Biomedical subjects

T Kumada

Publications and source records attributed to T Kumada.

At least 127 records · Page 7Linked to original sources

PubMed1989

Assessment of transesophageal Doppler echography in dissecting aortic aneurysm.

To assess the clinical value of transesophageal Doppler echography in the diagnosis of dissecting aortic aneurysm, both transesophageal and conventional echograms were performed in 22 cases of dissecting aortic aneurysm. Of the 22 patients, 17 underwent angiography; 8, X-ray computed tomography; 4, both; and 12, surgery. The performance of each method was assessed in the following four segments: A, ascending aorta; B, aortic arch; C, thoracic descending aorta; and D, upper abdominal aorta. The results by angiography were presumed to be correct. In the group of 17 patients who underwent angiography, the rate of correct detection of an intimal flap using the transesophageal approach was 100% in all four segments, significantly better than detection by the conventional approach (segment A, 65%; segment B, 47%; segment C, 35%; segment D, 53%) (p less than 0.01), and the rate of correct detection of the entry sites using the transesophageal approach was 100%, significantly better than that by conventional approach (42%) (p less than 0.05). X-ray computed tomography was not capable of detecting the site of entry in all cases. The presence of thrombus, aortic regurgitation and pericardial hemorrhage were all revealed clearly by the transesophageal approach, and the results were partly proved by other methods. In conclusion, transesophageal Doppler echography provides a rapid and accurate method of diagnosing and evaluating dissecting aortic aneurysm and permits prompt initiation of appropriate treatment.

Adult↗

PubMed1989

Usefulness of negative dP/dt upstroke pattern for assessment of left ventricular relaxation in coronary artery disease.

It has been reported that regional asynchrony due to acute ischemia disturbs the exponential nature of left ventricular (LV) pressure reduction and may alter the pattern of (-)dP/dt upstroke curve. If LV pressure decreases exponentially during the isovolumic relaxation period (P = Ae-t/T + B, where A and B = constants, t = time and T = time constant), the (-)dP/dt upstroke curve should also be exponential and upward-convex because dP/dt = A(-t/T)e-t/T. To test this theory in humans, the LV (-)dP/dt upstroke curve was analyzed in 9 normal subjects, 12 patients with effort angina pectoris (AP) and 15 with old myocardial infarction (MI) under the basal conditions. The (-)dP/dt upstroke was convex-upward in all normal subjects, but convex-downward in 9 of 12 patients with AP and in all patients with MI, which suggests nonexponential decrease in LV pressure in the groups with AP and MI. The dP/dt (20/60), which is the ratio of the (-)dP/dt value at 20 ms after peak (-)dP/dt to that at 60 ms after peak (-)dP/dt, was significantly lower in the group with AP (1.70 +/- 0.07) and in the group with MI (1.61 +/- 0.13) than in normal subjects (2.08 +/- 0.18) (p less than 0.005). This indicates that (-)dP/dt upstroke 20 to 60 ms after peak (-)dP/dt increases more slowly in the groups with AP and MI than in normal subjects. Theoretical consideration showed that such a slower increase of the upstroke resulted from impaired early to midrelaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Can new inodilators displace digitalis in the therapy of congestive heart failure?

New inodilators that possess both positive inotropic and vasodilator actions have many favorable effects in patients with congestive heart failure, even in those with refractory heart failure. These effects are expected to prevent myocardial injury, improve peripheral circulation, depress the excessive endogenous neurohumoral activation, and, finally, improve the quality of life, and increase lifespan. However, experience with new inodilators has only begun. Several questions remain to be answered before these drugs can be widely used with safety, including whether life-threatening adverse effects appear, mortality rate is lessened, and drug tolerance occurs. The therapeutic level of the dose and the relation between the effectiveness of the drug and the degree of the severity of heart failure should also be established. Therefore, long-term, randomized, double-blind, placebo-controlled clinical trials will be necessary before the new inodilators can take the place of digitalis and thus become the mainstay of the therapy of congestive heart failure.

