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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 505 records · Page 28Linked to original sources
PubMed1986

Excessive fibrinolysis in suspected amyloidosis: demonstration of plasmin-alpha 2-plasmin inhibitor complex and von Willebrand factor fragment in plasma.

We performed a hemostatic evaluation in detail in a patient with suspected amyloidosis who was suffering from several bleeding episodes. He had a shortened euglobulin clot lysis time, decreased alpha 2-plasmin inhibitor (alpha 2-PI), decreased plasminogen, elevated tissue-type plasminogen activator (t-PA), elevated plasmin-alpha 2-PI complex, and decreased ratio of ristocetin cofactor to von Willebrand factor (vWF) antigen. Fibrinogen and fibrin/fibrinogen degradation products levels fluctuated, with abnormal values on several occasions. On crossed immunoelectrophoresis, plasmin-alpha 2-PI complex and vWF fragment were demonstrated in the patient plasma. These abnormal findings and bleeding symptoms improved following the administration of tranexamic acid. Discontinuation of tranexamic acid resulted in deterioration of these parameters. These observations indicate that pathologic fibrinolysis (continuous intravascular plasmin generation) characterized by the consumption of alpha 2-PI and plasminogen, formation of plasmin-alpha 2-PI complex, and fragmentation of vWF contributed to the bleeding in this patient. It is important to recognize excessive fibrinolysis as the underlying cause of bleeding in these patients, since specific treatment with antifibrinolytic agents is effective in controlling the bleeding.

Amyloidosis↗
PubMed1986

Hemorrhagic necrosis of pheochromocytoma associated with reversible renal artery stenosis.

An unusual case of pheochromocytoma associated with renal artery stenosis is described. Despite the removal of bilateral adrenal pheochromocytoma, laboratory findings suggested the presence of residual pheochromocytoma and abdominal aortography revealed more pronounced stenosis of the right renal artery. Two months later, the undetected residual pheochromocytoma underwent hemorrhagic necrosis with acute cessation of catecholamine release. Thereafter, the patient's blood pressure decreased to a normal level with marked improvement in hypertensive symptoms. No remaining stenosis was demonstrated on follow up renal angiography. Our case suggests that constant local secretion of catecholamines may be responsible for the development of renal artery stenosis.

Adolescent↗
PubMed1986

Periodic changes in cycle length of ventricular tachycardia: a Wenckebach type exit block?

A 55-year-old female developed ventricular tachycardia (VT) which showed a Wenckebach periodicity in cycle length. She had had a myocardial infarction about ten years previous and, at age 51, felt fatigability and palpitations. The ECG showed VT. Thereafter, she had had palpitations of short duration two to three times a year. On the last admission she developed fatigability; the ECG showed VT. Lidocaine (100 mg i.v.) did not terminate VT. Procainamide (600 mg) could not terminate the VT, but the rate became slower. Programmed stimulation was given at bedside which effectively terminated VT. Electrophysiologic study induced VT in a reproducible manner. Ventricular tachycardia showed initial fluctuation in cycle length which stabilized at 270 msec. Disopyramide therapy (400 mg/day p.o.) was begun and electrophysiologic study was repeated one week later. VT was again induced but the cycle length was a little longer. A periodic change in cycle length from 328 to 442 msec was repeated. The change in cycle length was uniformly found in surface leads (I, II, V1) and intracardiac electrograms from the right ventricular apex and the His bundle region. No change in QRS complex was found and the periodicity was unrelated to atrial activity. A Wenckebach type exit block was therefore suggested; disopyramide might be responsible for the development of the block. We could not find another such case in the literature.

Bundle of His↗
PubMed1986

Inhibition of erythropoiesis by human parvovirus-containing serum from a patient with hereditary spherocytosis in aplastic crisis.

Aplastic phase serum from a patient with aplastic crisis of hereditary spherocytosis, which was demonstrated to contain human parvovirus, inhibited in vitro erythroid colony formation almost completely. Human parvovirus was resistant to heating for 30 min at 56 degrees C. The suppressive effect of the serum was completely abrogated by adding convalescent phase serum from another patient with aplastic crisis of hereditary spherocytosis. Some normal sera had similar neutralizing ability. The results suggested that aplastic crisis of a patient with hereditary spherocytosis is caused by human parvovirus and that the neutralizing test could offer a tool for predicting the future occurrence of aplastic crisis in the patients with chronic hemolytic anemia.

Adolescent↗
PubMed1986

A defect of platelet release reaction in a patient with SLE: impaired platelet aggregation induced by phorbol ester with a normal phosphorylation of 40K protein.

