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Biomedical subjects

S Morooka

Publications and source records attributed to S Morooka.

At least 91 records · Page 5Linked to original sources
PubMed1993

Oxygen demand-supply relationship in peripheral tissues as a therapeutic indicator in acute myocardial infarction with advanced heart failure.

Oxygen demand-supply relationships in peripheral tissues were studied in 14 patients who had acute myocardial infarction with advanced pump failure. Seven patients with acute myocardial infarction but without pump failure were studied as a control. In all patients, a Swan-Ganz catheter and a radial arterial cannula were inserted for the purpose of hemodynamic monitoring, and arterial and mixed venous blood were sampled. Initially, oxygen delivery (DO2) (p < 0.01) was lower, and oxygen extraction ratio (OER) (p < 0.001) and oxygen tension at 50% saturation (P50) (p < 0.01) were higher in patients with pump failure than in the controls. During the therapeutic course, with an increase in the cardiac index and DO2, oxygen uptake (VO2) did not change but OER (p < 0.001) and P50 (p < 0.01) significantly decreased in 6 survivors with pump failure. In contrast, an increased VO2 (p < 0.01) and no change of OER and P50 were observed in 8 nonsurvivors with pump failure. These results suggest that reversibility of oxygenokinetics might be an important factor for recovery from critical heart failure.

Aged↗
PubMed1993

Venoarterial carbon dioxide tension gradient in acute heart failure.

The venoarterial carbon dioxide tension gradient (P[v-a]CO2) was studied in patients with acute myocardial infarction. Seven patients with congestive heart failure (CHF group) and 10 patients without heart failure (control) were enrolled in this study. In all patients, hemodynamics were continuously monitored. Simultaneously, arterial and mixed venous blood were sampled, and blood gases and lactate concentration were analyzed. At the initial measurement before therapy, arterial and mixed venous pH and bicarbonate values were within the normal range, and there was no significant difference between the CHF group and controls. There was also no difference in arterial oxygen tension under the differential conditions of oxygen inhalation. However, cardiac index and mixed venous oxygen saturation (SvO2) were significantly lower, while the oxygen extraction ratio (OER) and arterial lactate were significantly higher in the CHF group than in the controls. On the other hand, P[v-a]CO2 was significantly higher in the CHF group (7.8 +/- 2.6 vs. 3.5 +/- 2.2 mm Hg, p < 0.01). This finding was due to the elevated mixed venous carbon dioxide tension in the CHF group, since arterial carbon dioxide tension was the same in both groups. Analysis of a total of 42 measurements obtained during the therapeutic course in the CHF group revealed a correlation of P[v-a]CO2 with cardiac index (r = -0.3, p < 0.05), OER (r = 0.57, p < 0.001), SvO2 (r = -0.56, p < 0.001) and lactate (r = 0.62, p < 0.001). The increase in P[v-a]CO2 observed in acute heart failure suggests the evidence of intracellular acidosis despite the absence of acidemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Features of coronary artery lesions related to left ventricular aneurysm formation in anterior myocardial infarction.

To determine the factors of left ventricular aneurysm formation in acute myocardial infarction, the authors studied the distribution of coronary artery lesions and the left ventricular wall motion of 43 patients with anterior myocardial infarction. Of 15 patients with aneurysm, 9 (60%) showed a single-vessel disease with severe stenosis of the proximal left anterior descending artery. Of 9 patients with triple-vessel disease, 8 (89%) had no aneurysm. In patients with the aneurysm, the Gensini score of the culprit lesion was significantly higher (p < 0.05) and the score except for the culprit lesion was less (chi 2 = 5.7, p < 0.05). In 23 patients with single-vessel disease, the collateral score was significantly less (p < 0.05) in patients with the aneurysm. The systolic wall motion on the ventriculogram appeared more impaired in the anterior infarct area but well maintained in the posterior noninfarct area in patients with the aneurysm. In conclusion, the important factors of left ventricular aneurysm formation were as follows: (1) A culprit lesion of the myocardial infarction was severe, but other coronary artery lesions were mild. (2) Collateral vessels were poor. (3) The left ventricular wall motion of the infarct area was impaired, but that of the noninfarct area was relatively good.

