfortunately died on the 58th postoperative day for multiple organ failure. Pathological examination of the excised gastric wall revealed ischemic change, not ulcer. This gastric perforation was possibly caused by ischemia after harvesting the right gastroepiploic artery.

Aged↗
PubMed1998

[Repair of complete atrioventricular septal defect with severe pulmonary hypertension--effect of re-pulmonary artery banding and analysis of lung biopsy: a case report].

We report a case complete atrioventricular defect with severe pulmonary hypertension. The patient was a girl aged 2 years and 6 months with Down's syndrome who had undergone pulmonary artery banding (PAB) 2 years previously. Postoperative catheterization after PAB showed severe pulmonary hypertension. Pulmonary resistance values were 9.3 and 7.3 units at 1 year and 5 months and 1 year and 9 months respectively. We performed re-PAB and lung biopsy when the patient was 2 years and 6 months old. The biopsy specimen at re-PAB classified as Heath-Edwards grade 3 and had an IPVD score of 1.7, indicating tolerance to radical operation. Six months after re-PAB, pulmonary vascular resistance decreased a level at which radical operation could be performed safely. Radical operation was performed 1 year and 4 months after re-PAB. The post operative course was uneventful, and pulmonary hypertensive crisis did not occur. The lung biopsy at the final operation was classified as Heath-Edwards grade 3, had an IPVD score of 1.1, and showed improvement when compared with the pathological findings at re-PAB.

Biopsy↗
PubMed1998

C-type natriuretic peptide inhibits rat mesangial cell proliferation by a phosphorylation-dependent mechanism.

We studied the effects of C-type natriuretic peptide (CNP) on rat cultured mesangial cell proliferation. (1) Exposure to CNP (10 nM-1 microM for 72 h) inhibited [3H]thymidine incorporation into mesangial cells in a concentration-dependent manner. Atrial natriuretic peptide (1 nM-1 microM), a peptide related to CNP, also decreased [3H]thymidine incorporation into these cells in a concentration-dependent manner. (2) Both CNP (10 nM- microM) and atrial natriuretic peptide (10 nM-1 microM) also decreased mesangial cell number. (3) The cyclic GMP analog, 8-bromo-cyclic GMP (100 microM and 1 microM), mimicked the inhibitory effects of CNP and atrial natriuretic peptide on [3H]thymidine incorporation into mesangial cells, whereas inhibitors of protein kinase C, protein kinase A, and protein kinase G reduced the effect of both natriuretic peptides. Moreover, the phosphatase inhibitor, calyculin A, increased [3H]thymidine incorporation into mesangial cells. (4) CNP and atrial natriuretic peptide decreased interleukin-1-, interleukin-6-, platelet derived growth factor-, angiotensin II-induced [3H]thymidine incorporation into mesangial cells. These results suggest that CNP exerts inhibitory effects on mesangial cell proliferation and that this effects depend on protein phosphorylation pathways.

Angiotensin II↗
PubMed1998

Ketamine interacts with the noradrenaline transporter at a site partly overlapping the desipramine binding site.

Effects of the intravenous anaesthetic ketamine on the desipramine-sensitive noradrenaline transporter (NAT) were examined in cultured bovine adrenal medullary cells and in transfected Xenopus laevis oocytes expressing the bovine NAT (bNAT). Incubation (1-3 h) of adrenal medullary cells with ketamine (10-300 microM) caused an increase in appearance of catecholamines in culture medium. Ketamine (10-1000 microM) inhibited desipramine-sensitive uptake of [3H]noradrenaline (NA) (IC50=97 microM). Saturation analysis showed that ketamine reduced Vmax of [3H]NA uptake without changing Km, indicating a non-competitive inhibition. Other inhibitors of NAT, namely cocaine and desipramine, showed a competitive inhibition of [3H]NA uptake while a derivative of ketamine, phencyclidine, showed a mixed type of inhibition. Ketamine (10-1000 microM) also inhibited the specific binding of [3H]desipramine to plasma membranes isolated from bovine adrenal medulla. Scatchard analysis of [3H]desipramine binding revealed that ketamine increased Kd without altering Bmax, indicating a competitive inhibition. In transfected Xenopus oocytes expressing the bNAT, ketamine attenuated [3H]NA uptake with a kinetic characteristic similar to that of cultured adrenal medullary cells. These findings are compatible with the idea that ketamine non-competitively inhibits the transport of NA by interacting with a site which partly overlaps the desipramine binding site on the NAT.

Adrenal Medulla↗
PubMed1998

An active metabolite of carbamazepine, carbamazepine-10,11-epoxide, inhibits ion channel-mediated catecholamine secretion in cultured bovine adrenal medullary cells.