Cardiotonic Agents↗

PubMed1989

Transcription of thrombomodulin mRNA in mouse hemangioma cells is increased by cycloheximide and thrombin.

We have measured mRNA levels for thrombomodulin, an endothelial membrane cofactor for the activation of protein C by thrombin, in a mouse hemangioma cell line. Cycloheximide, an inhibitor of protein synthesis, increased levels of thrombomodulin mRNA, as measured in an S1 nuclease protection assay, to 2.5-4.0 times control levels. Thrombomodulin transcription in response to cycloheximide treatment, as determined by nuclear run-on analysis, was 3.9 +/- 1.3 (mean +/- SD) times that found in untreated cells. Thrombin also increased thrombomodulin mRNA levels to 151 +/- 21% (mean +/- SD) of control levels after 2 hr. Transcription increased in response to thrombin by 2.1- to 7.3-fold. The combination of thrombin and cycloheximide had no additive effect on thrombomodulin mRNA levels. Thrombin treatment of hemangioma cells also caused an increase in thrombomodulin protein synthesis to 142 +/- 17% (mean +/- SD) of control levels as determined by immunoprecipitation of [32S]methionine-labeled thrombomodulin. We conclude that thrombomodulin expression is determined in part by the rate of transcription and that thrombomodulin mRNA levels in hemangioma cells are increased by treatment with cycloheximide or thrombin. The increased transcription in response to cycloheximide suggests the existence of a labile protein repressor of thrombomodulin transcription.

Animals↗

PubMed1989

[Four cases of adult Listeria monocytogenes infection in the last 5 years--hepatic necrotic foci in the adult septic case].

We have reported on the clinical courses of 4 cases of adult Listeria monocytogenes (Lm) infection, and the autopsy findings of 2 cases, those we have observed over the past 5 years. They were 2 cases of meningitis, 1 case of meningitis and sepsis and 1 case of sepsis. These 4 cases had CML, neoplastic angioendotheliosis, SLE and post-renal transplant condition, as their underlying diseases, and all were receiving immunosuppressive therapy. One meningitis patient who recovered showed mild liver dysfunction during her clinical course. The other 3 patients who died had jaundice at the time of onset and severe liver dysfunction. The 2 cases those were autopsied were the sepsis cases. The one with an acute course and hepatic failure showed multiple miliary necrotic foci in the liver, where the presence of Lm in the cells could be verified. The other autopsy case, which had received adequate antibiotic therapy and the Lm infection had been cured, showed no necrotic foci in the liver. The case that had necrotic foci in the liver was the first such adult case in Japan. We have discussed the hepatic Lm infection in adult compromised hosts, which conventionally has not been considered a serious problem.

Aged↗

PubMed1989

Protective effect of piperacillin against the nephrotoxicity of cisplatin in rats.

The protective effect of piperacillin against the nephrotoxicity of cisplatin was compared with that of fosfomycin in Fischer 344 rats. Blood urea nitrogen, serum creatinine, and morphological changes were evaluated as the renal toxicological parameters. Rats receiving 2 mg of cisplatin per kg of body weight for 5 days showed significant (P less than 0.01 by multiple-comparison test) elevation of blood urea nitrogen and serum creatinine concentrations compared with rats receiving saline alone and also exhibited development of cell lesions in the pars recta of the tubules in the outer stripe of the outer medulla. However, piperacillin (250 and 1,000 mg/kg) significantly (P less than 0.01 by multiple-comparison test) reduced these toxicological parameters in comparison with results for cisplatin alone. The protective effect of piperacillin was superior to that of fosfomycin, although platinum levels in the kidney were higher with the combination of cisplatin and piperacillin than with cisplatin plus fosfomycin. Although the nephrotoxicity of cisplatin was also reduced when cisplatin was administered concomitantly with sodium chloride in mole-equivalents to 250 and 1,000 mg of piperacillin per kg, its protective effect was less than that of the corresponding piperacillin dose. These results suggest that piperacillin may have a role as a protective agent against the nephrotoxicity of cisplatin.

Animals↗

PubMed1989

Effect of diltiazem on aortic pressure-diameter relationship in dogs.

