Search PubMed⌕ Search

Biomedical subjects

M Mohri

Publications and source records attributed to M Mohri.

At least 91 records · Page 5Linked to original sources

Disappearance of coronary artery-ventricular fistulas after a radical operation for tetralogy of Fallot.

A 42-year-old Japanese man was diagnosed as tetralogy of Fallot (TOF). Coronary arteriography demonstrated coronary artery-ventricular fistulas (left coronary artery to left ventricle, right coronary artery to right ventricle). A radical operation for TOF was performed, including a patch closure of the ventricular septal defect, right ventricular muscle resection and a patch enlargement of the right ventricular outflow tract. After the operation, coronary arteriography showed a marked decrease in the shunt flow through the coronary artery-ventricular fistulas. Six months later, the patient was diagnosed as postoperative constrictive pericarditis, while the fistulas had almost completely disappeared. After pericardiectomy, when all hemodynamic variables were normal, the fistulas did not reappear. This is the first report of TOF complicated with multiple coronary artery-ventricular fistulas which completely disappeared after a radical operation. It is conceivable that in our case coronary artery-ventricular fistulas partially compensated for reduced arterial O2 saturation and disappeared after surgical correction with an improvement in hemodynamic variables.

Adult↗

Evaluation of static work load in a helium-oxygen saturation dive at 31 ATA.

The purpose of the present study is to evaluate the static work load as a model work in Submersible Decompression Chamber (SDC) during a deep sea saturation dive with helium-oxygen gas mixture. Heart rate (HR) and electromyogram (EMG) power spectrum changes were studied during a 7-minute static work, half-rising posture or flexed knee posture in four healthy male subjects. During the static work, EMG of the rectus femoris was recorded with surface electrodes, and changes in the EMG power spectrum were presented in the ratio of a high-frequency to low-frequency band (H/L ratio) after the Fourier transform analysis. The HR decreased at 31 ATA and increased remarkably after the decompression to 1 ATA. HR at post-decompression was higher than pre-compression. The lowering phenomena of EMG presented by H/L ratios during the static work were similarly observed in all three conditions. But the changes of the high and low frequency components were different in the post-decompression condition from the pre-compression and 31 ATA conditions. HR as a parameter of static work load might underestimate the work load at the hyperbaric environment due to hyperbaric bradycardia and overestimate it after decompression by "decompression tachycardia." The EMG lowering phenomenon observed after decompression might not be caused by the same mechanism as seen in the pre-compression and hyperbaric environments. Extreme care must be taken to evaluate the static work load not only at hyperbaric helium-oxygen environments but after decompression from a deep saturation dive.

Adult↗

Bradykinin-induced vasodilation is impaired at the atherosclerotic site but is preserved at the spastic site of human coronary arteries in vivo.

