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Biomedical subjects

K Tobise

Publications and source records attributed to K Tobise.

At least 19 recordsLinked to original sources
PubMed1992

Time course of pulmonary vascular response to an acutely repetitive pulmonary microembolism in dogs--an analysis using pulmonary vascular impedance.

To understand the mechanism leading to progressive pulmonary hypertension, we investigated the time course of vascular response to an acutely repetitive pulmonary microembolism in dogs by using pulmonary vascular impedance. In a normal state, the mean pulmonary arterial pressure (mPAP) was transiently increased by emboli, and the impedance moduli of 0 Hz (= Rin), 1.5 Hz and 3 Hz were slightly increased. A four-element electrical vascular model showed the transient increase in peripheral pulmonary vascular resistance (R2) and inertia, and reduction in compliance (C). In contrast, in a state of a slight pulmonary hypertension, mPAP was continuously increased by the same amount of emboli, and the impedance moduli of both 0 Hz and 3 Hz were significantly increased. By a four-element model, a severe increase in R2 and reduction in C were observed, and these changes continued. Therefore, although the vascular response to pulmonary microembolism basically depends on the degree of mechanical obstruction, this response is thought to be modulated by the responsiveness of pulmonary vessels at that time, which is involved in the alteration in the local characteristics of pulmonary vessels, and/or the recruitment of a new blood flow.

Acute Disease↗
PubMed1992

Site of hypoxic pulmonary vasoconstriction in pulsatile perfused canine lung lobes.

To elucidate the site of hypoxic pulmonary vasoconstriction (HPV) in the dynamic lung, we studied the effect of alveolar hypoxia (0 approximately 4% O2) on excised canine lung lobes with pulsatile perfusion from artery to vein (antegrade perfusion: AP) or vein to artery (retrograde perfusion: RP), and compared responses to hypoxia with those to serotonin and histamine. In our preparation, increases in the pulmonary vascular resistance (R) resulted in a wide range of decreases in the flow wave amplitude at the lobar inflow site (FA). These decreases in FA reflected reductions in the compliance of the vasculature proximal to the main site of resistance. The FA/R ratios of serotonin were 2.29 in AP and 0.24 in RP indicating the predominant arterial constriction, those of histamine were 0.07 in AP and 1.24 in RP indicating the selective venous constriction. In contrast, the responses to hypoxia were 0.38 in AP and 0.42 in RP. These results suggest that HPV occurs not only on the arterial side but on the venous side in the dynamic lung, and the main site of HPV is located in the peripheral pulmonary vasculature, between muscular arteries and veins which are constricted by serotonin and histamine.

Animals↗
PubMed1992

The effect of acute hypoxia on left ventricular function with special reference to diastolic function--an analysis using ultrasonic method.

In order to evaluate the effect of acute hypoxia on left ventricular (LV) contractility and diastolic function, hemodynamics and LV wall motion were investigated in anesthetized open-chest paced dogs using M-mode or pulsed Doppler echocardiography. Animals were ventilated with 10% oxygen (Hypo 1) and 6.3% oxygen (Hypo 2). LV contractility and diastolic functions were enhanced under "Hypo 1" and at an early phase of "Hypo 2". However, LV functions, both systolic and diastolic, were simultaneously reduced in the presence of hypercapnic acidosis by "Hypo 2". Peak velocities of diastolic rapid filling flow (R) and atrial contraction flow (A) were increased under "Hypo 1", but showed a biphasic change (an increase and a subsequent decrease) under "Hypo 2". The ratio of A/R, known as an index of LV diastolic function, was not altered under hypoxia alone or even under hypercapnic acidosis. Even when hypoxia seems to enhance LV contractility, LV function has already begun to be depressed with a reduction of pH. This seems, however, to be compensated for by LV dilatation and increase in preload, or preservation of left atrial performance.

Acidosis↗
PubMed1992

[Effect of potassium channel openers on hypoxic pulmonary vasoconstriction].

The ATP-sensitive potassium channel (K+ATP) has been suggested as an important mechanism for the reactivity of vascular smooth muscle. We investigated the effects of K+ channel openers (lemakalim, pinacidil) on hypoxic pulmonary vasoconstriction (HPV) and angiotensin II (Ag II) induced vasoconstriction in isolated rat lungs (Sprague-Dawley rats: 300-450 g). Ventilation with hypoxic gas (2% O2, 5% CO2) was performed for 6 min after the injection of Ag II (0.1 microgram). Isolated lungs were perfused under constant flow (0.04 ml/g/min) using 20 ml of blood from donor rat. The perfusion pressure was used as the pulmonary artery pressure. Lemakalim or pinacidil was pre-administered through the reservoir. Pretreatment with pinacidil (10(-4) M) or lemakalim (10(-5) M) inhibited the pressor response to hypoxia, but did not inhibit the response to angiotensin II. Although the effect of lemakalim on HPV was reversed by administration of glibenclamide (10(-5) M) or tolbutamide (10(-3) M), the effect of pinacidil on HPV was not influenced by either drug. These results suggest that 1) K+ channel openers (lemakalim and pinacidil) inhibit the pressor response to hypoxia, and 2) lemakalim seems to act through K+ATP, whereas pinacidil may have other mechanisms of inhibition of vascular smooth muscle contraction. K+ATP may play an important role in the regulation of pulmonary vascular reactivity to hypoxia.