Cardiac Catheterization↗
PubMed1993

Pronounced ST-segment depression during paroxysmal supraventricular tachycardia.

To determine the clinical significance of ST-segment depression observed in paroxysmal supraventricular tachycardia (PSVT), we evaluated the 12-lead electrocardiogram (ECG) during spontaneous PSVT in 54 patients (27 men and 27 women: mean age +/- SD; 47 +/- 18 years), who came to our clinic for the treatment of PSVT. Coronary angiography was performed in 16 patients (16 to 74 years; mean = 50 +/- 18) and treadmill exercise testing was performed in 21 patients. A cardiac electrophysiological study was carried out in 24 patients. During PSVT, ST-segment score was calculated as the sum of the ST-segment depression in 12 leads. The correlations between the ST-segment score, PSVT rate and age of the patient were analyzed as follows: The most significant positive correlation was observed between the ST-segment score and the PSVT rate (r = 0.615, p < 0.000001). The next most significant correlation was found between the PSVT rate and the age of the patient (r = -0.500, p = 0.00011). A negative correlation was also observed between the ST-segment score and the age of the patient (r = -0.429, p = 0.0012). In 13 of 16 patients, coronary angiography did not reveal any significant (> or = 75% in area) stenosis. Exercise testing induced significant ST-segment depression in 3 patients, of whom two had significant coronary artery lesions. PSVT was due to atrioventricular reentry via an overt (n = 3) or concealed accessory pathway (n = 15), atrioventricular nodal reentry (n = 5) and sinus node reentry (n = 1). In conclusion, patients with a faster PSVT rate revealed more pronounced ST-segment depression than did those with a slower PSVT rate, possibly reflecting the modified repolarization process instead of coronary artery involvement.

Adult↗
PubMed1993

[Respiratory changes in the blood flow pattern of the superior vena cava in patients with chronic obstructive pulmonary diseases].

Blood flow patterns in the superior vena cava (SVC) obtained from 20 elderly cases of COPD (aged 60-81) were compared with those from 24 elderly normal subjects (aged 61-80). The peak flow velocity and duration of two major antegrade flows during systole and diastole (S & D wave) were both qualitatively and quantitatively assessed with pulsed Doppler echocardiography. While peak flow velocity and duration of the S and D waves increased during inspiration and decreased during expiration in normal subjects, respiratory variations of these antegrade waves were extremely greater in patients with COPD with augmented and/or fused antegrade waves during inspiration, and there decrease was associated with an upward shift above the zero level during expiration. The duration of the D wave was significantly longer in COPD patients than in normal subjects and also revealed a significantly positive correlation with FEV1.0%. These findings suggest that SVC flow pattern is useful for the assessment of early right ventricular dysfunction in patients with COPD, but further clinical studies are required to confirm this thesis.

Aged↗
PubMed1993

[A case of coronary artery embolism associated with combined valvular heart disease].

A 53-year-old-man afflicted with combined valvular heart disease and atrial fibrillation was admitted to our department complaining of chest pain. ST elevation on ECG (II, III, aVF) and elevated CPK value were recognized. He was diagnosed as having acute myocardial infarction, and percutaneous transluminal coronary recanalization was performed immediately. The coronary angiogram showed occlusions at the proximal left branch (#12). But these lesions could not be recanalized by 960000 IU urokinase administration. The cineangiogram after one month revealed perfect recanalization of these occlusions. Mitral stenosis with neovascularity to the left atrium and aortic regurgitation were recognized. We supposed this infarction caused by coronary embolism originated from left atrial thrombi. Acute myocardial infarction associated with mitral stenosis has been reported in fifteen cases previously in Japan, but only three cases revealed coronary occlusion in the acute phase with normal coronary artery in the chronic stage. However, there has been no report, except for this case, demonstrating occlusion in two coronary arteries at the same time. So, our case is the first report of the involvement of two coronary artery occlusions.

Aortic Valve Insufficiency↗
PubMed1993

[ST-T changes associated with severe hypoxia in a case of obstructive sleep apnea syndrome].