BACKGROUND: Bradykinin causes endothelium-dependent vasodilation of isolated human coronary arteries in vitro. However, the effect of bradykinin on vasomotion of human coronary arteries in vivo has not been studied. The aim of this study was to examine whether bradykinin-induced vasodilation is altered at the atherosclerotic or spastic site of human coronary arteries in vivo. METHODS AND RESULTS: The effect of bradykinin on vasomotion of epicardial coronary arteries was evaluated in 8 patients with normal coronary arteries (control group), 14 patients with organic coronary stenosis (coronary artery disease [CAD] group), and 8 patients with vasospastic angina (VSA group). Changes in the diameter of epicardial coronary artery were assessed by quantitative coronary arteriography. Intracoronary administration of bradykinin at graded doses (60, 200, and 600 ng) dilated epicardial coronary arteries without altering arterial pressure or heart rate in all patients of either group. In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction. The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean +/- SD: 6 +/- 6%, 11 +/- 9%, and 15 +/- 9%) were comparable to that (3 +/- 6%, 8 +/- 8%, and 13 +/- 9%) at the site with acetylcholine-induced constriction. In the CAD group, vasomotor responses of the stenotic site (% diameter stenosis, 15% to 50%) and nonstenotic site were examined. The bradykinin-induced dilation at the stenotic site (0 +/- 4%, 3 +/- 8%, and 5 +/- 9%) was significantly less (P < .01) than at the nonstenotic site (3 +/- 4%, 8 +/- 6%, and 16 +/- 11%) and in the control group. Coronary vasodilation with nitrate at the stenotic site (20 +/- 11%) was comparable to that at the nonstenotic site (22 +/- 16%) and in the control group (21 +/- 10%). In the VSA group, vasomotor responses of the site with acetylcholine-induced spasm and the site without spasm were examined. The bradykinin-induced vasodilation at the spastic site (5 +/- 5%, 16 +/- 15%, and 33 +/- 17%) was comparable to that at the nonspastic site (4 +/- 8%, 12 +/- 14%, and 21 +/- 9%). Nitrate-induced dilation was comparable at the spastic site (51 +/- 19%) and the nonspastic site (32 +/- 13%). The ratio of bradykinin-induced vasodilation to nitrate-induced vasodilation at the spastic site was comparable to the control group. CONCLUSIONS: These results suggest that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradykinin-induced endothelium-dependent vasodilation is impaired at the stenotic site but is preserved at the angiographically normal site where endothelium-dependent vasodilation by acetylcholine is impaired and at the spastic site.

Acetylcholine↗

Isoproterenol infusion provokes vasovagal response without upright tilt in a patient exhibiting syncopal episodes.

We report a case of a patient with vasovagal syncope, in whom isoproterenol infusion provoked vasovagal response without upright tilting. We subjected the patient, who had had two previous syncopal and several presyncopal episodes, to upright tilting with isoproterenol infusion. Before a control tilt was performed for 10 min (80 degrees), the patient was placed in the supine position for 5 min. The control tilt did not provoke a vasovagal response. With isoproterenol being infused at a dose of 1 mu g/min, the sequence of positioning in the supine position for 5 min and upright tilting for 10 min was repeated. This dose of isoproterenol infusion did not provoke any vasovagal response in the patient, either in the supine or in the upright position. When the dose of isoproterenol infusion was then increased to 2 mu g/min, the heart rate increased to 121/min, but then suddenly dropped to 74/min; systemic arterial pressure simultaneously fell from 148/80 to 108/80 mmHg. The patient complained of palpitation and anxiety, and showed profound cold sweating. The drop in the heart rate and the fall in blood pressure occurred when the patient was in the supine position, indicating that, unlike upright tilting with isoproterenol infusion, venous return was not decreased at the beginning of vasovagal response in this setting. This observation suggests that isoproterenol infusion, even without upright tilting, may provoke the vasovagal response in some patients.

Adult↗

Insulin-like growth factor I is involved in inflammation linked angiogenic processes after microembolisation in porcine heart.

OBJECTIVE: Angiogenesis in the porcine heart can be induced by myocardial ischaemia following vascular occlusions. This process is characterised by increased numbers of monocytes/macrophages, known to be potent producers of various mitogens such as insulin-like growth factors (IGF) and interleukins (IL). The aim of the study was to examine gene expression of these factors by means of northern blot hybridisation, slot blot analysis, and in situ hybridisation in a porcine model of coronary angiogenesis. METHODS: Experimental ischaemia and subsequent focal necroses were induced by selective injection of 25 microns microspheres into the left circumflex artery. The hearts were excised after 3-168 h of microembolisation, and tissue was collected from a non-ischaemic control area and the circumflex region of the same heart for further analysis. RESULTS: IGF-I was constitutively transcribed in normal porcine myocardium mainly by myocytes. Following microembolisation, IGF-I mRNA expression was significantly increased in the experimental region (1.8-fold) after 72 h and to a lesser extent after 168 h. In the ischaemic region, characterised by capillary sprouting, numerous mononuclear cells contained IGF-I mRNA. In contrast, IGF-II mRNA levels, constitutively produced by porcine myocytes, were not altered by microembolisation. IL-1 alpha, IL-1 beta, and IL-4 mRNA expression was undetectable in our animal model, whereas IL-6 was constitutively transcribed in normal and ischaemic heart and remained insensitive to microembolisation and focal necrosis. CONCLUSION: After microembolisation, increased IGF-I mRNA expression occurred by infiltrating monocytes in areas of microsphere induced focal necrosis, where capillary sprouting can be detected, suggesting that IGF-I is involved in inflammation linked angiogenic processes.