To study the effects of diltiazem (Dz) on aortic (Ao) pressure-diameter (P-D) relationships, the external diameter (D) of the thoracic Ao (sonomicrometry) and Ao pressure (AoP, micromanometer) were simultaneously measured in 10 anesthetized dogs. The P-D relationship from 80 ms after the dicrotic notch of AoP (t80) to 20 ms after the peak of the next R wave on the electrocardiogram (ECG) (t20) was plotted at 30-ms intervals. To depict the P-D relationship in a wide range of AoP, Ao occlusion immediately after the release of inferior vena caval (IVC) occlusion was performed both before and after a Dz (0.03 mg.kg-1.min-1, over 10 min) infusion. The P-D relationship so obtained was a sigmoid curve under both conditions and was reasonably described by a cubic curve (P = aD3 + bD2 + cD + d, where a, b, c, and d are constants and r greater than 0.99). The first derivative of cubic regression equation (dP/dD) value of the cubic curve was used as an index of Ao stiffness. In all dogs, the dP/dD-D relationship, which was parabolic, was similar to the delta P/delta D-D relationship measured from the actual P-D relationship (delta P/delta D is the ratio of the change in AoP to that in AoD), suggesting that it corresponded to a cubic curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Liver function in congestive heart failure: abnormal elevation of serum hepatic enzyme and hepatic venous flow velocity.

Fifty one patients (pts) with various heart diseases and 6 normal subjects (N) were studied. Four of the 51 pts showed unusually high GOT values (greater than 3000 IU) without preceding evidence of acute heart failure, myocardial infarction, or hepatitis. Of these 4 pts, either ventricular tachyarrhythmias, marked bradycardia, or rapid ventricular response with atrial fibrillation (af) were evident a few days prior to the GOT elevation. GOT values returned to below 100 IU within a few days, but hypotension and frequent arrhythmias were sustained in 3 of the 4 pts and these 3 pts died about one month later. The symptoms of the remaining one improved but he too died 9 months later of ventricular fibrillation. A postmortem histological examination revealed centrilobular necrosis of the liver cells. Thus, abnormal GOT elevation may result from hepatic cell necrosis, which is probably due to tissue hypoperfusion caused by severe arrhythmias. Hepatic venous flow velocity (HFV) was measured in the remaining 47 pts and 6N using a pulsed doppler echocardiogram. The HFV curve was biphasic, with the first curve corresponding to the forward flow velocity during ventricular systole (s-HFV) and the second corresponding to ventricular diastole (d-HFV). The ratio of the area under s-HFV curve to the sum of areas under s-HFV and d-HFV curves was defined as the VI ratio. In N, the VI ratio was 0.7 +/- 0.06 whereas the VI ratio in pts in sinus rhythm tended to be above 0.7. This indicated that s-HFV is greater than d-HFV in N while s-HFV is less than d-HFV in pts in sinus rhythm. There was a good negative correlation (n = 15: r = -0.70) between VI ratio and cardiac index (CI) in these pts, suggesting that the contribution of s-HFV to the venous return becomes greater as the cardiac function becomes more impaired. In pts with af, the VI ratio was below 0.5 and there was a good positive correlation (n = 14: r = 0.82) between the VI ratio and CI. This suggested that the s-HFV may be reduced due to a lack of atrial contribution in af so that contribution of d-HFV to venous return becomes greater as the cardiac function becomes more impaired. Thus, the HFV pattern may reflect the abnormality of the cardiac pump function in human beings.

Adult↗

PubMed1989

The effect of left ventricular wall motion during isovolumetric relaxation period in coronary artery disease.