A 59-year-old man with obesity was admitted with nocturnal dyspnea and nocturnal precordial oppression. Catheter data disclosed no cardiac failure. Polysomnography was performed for a total of 3 nights. The diagnosis of obstructive sleep apnea syndrome was made because apnea index was 50 times/hour in average, the max apnea time was about 80 seconds and disappearance of airflow during decrease of endoesophageal pressure was observed. At the max apnea time, ST-T change in leads V2-5 was observed with severe desaturation (arterial oxygen saturation: 49%). It was considered that myocardial hypoxia following sleep apnea might be the cause of nocturnal precordial oppression.

Electrocardiography↗
PubMed1992

In vitro study of a novel atypical beta-adrenoceptor agonist, SM-11044.

SM-11044 (L-threo-3-(3,4-dihydroxyphenyl)-N-[3-(4-fluorophenyl) propyl] serine pyrrolidine amide hydrobromide) stimulated the relaxation of guinea pig ileum (EC50: 3.0 x 10(-8) M), trachea (EC50: 1.3 x 10(-7) M), lung parenchyma (EC50: 2.1 x 10(-6) M) and the increase in right atrial rate (EC50: 6.9 x 10(-6) M). It also induced lipolysis of rat white adipocytes (EC50: 1.2 x 10(-6) M). Both the relaxant response of ileum and the lipolytic response of adipocytes to SM-11044 were resistant to inhibition by propranolol (10(-6) M), but were antagonized by cyanopindolol (10(-6) M). In contrast, the responses to SM-11044 in trachea, lung parenchyma and right atrium were almost completely abolished by propranolol (10(-6) M). Furthermore, the selectivity of SM-11044 relative to isoproterenol was ileum greater than adipocytes greater than trachea (beta 2) greater than lung (beta 2) greater than atrium (beta 1). These results suggest that SM-11044 is a selective agonist of atypical beta-adrenoceptors that are resistant to antagonism by propranolol but sensitive to cyanopindolol. The receptor binding and adenylate cyclase stimulating activity of SM-11044 were also examined on transfected Chinese hamster ovary cells expressing human beta 1-, beta 2- or beta 3-adrenoceptors. SM-11044 inhibited the binding of [125I]iodocyanopindolol to the three types of receptors in a concentration-dependent manner. The selectivity in terms of Ki values was beta 3 (Ki: 1.3 x 10(-6) M) greater than beta 2 (Ki: 4.1 x 10(-6) M) greater than beta 1 (Ki: 18.1 x 10(-6) M)-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1992

Hemofiltration as treatment for patients with refractory heart failure.

Hemofiltration was performed in 15 patients with refractory congestive heart failure. All of these patients had oliguria, although intensive treatment with diuretics, digitalis, vasodilators, and catecholamines was prescribed. Hemofiltration was performed under hemodynamic monitoring in 14 patients. The water removal by hemofiltration decreased pulmonary arterial pressure, pulmonary capillary wedge pressure and right atrial pressure. Despite these hemodynamic improvements, nine patients (60%) died within one month after the start of hemofiltration; the causes were fatal arrhythmia in three, renal failure in two, sepsis in one and irreversible cardiogenic shock in three. Oliguria for over 15 h or a serum creatinine concentration of more than 4.0 mg/dl at the start of hemofiltration related to poor prognosis. In view of these results, hemofiltration for refractory heart failure should be started earlier and performed carefully in order to avoid arrhythmia, cardiogenic shock, and other complications.

Adult↗
PubMed1992

Left ventricular diastolic dysfunction in coronary artery disease: effects of coronary revascularization.