Animals↗

Cardiovascular deconditioning occurs during a 7-day saturation dive at 31 ATA.

Cardiovascular deconditioning (CD) has been reported to occur within 24-48 h of exposure to 4, 11, or 31 ATA environment and following decompression to sea level pressure. The CD was indicated by orthostatic intolerance, exaggerated cardiovascular responses to a passive tilt, an elevated resting heart rate and a reduced stroke volume postdive. In this dive, one of the New Seatopia series, we used a non-syncope criterion, the cardiovascular index of deconditioning (CID; Bungo MW, Johnson PJ Jr. Aviat Space Environ Med 1983; 54:1001), to evaluate CD in 3 male subjects. The CID sums the changes in heart rate and blood pressure in response to orthostatic stress. An elevated CID indicates CD. We used a passive 70 degrees head up tilt as the orthostatic stress. The CID was measured before and after a bout of underwater exercise at predive, during the early, mid, and late exposure of the 7-d 31 ATA, and after the dive. The CID and circulatory responses to tilt were similar before and after the exercise. The CID increased (p < 0.05) from the predive value of 20 +/- 1.6 to 25 +/- 0.9 on the 2nd day, to 25 +/- 0.8 on the 4th day at 31 ATA, indicating the presence of CD at the early and mid periods of hyperbaric exposure. However, CID was indifferent (18 +/- 0.6) from the predive on the 7th day at 31 ATA. The increased CID corresponded to decreases in plasma volume during the early and mid periods of 31 ATA exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Maximum sustained fin-kick thrust in underwater swimming.

We examined the upper limit of a diver's fin-kick thrust force using a stationary-swimming ergometer. Heart rate, respiratory minute volume, oxygen uptake, and performance rate were measured in four male subjects who swam constantly for 8 min to maintain a horizontal position against an applied force at a depth of 0.7 m. The water temperature was controlled at 26 degrees +/- 1 degree C. The performance rate, which was the parameter of how well the subjects compensated for the applied load, showed an upper limit around 64 N of sustainable thrust force. This meant that the diver could generate the swimming thrust force within 64 N continuously for 8 min in a steady state. Heart rate, respiratory minute volume, and O2 uptake showed almost proportional increases to the applied load within 64 N and tended to plateau about 69 N.

Adolescent↗

Diving patterns of ama divers of Hegura Island, Japan.

Daily diving patterns, especially depth-time profiles, were continuously recorded during the entire work shift in four cachido and four funado divers of Hegura Island, Japan. All Hegura divers (cachido and funado alike) were female and habitually wore wet suits. Cachidos dive free and unassisted from a boat or float, whereas funado divers are assisted by weighted descent and during the ascent by being pulled by a partner into a boat on the water surface. Both funado and cachido divers spent 250-280 min/day on the sea at their diving locations; the actual diving time was 100-120 min. The divers made 90-120 dives/day to a depth of 13-22 m, each dive lasting approximately 60 s, considerably longer and deeper than those observed and recorded previously in ama divers in the Chiba and Miura regions. These dive profiles are similar to those reported by Paulev in which he observed apparent signs of decompression sickness when the subject dived to a depth of 15-20 m 100 times in 5 h. The average bottom time for each dive of Hegura funados was 23.6 s which is approximately 10 s longer than that of Korean female ama. The rate of ascent in the funado divers was 1.5 m/s, which is nearly twice that of the cachido divers (0.8 m/s). The dive frequency of Hegura funados (109 dives/day) was greater than the Chiba male funados (23 dives/day). Accordingly, cumulative bottom time of Hegura funado was 48 min/day, whereas that of Chiba funado was 17 min/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Diurnal renal responses in man to water loading at sea level and 31 atm abs.