A 37-year-old female who suffered from SLE had a bleeding disorder. At the time of initial evaluation, the main disease demonstrated was a delta-storage pool deficiency. After this improved, a marked decrease of aggregation still remained, when induced by either ADP, epinephrine, collagen, A23187, thrombin, or PAF-acether. Although arachidonate-induced aggregation was slightly decreased, thromboxane B2 was produced normally in response to exogenous arachidonate. The patient's endoperoxides and/or thromboxane A2 aggregated aspirin-treated platelets, though her platelets were themselves unresponsive. Impaired aggregability induced by TPA (12-0-tetradecanoylphorbol-13-acetate) or OAG (1-oleoyl-2-acetyl-glycerol) was also found. However, the phosphorylation of P43 and P20 induced by several stimulators including CA++ ionophore was normal, using 32P-labelled platelets. It is suggested that TPA or OAG-induced platelet aggregation requires not only the phosphorylation of those proteins, but also another unknown mechanism after the phosphorylation, and that the platelet dysfunction of this patient was due to a defect of some mechanism involving Ca++ uptake or mobilization of cytoplasmic Ca++ from intracellular storage sites.

Adenosine Diphosphate↗
PubMed1986

Recurrent paroxysmal hypotension and bradycardia in a patient with pharynx tumor metastasis to the cervical lymph nodes.

In a 64-year-old male, recurrent syncope, hypotension and bradycardia developed repeatedly. The systolic blood pressure fell and could not be measured by auscultation method and the heart rate decreased to under 20 bpm. He recovered from unconsciousness in several minutes. No precipitating cause was apparent for such episodes. Physical examination revealed swollen lymph nodes in the upper cervical regions. Carotid sinus massage caused a fall of systolic blood pressure by 40 mmHg and the P-P interval lengthened to 1.96 sec. The otolaryngeal examination showed neoplasma in the pharynx. He received irradiation therapy on the primary lesion and the bilateral metastatic lesions. After irradiation (4,000 rad), the paroxysmal hypotension and bradycardia disappeared concomitantly with the reduction in size of the metastatic tumor. Hypersensitivity to carotid sinus massage, however, remained unchanged. In this case, the metastatic tumor around the carotid sinus seemed to be related to the syncope and the hemodynamic collapse.

Bradycardia↗
PubMed1986

Late sustained ventricular tachycardia after complete repair of tetralogy of Fallot--a case report.

A female patient had recurrent sustained ventricular tachycardia (VT) as a late sequela after complete repair of tetralogy of Fallot, and the clinically documented VT could be induced and terminated in a reproducible manner by programmed stimulation. VT was accompanied by fragmented electrical activities when the electrode was positioned at the outflow tract of the right ventricle where myotomy was added on the previous scar. The electrophysiological study revealed that the mechanism of VT was re-entry and that the focus of VT was located at the right ventricular outflow tract.

Adult↗
PubMed1986

Five cases of arrhythmogenic left ventricular aneurysm unrelated to coronary occlusion.

Five among 19 cases of sustained ventricular tachycardia (VT) treated in the last two years had left ventricular aneurysms, but the patients denied any previous attack of chest pains that would indicate acute myocardial infarction. Laboratory findings including serum electrolytes were normal and no signs of inflammation were found. Coronary angiograms were normal but the left ventriculograms showed aneurysms in four patients and akinetic to aneurysmal wall motion in one patient. Electrophysiologic studies (EPS) were done in four patients. VT was induced reproducibly by programmed electrical stimulation in three patients and it was terminated by programmed stimulation within 30 seconds. The foci of VT were determined by EPS. One case who showed acceleration of the VT rate following the second induction of VT developed a fulminant course; Adams-Stokes attacks from VT, more than ten times a night in spite of intravenous administration of a large dose of procainamide, were terminated by DC shock. VT was determined to originate from the aneurysm that was resected operatively. In the other two cases, the foci were resected and the intraoperative EPS confirmed the preoperative foci. The postoperative EPS showed no inducibility of VT in three surgical cases. Though the induction of VT may not be indicated in every case of VT, we believe that EPS is required to determine the focus for the operation and to evaluate the precise drug efficacy in rapid VT. It is further stressed that the sustained VT of our patients including the present five, lasted for several hours until it was terminated in the hospital.

Aged↗
PubMed1986

Effect of nifedipine on neuropeptide Y-induced coronary vasoconstriction in anesthetized dogs.

The coronary vasoconstrictor effects of neuropeptide Y (NPY) were confirmed in anesthetized closed-chest dogs. This NPY-induced vasoconstriction was not affected by alpha- or beta-adrenergic blockers and nifedipine given into the perfusion circuit abolished the constriction. After intracoronary nifedipine administration, coronary flow exceeded the control level within 60 sec, then returned to a level between the control value before NPY and the lowest value elicited by NPY after 10 min. When nifedipine was given systemically before NPY, the peak response to NPY was attenuated, suggesting a preventive effect of nifedipine on the NPY-induced coronary vasoconstriction. Since NPY is found in the hearts of many species, including man, NPY may cause coronary vasospasms. An effect on NPY-induced coronary vasoconstriction of nifedipine may be compatible with the beneficial clinical effects of this drug.

Animals↗
PubMed1986

A successful electrical ablation of recurrent sustained ventricular tachycardia in a postoperative case of tetralogy of Fallot.