We have recently reported inhibitory effects of carbamazepine (CBZ) on ion channel-mediated secretion of catecholamines in bovine adrenal medullary cells. Here, we report the effects of carbamazepine-10,11-epoxide (CBZ-E), an active metabolite of CBZ, and carbamazepine-10,11-diol (CBZ-D), a non-active metabolite, on 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured adrenal medullary cells. CBZ-E, but not CBZ-D inhibited 22Na+ influx, 45Ca2+ influx and catecholamine secretion induced by carbachol or veratridine with a half-maximal inhibitory concentration (IC50) of 0.26 or 0.68 microg/ml, respectively. CBZ-E also inhibited high K+-evoked 45Ca2+ influx and catecholamine secretion (IC50 = 0.3 microg/ml), but CBZ-D did not. These findings suggest that CBZ-E, but not CBZ-D, attenuates catecholamine secretion by inhibiting nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and voltage-dependent Ca2+ channels in the cells. This inhibition of CBZ-E as well as CBZ may be related to the clinical effects in neuropsychiatric disorders.

Adrenal Medulla↗
PubMed1998

[Acute aortic dissection (Stanford A) with pericardial tamponade--extension of the dissection after emergency pericardial puncture].

The hemodynamic deterioration associated with acute aortic dissection (Stanford A) is caused by an acute loss of volume, acute aortic valve insufficiency, or possibly by hemopericardium with tamponade. In the latter case, a pericardiocentesis may restore hemodynamic stability. However, it is only indicated in the case of reduced perfusion of vital organs. The relief of the pericardial effusion can produce a pressure gradient between dissection and pericardial space, which again might cause hemodynamic deterioration by the blood flow into the pericardial space as well as extension of the aortic dissection. Following pericardiocentesis immediate surgery is indicated. In the present case, after a primarily effect hemodynamic stabilization by pericardiocentesis, this mechanism has very probably led to a repeated tamponade and extension of aortic dissection, which was successfully repaired by the implantation of a vascular prosthesis immediately following invasive diagnosis.

Aortic Dissection↗
PubMed1998

Influence of forskolin on the force-frequency behavior in nonfailing and end-stage failing human myocardium.

UNLABELLED: End-stage failing human myocardium is characterized by a negative force-frequency relationship (FFR), possibly as a result of reduced SR Ca2+ uptake capacity. We investigated the effects of the direct adenylate cyclase stimulator, forskolin, on force of contraction and FFR in isolated human myocardium from 7 nonfailing hearts (NF) and end-stage failing hearts (NYHA IV) due to either ischemic (ICM; n = 13) or dilated cardiomyopathy (DCM; n = 16). METHODS: Isolated left ventricular muscle strips, isometric contraction, electrical stimulation at a basal stimulation rate of 1 Hz (37 degrees C). Inotropic responses: Cumulative concentration-response curves for forskolin (0.01-10 microM) and for Ca2+ (2.5-15 mM). Force-frequency experiments: stepwise increase in stimulation rate from 0.5 to 3.0 Hz without and in the presence of 0.3, 1.0 or 3.0 microM forskolin. RESULTS: Forskolin concentration-dependently increased force of contraction to 386 +/- 28% (n = 5) in NF, to 256 +/- 48% (n = 7) in ICM, and to 212 +/- 13% (n = 14) in DCM. The effectiveness of forskolin was significantly reduced in failing myocardium. Ca2+ increased force of contraction to maximally 438 +/- 108% in NF, to 267 +/- 15% in ICM, and to 292 +/- 20% in DCM. Again, the effectiveness of Ca2+ was significantly reduced in failing myocardium. Forskolin activated contractile reserve to similar extents in all types of myocardium (90%, 95%, and 82%, respectively). Force of contraction continuously increased with increasing stimulation rates in nonfailing myocardium (positive FFR), but was blunted or inversed in ICM and DCM. Prestimulation with forskolin (0.3 microM) further enhanced frequency-potentiation in nonfailing, and normalized the slope and optimum stimulation frequency in ICM and DCM. However, at higher concentrations of forskolin, FFR was blunted or inversed in non-failing myocardium, and further impaired in failing myocardium. CONCLUSION: Low concentrations of forskolin with only marginal inotropic effects may partially normalize the inverse force-frequency relation in end-stage failing human myocardium. Reduced cAMP levels in conjunction with reduced expression of SR Ca2+ ATPase may be the underlying cause for altered excitation-contraction coupling in diseased human hearts.

Biomechanical Phenomena↗
PubMed1998

Cardiopulmonary resuscitation after cardiac surgery: a two-year study.