The hyperbaric environment causes a sustained diuresis accompanied by normal water intake and a decrease in insensible water loss. The maintained water intake may be necessary for the maintenance of water balance because of a reduced ability of the kidney to retain water, or may be causal in the diuresis. This problem was studied in four male subjects. Each ingested 1 liter of water (15 degrees C) at 0800 and 2000 h on different days, at 1 atm abs during a predive control, at 31 atm abs, and at 1 atm abs during the postdive control period. Urine was collected 30 min before and 3 h after the drink. Plasma vasopressin (VP) showed a circadian rhythm only at 1 atm abs, higher during the daytime. Because of this, and slightly lower VP levels at hyperbaria, a decrease in VP in response to the water load was significantly detectable only at 1 atm abs during the daytime. At 60 min after all water loads, there were no differences in plasma VP or plasma or urinary osmolality. Variability in the length of time of similarly reduced urine osmolality and increased free water excretion accounted for the increased urine flow during day compared to night (P < 0.05) at 120 and 150 min after the water load. The ability to excrete a water load both day (free water clear-ance, P < 0.05 at 60 min post-drink) and night (free water clearance, P < 0.05 at 60, 90, and 120 min post-drink) at 31 atm abs was enhanced. It is concluded that maintained water intake at hyperbaria is necessary to maintain water balance because there is a reduced ability of the body through renal mechanisms to retain a water load.

Adult↗

Intravenous extended infusion of recombinant human soluble thrombomodulin prevented tissue factor-induced disseminated intravascular coagulation in rats.

This study demonstrated that intravenous infusion of recombinant human soluble thrombomodulin (rhs-TM) could inhibit disseminated intravascular coagulation (DIC) caused by 4 hr infusion of tissue factor (TF) in rats. Extended infusion of TF reduced fibrinogen and platelet counts and elevated serum FDP level. Pretreatment and coinfusion of rhs-TM could block changes of these DIC-parameters without prolongation of APTT. Heparin, which is a potent anti-DIC drug, could also inhibit these changes with extra prolongation of APTT and PT. Thus, these results suggest thrombomodulin prevent DIC less bleeding tendency than heparin.

Animals↗

Antithrombotic effects of recombinant human soluble thrombomodulin (rhs-TM) on arteriovenous shunt thrombosis in rats.

We examined the antithrombotic effect of recombinant human soluble thrombomodulin (rhs-TM) using an arteriovenous shunt thrombosis model and its influence on hemostasis in rats. Intravenous administration of rhs-TM (0.5-4 mg/kg) significantly inhibited thrombus formation and prolonged ex vivo activated partial thromboplastin time (APTT) in a dose-dependent manner. Thrombus formation was inhibited to the same extent in animals treated with heparin (25-200 U/kg) and in those treated with rhs-TM (0.5-4 mg/kg), but heparin had a much stronger effect on prolonging APTT. In the hemorrhagic study using the rat template bleeding time method, rhs-TM exhibited the prolongation of the bleeding time only at the highest effective dose (rhs-TM; 4 mg/kg) of the thrombosis experiments. Thus, rhs-TM exhibits the inhibitory effect on thrombus formation with less APTT prolongation in comparison with heparin and without significant pertubation of hemostasis.

Animals↗

Neoglottic activity in tracheoesophageal phonation.

It has been generally accepted that the retropharyngeal wall protrudes into the lumen and forms a prominence during alaryngeal phonation. Although the prominence is thought to be responsible for the vibratory source, the relationship between the vocalization process and the dynamics of the prominence is not well known. This study is undertaken to clarify the above-described relationship during tracheoesophageal (TE) phonation, one of the most common forms of voice restoration following total laryngectomy. Electromyography (EMG) with simultaneous manometry and fiberoptic observation of the hypopharynx were done in 7 subjects who underwent TE fistulization at the time of laryngectomy. Fiberscopy revealed prephonatory closure of the hypopharyngeal lumen, and subsequently, a definite configuration of the lumen where diverted air can escape with mucosal vibration during phonation. The EMG disclosed a characteristic pattern that had two bursts of activity with an intervening quiet period. It may be concluded that TE phonation consists of two steps: The first step, associated with the first burst and regarded as the preparatory stage, consists of the hypopharyngeal closure which forms a small lumen. The second step, associated with the second burst and regarded as the phonatory stage, consists of the vibration of the neoglottis with a definite configuration which is maintained by the hypopharyngeal muscle contraction.