A 26 year old female patient developed recurrent sustained ventricular tachycardia (VT) after undergoing heart surgery for the third time for chronic pulmonary regurgitation following repair of tetralogy of Fallot. At the last surgery, ventriculotomy was again performed in the outflow tract of the right ventricle. At that time, scar formation and thinning of the cardiac wall were obvious. The surgical result was excellent. Three months later, she lost consciousness. ECG showed VT which was refractory to tolerated doses of antiarrhythmic drugs. Electrophysiologic study showed fragmented activity in the outflow tract of the right ventricle during VT which could be induced and terminated by programmed electrical stimulations. DC energy delivery of 200 Joules to catheter electrodes which recorded local activity 20 msec prior to the onset of the QRS of VT was successful in preventing VT. VT could not be induced by extensive programmed stimulation 1 month later.

Adult↗
PubMed1986

A case of atrial septal defect complicating myocardial infarction. Severe heart failure induced by balloon occlusion of ASD.

A 58 year old man with an acute, extensive anterior myocardial infarction was found to also have an atrial septal defect secundum. A cardiac catheterization study showed a large left to right shunt (Qp/Qs: 6.0). Since other clinical findings were not consistent with the prolonged existence of a large shunt, we considered it to be secondary to the myocardial infarction. Balloon occlusion of the ASD was carried out to predict the hemodynamics after the surgical correction, which soon resulted in severe left ventricular failure. Therefore, an operation was not feasible in this case.

Cardiac Catheterization↗
PubMed1986

Evaluation of left ventricular residual function using postextrasystolic potentiation. Relation between systolic time intervals and angiographic study.

The effects of postextrasystolic potentiation (PESP) on systolic time intervals and left ventricular wall motion were studied during diagnostic cardiac catheterization in 20 patients (4 normal individuals, 11 patients with coronary artery disease and 5 patients with idiopathic dilated cardiomyopathy). Postextrasystolic changes in the aortic pressure and systolic time intervals were measured from the electrocardiogram and aortic pressure tracing. After a micromanometer-tipped catheter was positioned in the ascending aorta just above the aortic valve, a single ventricular premature beat was introduced using an R-wave coupled stimulator. PESP was then studied during left ventriculography which was undertaken simultaneously in the right anterior oblique 30 degrees and left anterior oblique 60 degrees positions. Following two or three normal sinus beats, a right ventricular extrastimulus was delivered again under the same stimulating condition. PESP in all patients caused a decrease in the ratio of the preejection period to the left ventricular ejection time (PEP/ET). The average percent decrease was 21% (from 0.429 +/- 0.162 to 0.339 +/- 0.102, p less than 0.001). The left ventricular ejection fraction (EF) increased in all patients with PESP from 0.52 +/- 0.20 to 0.61 +/- 0.17 (p less than 0.001). The postextrasystolic changes in the PEP/ET ratio and EF were greater in patients with low cardiac performance. There was a good correlation (r = -0.85, p less than 0.001) between the changes in the EF and those in PEP/ET in PESP. Thus, it is possible to determine left ventricular residual function (the postextrasystolic change in the global EF) using the postextrasystolic change in PEP/ET in patients with coronary artery disease and dilated cardiomyopathy.

Adult↗
PubMed1986

Plasma levels of protein C and vitamin K-dependent coagulation factors in patients on long-term oral anticoagulant therapy.

Plasma levels of protein C (PC) and vitamin K-dependent coagulation factors (factors II, VII, IX and X) were measured in 100 specimens from patients on long-term warfarin therapy. Both activities and antigens of these coagulation factors were decreased, depending on the thrombotest values. Factor II activity/antigen ratio and factor X activity/antigen ratio were correlated well with thrombotest values, indicating that the concentration of inactive molecules (PIVKAs) relative to normal proteins increases with increasing intensity of anticoagulation. Although PC antigen (PC:Ag) was also decreased, the ratios between PC:Ag and vitamin K-dependent coagulation factor antigens remained constant, being independent of the intensity of warfarin therapy. These findings indicate that long-term oral anticoagulant therapy results in the suppression of the synthesis of both vitamin K-dependent coagulation factors and PC, but the production of the coagulant and anticoagulant proteins is well-balanced.

Blood Coagulation Factors↗
PubMed1986

Immunohistochemical demonstration of S-100 protein in fibroblast-like cells of the guinea-pig heart.

The immunocytochemical localization of S-100 protein was examined in the hearts of adult guinea-pigs. In addition to Schwann cells, adipose cells and chondrocytes, fibroblast-like cells densely distributed in the cardiac skeleton, all of the four valves and tendinous chordae were immunoreactive for S-100 protein. The S-100-positive fibroblast-like cells were conspicuously rounded in shape and extended their thin, thread-like cell processes in opposite directions; the cytoplasm was restricted to perinuclear region. In these morphological features, the cells were distinctly different from ordinary fibroblasts which were immunonegative for S-100 protein. Electron microscopic observation revealed that the S-100-like immunoreactivity was distributed throughout the cytoplasmic matrix in the cell body and processes, but absent from the nuclei and cell organelles. The significance of the S-100 immunopositive fibroblast-like cells was discussed in relation to cartilaginous tissues, which have the potential to form in the region of the cardiac skeleton and valves under both normal and abnormal conditions.

Animals↗