OBJECTIVE: The aim of this study was to investigate the incidence of cardiopulmonary resuscitation (CPR) after cardiac surgery and to find predictors of survival. DESIGN: A retrospective study with data obtained by chart review. SETTING: A university hospital 24-bed cardiac surgical intensive care unit (ICU). PARTICIPANTS: Between 1993 and 1994, 4,968 consecutive adult patients who underwent cardiac surgery at the authors' hospital were studied. INTERVENTIONS: None. MAIN RESULTS: One hundred thirteen of these patients (2.3%) were resuscitated. Seventy-nine patients (70%) survived to be discharged from the hospital. Significant predictors of survival were the time between admission to the ICU and initiation of CPR, CPR time, and creatine kinase (CK) and CK-MB values. CONCLUSIONS: The incidence of CPR after cardiac surgery was 2.3% with no difference between valve surgery and CABG. Best results were achieved when arrhythmias or bleeding were the predisposing causes. Further studies have to be undertaken concerning long-term results and quality of life of the discharged patients.

Adult↗
PubMed1998

Colon-specific drug delivery based on a cyclodextrin prodrug: release behavior of biphenylylacetic acid from its cyclodextrin conjugates in rat intestinal tracts after oral administration.

An antiinflammatory drug biphenylylacetic acid (BPAA) as a model drug was selectively conjugated onto one of the primary hydroxyl groups of alpha-, beta-, and gamma-cyclodextrins (CyDs) through an ester or amide linkage, and the in vivo drug release behavior of these prodrugs in rat gastrointestinal tracts after oral administration was investigated. The CyD prodrugs were stable in rat stomach and small intestine and negligibly absorbed from these tracts. Three to six hours after the oral administration, most of the prodrugs had moved to the cecum and colon. The alpha- and gamma-CyD amide prodrugs were hydrolyzed to the maltose conjugate in the cecum and colon, and these prodrugs and the conjugate were negligibly absorbed. On the other hand, the alpha- and gamma-CyD ester prodrugs produced BPAA in the cecum and colon, and BPAA appeared in the blood after 3-6 h. Both beta-CyD amide and ester prodrugs released only small or negligible amounts of the maltose conjugate or BPAA in the cecum and colon, within 24 h, probably due to the low solubility in the biological media. Further, the antiinflammatory effect of the gamma-CyD ester prodrug was evaluated using the model of carageenan-induced acute edema in rat paw and compared with those of BPAA alone and the BPAA/beta-CyD complex prepared by the kneading method in a molar ratio of 1:1. In the case of the beta-CyD complex, a rapid antiinflammatory response was observed, compared to BPAA alone, because the drug is mainly absorbed from the small intestine after a fast dissolution of the complex. In sharp contrast, the gamma-CyD ester prodrug needed a fairly long lag time to exhibit the drug activity, because BPAA is produced after the prodrug had reached the cecum and colon. The present results clearly suggest that the CyD prodrug approach can provide a versatile means for constructions of not only colon-specific delivery systems but also delayed-release system of certain drugs.

Administration, Oral↗
PubMed1998

Down-regulation of the noradrenaline transporter by interferon-alpha in cultured bovine adrenal medullary cells.

The aim of this study was to investigate the effect of long-term treatment with interferon (IFN)-alpha on the noradrenaline transporter of bovine adrenal medullary cells. Treatment of cultured adrenal medullary cells with IFN-alpha caused a decrease in uptake of [3H]noradrenaline by the cells in time (4-48 h)- and concentration (300-1,000 U/ml)-dependent manners. IFN-beta also inhibited [3H]noradrenaline uptake to a lesser extent than did IFN-alpha, whereas IFN-gamma had little effect. An anti-IFN-alpha antibody reduced the effect of IFN-alpha on [3H]noradrenaline uptake. Saturation analysis of [3H]noradrenaline uptake showed that the inhibitory effect of IFN-alpha was due to a reduction in the maximal uptake velocity (Vmax) values without altering apparent Michaelis constant (Km) values. Incubation of cells with IFN-alpha caused a translocation of protein kinase C from the soluble to the particulate fraction in the cells. The effect of IFN-alpha on [3H]noradrenaline uptake was diminished in protein kinase C-down-regulated cells. Incubation of cells with IFN-alpha for 48 h significantly reduced the specific binding of [3H]desipramine to crude plasma membranes isolated from cells. Scatchard analysis of [3H]desipramine binding revealed that IFN-alpha decreased the maximal binding (Bmax) values without any change in the dissociation constant (K(D)) values. These findings suggest that IFN-alpha suppresses the function of noradrenaline transporter by reducing the density of the transporter in cell membranes through, at least in part, a protein kinase C pathway.

Adrenal Medulla↗