Aged↗

Effects of a new Na+/H+ antiporter inhibitor on postischemic reperfusion in pig heart.

We investigated the effects of a new compound (3-methylsulfonyl-4-piperidinobenzoyl) guanidine hydrochloride (HOE 694) known to inhibit the Na+/H+ exchanger in a porcine model of ischemia/reperfusion. Ischemia was induced by coronary occlusion (twice for 10 min, with a 30-min reperfusion interval) followed by a 4-h reperfusion period. Treated animals (n = 8) received HOE 694 as a bolus (7 mg/kg) 20 min before ischemia and subsequently as a continuous infusion (0.07 mg/kg) throughout the experiment. Control pigs (n = 11) received vehicle. Regional wall function (percentage of segment shortening, % SS) of the treated animals was significantly improved as compared with that of controls after the 4-h reperfusion period (74.1 +/- 2.5 vs. 50.9 +/- 5.4, p < 0.005). Ventricular fibrillation (VF) could be prevented completely in treated pigs but occurred in 9 of 11 control animals (p < 0.001). Ultrastructural changes after ischemia and reperfusion were moderate and slightly abnormal in controls but much milder and completely recovered in the treated group, respectively. The tissue content of high-energy phosphates did not show a significant difference between groups. Inhibition of the sarcolemmal Na+/H+ antiporter with HOC 694 is antiarrhythmic and diminishes myocardial ischemic cell injury by preventing Na+ overload.

Adenine Nucleotides↗

Collateral development induced by repetitive brief coronary occlusion relates to the functional state of pre-existing collaterals.

The effects of pre-existing collaterals (PC) and the perfusion size (PS) on the ischemia-induced collateral development were studied in a canine model. Under aseptic conditions, the dogs were instrumented with pairs of ultrasonic crystals to measure regional wall motion in the territory of the left circumflex (LCX) and left anterior descending coronary artery. A micromanometer was used to measure left ventricular (LV) pressure. Two to 3 weeks after surgery, 2 min coronary occlusion (CO) of LCX was repeated every 32 min consecutively day and night using a remote control, motor-driven hydraulic cuff occluder. Regional wall motion and LV pressure were monitored via a telemetry system in 23 dogs. The functional state of PC was estimated by the level of % reduction of regional wall motion at the end of the first 2 min CO, which ranged from -11 to -141%. PS of LCX area at risk determined by the post mortem angiograms ranged from 35 to 54% (mean +/- SEM; 44 +/- 1%) of LV. Number of CO needed for collateral development ranged from 8 to 628, and was exponentially related to the functional state of PC (r = -0.77, n = 23, p < 0.01), but not to PS (r = 0.43, n = 19, p = 0.07). These results suggest that the functional maturity of pre-existing collaterals is one of the major determinants of collateral development related to ischemic stimuli.

Animals↗

[Mechanism of neoglottic adjustment for voice variation in tracheoesophageal speech].