Angiotensin II↗
PubMed1991

Prolonged period of global ischemia causes no change in the GTP-binding proteins in the isolated perfused rat heart.

The response of the beta-adrenoceptor transduction system to global ischemia for 40 min was investigated in isolated working heart of rat. The enhancement of beta-adrenoceptors was not observed in the ischemic myocardium. A depression of forskolin-stimulated adenylate cyclase enzyme occurred with global ischemia, but no change in Gs or Gi2 was detected. Thus, the present in vitro ischemic heart model may not necessarily reflect the identical milieu induced by the in vivo myocardial ischemia.

Adenylyl Cyclases↗
PubMed1991

Transient pulsus alternans induced by isosorbide dinitrate: echocardiographic and hemodynamic evidence of reduced venous return--a case report.

Transient pulsus alternans was induced by isosorbide dinitrate (ISDN) in a patient with postmyocarditis congestive heart failure under diuretic therapy. The severity and duration of pulsus alternans depended on the dose of ISDN. According to the echocardiographic and hemodynamic examinations, the superimposed preload reduction caused by ISDN combined with decreased blood volume owing to diuretic therapy most likely contributed to the development of pulsus alternans.

Adult↗
PubMed1991

[A case of sleep apnea syndrome with variant angina].

A 56-year-old male was admitted because of respiration arrest during sleep, and precordial crushing sensation which repeatedly occurred early in the morning. He had been hypertensive and aware of daytime sleepiness for ten years. After admission, all night polysomnography was recorded a total of four times. Apnea index was 37.5 times/hour, and central type apnea was predominant. The diagnosis of sleep apnea syndrome was made. In the early morning of the fourteenth day after admission, the patient developed anterior chest pain associated with ST elevation in leads II, III, and aVF of the electrocardiogram. Thus, the case was thought to be complicated by variant angina. There were no anginal attacks during the all night polysomnography recordings. However, a causal relationship between the sleep apnea and variant anginal attacks was suspected. Since both the sleep apnea and the variant anginal attacks tended to occur during the stages of REM sleep, and they are both related to changes in activity of the autonomic nervous system. It was considered that hypoxemia following sleep apnea and/or the hyperventilation after the apneic episodes might be the cause of the variant anginal attacks.

Angina Pectoris, Variant↗
PubMed1991

[Technetium-99m-pyrophosphate myocardial scintigraphy in polymyositis--a case report].

A patient with polymyositis who had cardiac involvement underwent myocardial scan with technetium-99m-pyrophosphate. We used Activity Index for evaluating myocardial uptake of technetium-99m-pyrophosphate, which correlated with the degree of serum creatine phosphokinase elevation. Our findings indicate that these examinations may be helpful for identifying patients who have cardiac involvement and evaluating their response to the treatment with corticosteroids or immunosuppressants.

Cardiomyopathies↗
PubMed1991

[A case of right atrial myxoma--the availability of transesophageal echocardiography in the detection of right atrial myxoma].

A 72-year-old woman had experienced palpitation and fatigue during exertion for two months and was referred to our hospital from her nearby hospital. On physical examination, a systolic murmur was heard in the left fourth intercostal space. A chest X-ray film showed cardiac enlargement (CTR 64%). An ECG showed elevated P waves in leads II, III. Transthoracic echocardiography revealed a large oval heterogeneous mass in the right atrium. Transesophageal echocardiography (TEE) revealed the right atrial mass clearly, which was attached to the atrial septum with a short wide stalk. This mass prolapsed from the right atrium into the right ventricle in diastole. And there were some cysts in the homogeneous high-echoic lesion. The chest CT and MRI also showed the mass in the right atrium. However, these images were not clear. Surgical excision of the mass was undertaken. A solid mass measuring 75 x 50 x 45 mm was attached to the fossa ovalis with a wide short stalk. There were several cysts in the mass. Pathological examination showed myxomatous tissue. In this case, TEE was the most valuable means for evaluation of the right atrial mass.

Aged↗
PubMed1990

Changes in the pulmonary vascular input impedance in patients with atrial septal defect after surgical correction.