The effect of the left ventricular (LV) regional wall motion during isovolumetric relaxation period (IRP) were studied in 9 patients with old anteroseptal myocardial infarction (OMI) and 8 normal subjects (NOR). There were no significant differences in heart rate, peak LV systolic pressure and peak (+) dP/dt between the groups. LV cavity was divided into the anterior and inferior sides by a long axis, which was equally divided with 3 perpendicular lines, creating 4 areas in each side. The sums of the 2 middle areas in each side were defined as Aa and Ab, respectively. During IRP the pattern of (-) dP/dt at the upstroke phase was convex-downward in OMI, but convex-upward in NOR. Time constant (T) was significantly prolonged in OMI compared with NOR (50 +/- 9 vs 37 +/- 6 msec; p less than 0.01). On NOR, Aa increased significantly after 33.4 msec from peak (-) dP/dt, while Ab remained unchanged. In OMI, Ab increased after 50.1 msec from peak (-) dP/dt, associated with decrease in Aa, suggesting the passive shortening of the anterior wall by the active expansion of the inferior. Such asynchronous LV wall motions during IRP might impair LV relaxation and influence the upstroke pattern of (-) dP/dt.

Adult↗

PubMed1989

[Transesophageal Doppler echocardiography in the diagnosis of dissecting aortic aneurysm].

Transesophageal Doppler echocardiography (TEDE) was performed in three patients with proven or suspected DeBakey type I and type III aortic dissection. Case 1: A 66-year-old woman, with DeBakey type I aortic dissection. Clear images of a widened dissected aorta and an intimal flap were obtained in both the ascending and descending aorta, including the aortic arch. The site of an entry into the false lumen was identified by the defect of the intimal flap and the pulsatile entry flow through it. The reentry into the true lumen was also identified near the orifice of the celiac trunk. In this case, the observation was performed using this technique during the operation; i.e., replacement of the ascending aorta with an artificial graft. Case 2: A 77-year-old man, DeBakey type III aortic dissection. The study was performed after surgery which consisted of replacement of the descending aorta with an artificial graft. TEDE provided clear images of the artificial graft, the aorta, and their boundaries. The remaining intimal flap was clearly confirmed. Case 3: An 80-year-old man, DeBakey type III aortic dissection. In this case, though abdominal echography suggested aortic dissection, angiography and X-ray CT failed to facilitate the diagnosis. Only TEDE confirmed the diagnosis. The abnormal flow via the entry directing toward the false lumen was clearly demonstrated on the color Doppler images. We therefore conclude that TEDE is a useful and reliable means of diagnosing dissecting aortic aneurysm.

Aged↗

PubMed1988

The structure and function of mouse thrombomodulin. Phorbol myristate acetate stimulates degradation and synthesis of thrombomodulin without affecting mRNA levels in hemangioma cells.

Thrombomodulin is an endothelial membrane anticoagulant protein that is a cofactor for protein C activation. We have evaluated the expression of thrombomodulin in cultured mouse hemangioma cells before and after treatment with phorbol myristate acetate (PMA), an agent that stimulates protein kinase C. We also isolated a cDNA encoding 481 amino acids of mouse thrombomodulin and the entire 3'-untranslated portion of its mRNA. The deduced amino acid sequence of mouse thrombomodulin is similar to those determined for human and bovine thrombomodulin. An S1 nuclease protection assay was used to measure thrombomodulin mRNA in hemangioma cells. The half-life for thrombomodulin mRNA was 8.9 +/- 1.8 h (S.D.) in cells treated with actinomycin D. Treatment with PMA had no effect on thrombomodulin mRNA levels. Thrombomodulin turnover was evaluated by immunoprecipitation of [35S]methionine-labeled thrombomodulin. The t1/2 was 19.8 +/- 3.9 h (S.D.); PMA treatment decreased the t1/2 to 10.9 +/- 1.1 h (S.D.) while increasing the rate of synthesis to a maximum of 190% of control. Protein C cofactor activity on hemangioma cells was reduced 35 +/- 4% by treatment with PMA within 30 min. This decrease was associated with a parallel decline in cell surface thrombomodulin antigen and with enhanced phosphorylation of thrombomodulin on serine residues. We conclude that thrombomodulin is phosphorylated in response to treatment of hemangioma cells with PMA which leads to decreased protein C cofactor activity and both increased degradation and synthesis of thrombomodulin.

Amino Acid Sequence↗

PubMed1988

Recurrent left ventricular mural thrombi in a patient with acute myocarditis.