Left ventricular diastolic dysfunction was studied globally and regionally in patients with coronary artery disease, and the effects of coronary revascularization were evaluated. A total of 25 patients with angina pectoris who had a stenotic lesion (greater than or equal to 90%) in only left anterior descending branch underwent coronary revascularization [percutaneous transluminal coronary angioplasty (PTCA) in 13 patients and coronary artery bypass graft (CABG) in 12]. Nine patients with normal coronary artery were studied as controls. Left ventricular volume and radial axes were measured on serial frames of one cardiac cycle by cine left ventriculography. The radial axes were drawn from the left ventricular gravity to left ventricular wall at every 20 degrees. Left ventricular filling fraction and distension rate of radial axes were calculated at the times of 25%, 50%, 75%, and 100% of diastolic period, 100% being end-diastole. Although there were no significant changes of the systolic function by revascularization, the filling fraction increased from 11.2 +/- 2.6 to 14.5 +/- 3.5% (p less than 0.001) at 25% time of diastole, from 29.9 +/- 4.9 to 32.5 +/- 5.0% (p less than 0.05) at 50% time in the PTCA group, and from 11.8 +/- 3.7 to 13.4 +/- 3.8% (p less than 0.01) at 25% time in the CABG group. The distension rate of radial axis to the anterior wall also increased significantly at 25% and 50% time of diastole after revascularization, and the change was marked in the PTCA group. However, these increases did not apply to the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1992

Effect of BRL-35135 on LTB4-induced guinea pig eosinophil chemotaxis.

The effect of an atypical beta-adrenoceptor agonist, BRL-35135 on leukotriene B4-induced-guinea pig eosinophil chemotaxis was studied. BRL-35135 and SC-41930 (leukotriene B4-antagonist) inhibited the chemotaxis in a concentration-dependent manner (IC50 = 9.0 x 10(-6) and 2.6 x 10(-7) M, respectively). However, isoproterenol, fenoterol and another atypical beta-agonist, BRL-37344 had no effects. The inhibitory effect of BRL-35135 was not affected by (+/-)-propranolol (10(-4) M). In contrast, the nonselective beta-adrenoceptor antagonist, (-)-alprenolol (10(-4) M) dextrally shifted the inhibitory curve of BRL-35135. The response to BRL-35135 was antagonized in a competitive manner by (-)-alprenolol, with the slope of the Schild plot close to unity, and a pA2 value of 5.62. These findings suggest that guinea pig eosinophils possess an "atypical receptor", which differs from either beta 1-, beta 2- or atypical beta-adrenoceptor on guinea pig ileum, and through which eosinophil chemotaxis can be modulated by BRL-35135.

Adrenergic beta-Agonists↗
PubMed1992

Platelet-activating factor (PAF) plays an important role in the immediate asthmatic response in guinea-pig by augmenting the response to histamine.

1. To investigate the role of platelet activating factor (PAF) in the immediate asthmatic response, we examined the bronchial reactivity to histamine after administration of PAF to guinea-pigs or antigen challenge to passively sensitized guinea-pigs. 2. A bolus injection of PAF (20-40 ng kg-1), which did not cause a significant increase in intrathoracic pressure (ITP), augmented the bronchial response to histamine almost 8 fold. This airway hyperreactivity was observed even 1 min after PAF treatment. 3. A subthreshold dose of antigen (0.01 mg kg-1, i.v.) also provoked hyperreactivity to histamine, which became significant 6 and 11 min after the antigen treatment. 4. The specific PAF-antagonists, SM-10661 and CV-6209 (i.v.) dose-dependently inhibited both PAF- and antigen-induced airway hyperreactivities to histamine. 5. These results suggest that PAF plays an important role in antigen-induced acute airway responses by augmenting the activities of spasmogens.

Anaphylaxis↗
PubMed1992

Effects of secondary organ failure on compensation of acute heart failure in patients with myocardial infarct and dilated cardiomyopathy.

Compensation for heart failure can be influenced by cardiac loads due to organ failure. This investigation studied the effect of secondary organ failure on the hemodynamics of acute heart failure. Of 106 patients with acute heart failure due to myocardial infarction or dilated cardiomyopathy, 49 (46%) patients had secondary organ failure, either kidney, liver, brain or blood. Their acute heart failure was sustained for significantly longer than that of 57 patients without organ failure. A transient but severe decompensation induced secondary organ failure, although the left ventricular ejection fraction was not different from that of the control without heart failure. Hypervolemia in cases of renal failure, bradycardia in loss of consciousness, hyperdynamic state in anemia and low blood pressure in liver dysfunction caused the sustained acute heart failure. These results suggested that secondary organ failure might occur in 46% of patients with acute heart failure, and might disrupt compensation by different kinds of hemodynamic loads in low cardiac function.