In order to evaluate whether there is pulmonary vascular disease in patients with atrial septal defect (ASD), we used the pulmonary vascular input impedance to estimate the stiffness of the pulmonary vessels with before and after surgical intervention. Ten control subjects and 11 patients with ASD (9 operable and 2 inoperable) were examined. In preoperative patients the decreased total pulmonary resistance (Rin) and pulmonary vascular resistance appeared to open new parallel vascular channels with increased blood flow. Further, there were no significant differences in the pulmonary vascular input impedance spectrum and phase, and characteristic impedance among control subjects, preoperative and postoperative patients. Although distensibility of the pulmonary vascular wall in operable patients was similar to that in control subjects, an excessive elevation in Rin and input impedance modulus was observed in inoperable patients. The results demonstrate that the normal input impedance spectrum and phase in patients with ASD is predictive of a good prognosis after successful surgical correction.

Adolescent↗
PubMed1990

Ca2(+)-induced contraction and hyperreactivity of pulmonary arterial smooth muscle in monocrotaline-treated rats.

The mechanism of progressive pulmonary hypertension induced by monocrotaline (MCT) remains controversial. To determine whether or not functional changes in pulmonary arterial smooth muscle contribute to the development of pulmonary hypertension, we examined the reactivity of isolated pulmonary artery segments 7, 14 and 21 days after a single subcutaneous injection of MCT. In Ca2(+)-free buffer, pulmonary arteries from MCT-treated rats contracted when CaCl2 was added without any other stimulation. The pulmonary artery exposed to MCT also exhibited hyperreactivity to KCl and 5-hydroxytryptamine. These functional changes in the pulmonary artery preceded the elevation of right ventricular systolic pressure and right ventricular hypertrophy. The contraction in response to Ca2+ suggests that the pulmonary artery of rats given MCT may be contracted in situ. Vasoconstriction due to these alterations may play an important role in the development of pulmonary hypertension according to this model.

Animals↗
PubMed1990

[Respiratory pathophysiology during sleep in patients with myotonic dystrophy].

Myotonic dystrophy is a genetic disorder inherited as an autosomal dominant trait. It is known to be associated with endocrine dysfunction, polar cataracts, cardiac abnormalities and other conditions. Respiratory distress constituents the principal problem in myotonic dystrophy. The author investigated postural change of respiratory function in 12 patients with myotonic dystrophy (MYD), and 7 patients with limb-girdle dystrophy (LG) and overnight polysomnography was performed on 10 patients with MYD and 5 patients with LG. The respiratory function in seated posture showed no significant difference between LG and MYD, but in patients with MYD, the vital capacity and the expiratory reserve volume in a supine posture was reduced in comparison to that during seated posture. However, the respiratory function in patients with LG was not significantly different in seated and supine postures. Also, in patients with MYD, there was a significant decrease in arterial PO2 from the seated posture to the supine posture, without a significant change in the arterial PCO2. However, in patients with LG, there was no significant change in arterial blood gas analysis parameters. It was speculated that these findings concerning respiratory function and blood gas analysis in patients with MYD were caused by the involvement of the diaphragm. In the supine posture, the diaphragm shifted to the cranial position because of the abdominal contents rising into thorax, therefore the lung volume was reduced and the ventilation-perfusion ratio deteriorated. The changes of respiratory function parameters and PaO2 were partly responsible for the hypoxemia observed during sleep in patients with MYD. Overnight polysomnography showed that 9 of the 10 patients with MYD and 1 of the 5 patients with LG presented apneas during sleep, particularly during REM, stage 1 and stage 2. Almost all apneas were central type, with a low percentage of obstructive apneas and the apnea index was 19.0/h (mean) in MYD, 6.5/h in one case of LG. These result strongly suggest that sleep apnea is of central origin, but the distinction between a central and an obstructive etiology is difficult in neuromuscular disease and particularly when a disorder of central ventilatory responsiveness is suspected. The respiratory function of MYD and LG in seated and supine postures was studied and overnight polysomnography performed. It was emphasized that it was important for the respiratory care of neuromuscular disease to consider the influence of postural changes in the respiratory function. The present series of studies revealed central sleep apnea in the patients with myotonic dystrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

[Obstructive sleep apnea syndrome with reversible interventricular septal displacement during sleep: a case report].

A case of the obstructive sleep apnea syndrome revealed reversible leftward displacement of the interventricular septum by echocardiography during sleep. A 46-year-old housewife with congenital micrognathia was admitted to our hospital complaining of severe dyspnea and general edema. On admission, she had severe hypoxemia (PaO2 = 35.2 mmHg), pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) and right heart failure. Her echocardiograms revealed enlargement of the right ventricle with a flattened left ventricle. A sleep study performed after partial resolution of her right heart failure disclosed that severe hypoxemia and pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) occurred after relatively long periods of apnea. With vigorous inspiratory efforts during sleep apnea, transient enlargement of the right ventricle and leftward displacement of the septum causing the flattened left ventricle were observed echocardiographically. A concomitant decrease in left ventricular inflow velocities was also observed by the pulsed Doppler method. However, these findings immediately returned to normal with the resumption of ventilation. We concluded that these repetitive apneic events due to obstruction of the airway during sleep might accelerate complete eventual pulmonary hypertension and right heart failure.

Echocardiography↗