A case of acute myocarditis with recurrent left ventricular mural thrombi in a 59-year-old man is reported. Two-dimensional echocardiogram demonstrated left ventricular mural thrombus with apical dyskinesis on the 2nd day after the onset of chest oppression. No hemoagglutination abnormalities were present. Anticoagulation treatment with heparin was initiated. A two-dimensional echocardiogram obtained on the 15th day showed that the left ventricular wall motion had become normal and that the thrombus had disappeared. However, on the 38th day, a new pedunculated free mobile thrombus was found in the apical part of the left ventricle despite the normal wall motion. By the 46th day, the new thrombus had disappeared. The present case suggests that mural thrombi can occur in the absence of left ventricular dyskinesis and dilatation. Anticoagulation therapy resolved the mural thrombi but could not prevent the recurrence at the apex. Thus, in acute myocarditis, a mural thrombus may appear as a result of the endocardial damage, even when blood stasis is absent.

Acute Disease↗

PubMed1988

Protective effect of piperacillin against nephrotoxicity of cephaloridine and gentamicin in animals.

The protective effect of piperacillin against the nephrotoxicity of cephaloridine and gentamicin was examined in experimental animals. In rabbits, piperacillin was infused at a dose of 1 mg/kg (body weight) per min over 225 min and cephaloridine (300 mg/kg) was intravenously administered as a bolus 45 min after the start of a drip infusion. Blood urea nitrogen, serum creatinine, and N-acetyl-beta-D-glucosaminidase (NAG) in urine were measured as the renal toxicological parameters before and 24 h after cephaloridine dosing. Although the single administration of cephaloridine significantly elevated these parameters, the elevation was prevented by the concomitant administration of piperacillin. The protective effect of piperacillin was superior to those of cephalothin and fosfomycin. In rats, piperacillin (1,000 mg/kg) was intravenously administered and immediately followed by the intramuscular administration of gentamicin (100 mg/kg) every 24 h for 5 days. When piperacillin was concomitantly administered with gentamicin, the elevations of blood urea nitrogen, serum creatinine, and urinary NAG were significantly lower than when gentamicin was given alone. The concomitant administration of piperacillin resulted in a significant protective effect against the nephrotoxicity of cephaloridine in rabbits and of gentamicin in rats. Histopathological observation also supported the protective effect of piperacillin. The protective mechanism of piperacillin might be the inhibition of transport from the peritubular side to tubular cells for cephaloridine and from both the peritubular and luminal sides for gentamicin.

Animals↗

PubMed1988

Effect of afterload on the left ventricular pressure fall during isovolumic relaxation period in man.

To assess the effect of afterload on the left ventricular pressure (LVP) fall during isovolumic relaxation period (IRP) in man, we examined the peak (-)dP/dt, (-)dP/dt upstroke pattern in IRP, and time constant (T) in 15 patients [normal (N): 5 valvular heart disease (VHD): 5, dilated cardiomyopathy (DCM): 5]. LVP and echocardiographic internal diameter were measured simultaneously at rest and after about 30 mmHg increment of LV peak systolic pressure (PSP) by drip infusion of angiotensin (20 ng/kg/min). After augmentation in afterload, heart rate (HR) increased slightly in VHD. T increased significantly (p less than 0.05) in N (from 32 +/- 3 to 39 +/- 4 ms) and DCM (from 56 +/- 18 to 72 +/- 12 ms), but not in VHD (from 41 +/- 5 to 46 +/- 8 ms) probably due to increased HR. LV end-systolic dimension had the same trend as T. Although there was no significant change in peak (-)dP/dt in N (from 1937 +/- 385 to 1945 +/- 189 mmHg/s), VHD (from 1521 +/- 210 to 1730 +/- 462 mmHg/s), or DCM (from 814 +/- 143 to 814 +/- 131 mmHg/s), the (-)dP/dt upstroke pattern during IRP became nonexponential in N and more downward convex in VHD or DCM. Thus, these changes of T and (-)dP/dt upstroke pattern suggest the afterload dependence of LVP fall during IRP in normal and diseased hearts.