Over the past 17 years, we have been performing tracheoesophageal (TE) fistulization for voice restoration following total laryngectomy. The purpose of this technique is to divert the exhaled air through the TE fistula into the hypopharynx where the inferior constrictor muscle forms the retropharyngeal prominence on which the neoglottis is located. It is generally accepted that both pulmonary power and laryngeal adjustment control voice frequency and intensity change in laryngeal phonation. Regularity at various pitches and voice intensities was seen in TE phonation, despite laryngeal adjustment being lost. Regular voice production with various pitches and intensities requires a regulatory mechanism for both pulmonary power and the neoglottis. This study was designed to clarify the mechanism of neoglottic adjustment in TE phonation. Ten speakers with TE fistula were subjected to aerodynamic and electrophysiological investigations. Tracheal pressure, fundamental frequency, intensity, and airflow rate were measured for easy phonation, a high-pitched voice, and a loud voice. Resistance and efficiency of the neoglottis were calculated from the data obtained. Electromyograms of the inferior constrictor muscle and tracheal pressure were simultaneously recorded when the pitch or intensity of the voice increased. Six of the ten subjects examined were able to produce a high-pitched voice. Tracheal pressure increased in all six, the airflow rate in four, and neoglottal resistance in five, as compared with the data obtained during easy phonation. Nine of the ten subjects examined were able to produce a loud voice. In all nine, both tracheal pressure and the airflow rate increased as compared with the values measured during easy phonation. Neoglottal resistance had no definite pattern in relation to voice intensity changes. Electrophysiological study demonstrated that the activity of the inferior constrictor muscle increased as tracheal pressure increased so as to raise the pitch or increase the intensity of the voice. These results indicate that the adjustment of neoglottic closure and stiffness produced by the inferior constrictor muscle has the role of varying the frequency or intensity of the voice.

Aged↗

[Lung pathology of cryptococcosis].

To elucidate the relationship between the clinical manifestations and pathologic findings of the lung in patients with cryptococcosis, we reviewed 14 autopsied cases of cryptococcosis. Five patients had pulmonary cryptococcosis and 9 had disseminated cryptococcosis. Patients with pulmonary cryptococcosis showed granulomatous reactions of the lung, such as fibrocaseous cryptococcoma (n = 2), discrete granuloma (n = 2), and granulomatous pneumonia (n = 1). Patients with disseminated cryptococcosis showed intracapillary/interstitial involvement (n = 2), mucoid pneumonia (n = 3), histiocytic pneumonia (n = 1), and granulomatous pneumonia (n = 3). There was a distinct difference between pulmonary cryptococcosis and disseminated cryptococcosis in lung pathology. Intracapillary/interstitial involvement and mucoid pneumonia were fatal because of extensive hematogeneous dissemination to other organs. Hilar lymph node involvement of cryptococcosis was found in all of the nine patients with disseminated cryptococcosis and in one of the five patients with pulmonary cryptococcosis. Pleural involvement of cryptococcosis was found in six of the nine patients with disseminated cryptococcosis. We conclude that the clinical manifestations of cryptococcosis are closely associated with the variety of lung pathology of cryptococcosis. Clinicians should understand the morphologic features to cope with patients with cryptococcosis.

Adult↗

Effects of recombinant human soluble thrombomodulin (rhs-TM) on a rat model of disseminated intravascular coagulation with decreased levels of plasma antithrombin III.

We reported that recombinant human soluble thrombomodulin (rhs-TM) is effective for disseminated intravascular coagulation (DIC) in vivo, in mice and rats. In the present work, we investigated the effects of decreased plasma antithrombin III (ATIII) levels on anticoagulant effects of rhs-TM, as compared to findings with heparin, of which effect is lowered by the decreased plasma ATIII levels in patients with DIC. Rat plasma ATIII levels decreased when we mixed plasma with anti-rat ATIII antibody and the potential of heparin to prolong APTT or PT was markedly diminished. The potential of rhs-TM to prolong APTT and PT was not affected. In rats injected with anti-rat ATIII antibody, plasma ATIII levels decreased immediately. When the rats were infused with tissue factor (TF), DIC was induced. At doses of rhs-TM and heparin which were equally effective at inhibiting the decrease in platelet count and fibrinogen level in control rats treated with TF, only rhs-TM remained effective in preventing DIC in rats with reduced ATIII levels. Heparin was not effective when administered to these rats with reduced ATIII levels. Therefore, rhs-TM effectively inhibits coagulation independent of ATIII levels, in contrast to heparin, which depends on the ATIII level.

Animals↗