Acute Disease↗
PubMed1992

Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression.

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.

Coronary Angiography↗
PubMed1992

[Left ventricular filling disturbances in cardiac amyloidosis: a study of atrial sound and diastolic inflow velocities].

Cardiac amyloidosis is characterized by left ventricular filling disturbances in a relatively early stage. To investigate such disturbances more precisely, we studied atrial sound and left ventricular inflow velocity patterns. Twelve cases diagnosed as cardiac amyloidosis according to the clinical criteria including rectal biopsies and serum amyloid proteins or at autopsy were reviewed and analyzed. Their mean age was 60.9 +/- 12.5 years. Twelve age-matched cases with hypertrophic cardiomyopathy (HCM) served as the controls. We measured the amplitude of atrial sound by low-frequency phonocardiograms and the ratio of the heights of the A wave of apexcardiograms (ACG) to the total amplitude of the ACG. The mitral inflow velocity patterns were recorded using pulsed Doppler echocardiography. The rapid filling wave (R), atrial filling wave (A) and the ratio of A to R (A/R) were measured. In the amyloidosis group, atrial sound moderately increased in 2 cases, it was faint in 9 and not manifest in the remaining one. The A wave in the amyloidosis group was significantly smaller than that in the HCM group (p < 0.001) (12.4 +/- 3.9 vs 22.4 +/- 5.6%). In the left ventricular inflow velocity patterns, the R in amyloidosis was smaller than that in HCM (41.7 +/- 16.0 vs 56.4 +/- 12.1 cm/sec) (p < 0.02). The A in amyloidosis was also smaller than that in HCM (40.5 +/- 13.4 vs 58.1 +/- 13.0 cm/sec) (p < 0.006). The A/R was 1.0 +/- 0.34 in amyloidosis and 1.1 +/- 0.32 in HCM (N.S.). Both A and R were significantly less in amyloidosis than those in HCM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[A case of angina pectoris with cardiac arrest at treadmill stress test].

We reported a case of angina pectoris with cardiac arrest immediately after treadmill exercise test, and the effect of PTCA in the same case. A 69-year-old Japanese male had chest oppression on exertion. Initial treadmill test showed 2 mm ST-segment depression in leads V4-6. Two minutes after exercise, he had atrio-ventricular (A-V) block and cardiac arrest with episodes of fainting. He was resuscitated by chest thump. Coronary angiography showed 90% stenosis in the right coronary artery (RCA). PTCA for RCA was able to dilate the stenotic lesion. The second treadmill test after PTCA did not induce bradycardia nor A-V block. It was suggested that the RCA lesion may play a critical role.

Aged↗
PubMed1991

Left ventricular diastolic filling in patients with coronary artery disease without myocardial infarction.

Left ventricular diastolic dysfunction at rest was studied in 24 patients with coronary artery disease but no evidence of previous myocardial infarction. Seven patients with normal coronary arteries were studied as control. Diastolic filling was analyzed by the serial left ventricular volume and 14 radial axes from the gravity point of the left ventricle with cine left ventriculography. There were no differences in the systolic function between coronary artery disease and the normal control. Peak filling rate was decreased significantly in the groups with left anterior descending artery disease (LAD, p less than 0.05) and multivessel disease (MVD, p less than 0.05), but not in the group with right coronary artery disease (RCA). Time to peak filling rate was prolonged in each group of LAD (p less than 0.05), RCA (p less than 0.05), and MVD (p less than 0.001), compared with controls. The time-volume curve showed disturbed rapid filling in the LAD and RCA groups, and also both depressed rapid and slow filling in the MVD group. In the LAD group, the filling fraction was decreased significantly at the time of 25% of the diastolic period (p less than 0.001) and radial distension to the anterior wall was decreased at the time of 25%, 50%, and 75% of the diastolic period, compared with controls. In the RCA group, the filling fraction (p less than 0.001) and radial distension to the posterior wall were decreased only at the time of 25% of the diastolic period. In the MVD group, filling fraction and radial distension to the most wall were decreased at 25%, 50%, and 75% of the diastolic period.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