Adult↗

PubMed1988

[Distribution of spatial attention in position recognition].

Spatial limitation in visual information processing was examined with dot-in-matrix patterns by using a probe recognition procedure. The independent variables were the number (1-16 dots) and the position of target dots. Subjects were four undergraduate students. The data were analyzed and discussed from three points of view; span of attention, spatial limitation of recognition and visual attention. The following became clear: First, the span of position recognition was 4.8. Second, "spatial span of attention" was defined as the range of dot positions at which subjects can perceive target dots with 75% or more accuracy. It extended around the fixation point and shrinked with the increase of the number of target dots. Finally, the distribution of spatial attention was estimated for each target dot condition under the assumption that the hit RT at each probe position reflects the amount of attention allocated there. Distributions estimated were cone-shaped, and the height and extent changed with the number of target dots. It was suggested that spatial limitation (i.e. spatial span of attention) in the processing of spatial positions can be explained by the notion of distribution of spatial attention.

Attention↗

PubMed1988

A role for thrombomodulin in the pathogenesis of thrombin-induced thromboembolism in mice.

The antithrombotic action of thrombomodulin was studied in mice. Rat and mouse thrombomodulin were isolated from lung acetone powders, and anti-rat thrombomodulin antibodies were prepared in rabbits. The antibodies neutralized both mouse (Kd approximately 150 nM) and rat thrombomodulin (Kd approximately 50 nM). A role for thrombomodulin in vivo was shown in mice injected intravenously (IV) with thrombin. All mice injected with 15 U thrombin (bolus) died of thromboembolism (mean survival 55 minutes), whereas those injected with a lower dosage survived. Prior injection with anti-rat thrombomodulin (1.8 mg IgG/mouse) potentiated the lethal effects of subsequent thrombin, whereas injection of thrombomodulin (isolated from mouse lung) prior to thrombin prolonged survival in a thrombomodulin concentration-dependent manner. The protective effect of thrombomodulin persisted for 30 minutes but after one hour thrombin injection was as toxic as in control animals. The half life (t1/2) for plasma clearance of 125I-mouse lung thrombomodulin was nine minutes. The major site of clearance was the liver, although thrombomodulin accumulated in several organs ten minutes after injection. The mechanism by which antithrombomodulin antibodies potentiated the lethal effects of thrombin was studied by measuring the protein C activating cofactor activity on vena cava removed from animals injected with antibodies. Protein C activation was inhibited by antibodies, suggesting a role for activated protein C in prevention of lethal thromboembolism. We found no effect of antibodies on the clearance of thrombin from mouse plasma, suggesting that blockade of endothelial endocytosis of thrombin does not play a significant role in the effects of antibodies. These results indicate that thrombomodulin participates in the defense against thrombosis in vivo.

Animals↗

PubMed1988

[Venous flow velocity patterns and cardiac function studied by Doppler echocardiography].

To study the relations of central venous flow velocity (VFV) to cardiac pump function, hepatic venous flow velocity was recorded using Doppler echocardiography in six normal subjects and 47 patients with heart disease, of whom 28 had sinus rhythm and 19, atrial fibrillation. The area under the VFV profile during systole and diastole in a cardiac cycle was computed, and termed the VIs (systolic time-velocity integral) and VId (diastolic time-velocity integral), respectively. VIs was divided by the sum of VIs and VId [VIs/(VIs + VId)], and this was termed the VI ratio. The cardiac index (CI) was estimated by Doppler echocardiography. In normal subjects, the VFV pattern in a cardiac cycle was biphasic, the systolic VFV being dominant. In patients with atrial fibrillation, the systolic VFV was attenuated or absent, the diastolic VFV being dominant. The CI correlated well with the VI ratio (r = 0.80; p less than .001) in 14 patients with atrial fibrillation except for five patients with tricuspid regurgitation. Four patients in whom atrial fibrillation converted spontaneously to sinus rhythm showed an increase in the CI and the VI ratio according to the CI-VI ratio relationship. In patients with sinus rhythm, the CI tended to decrease as the VI ratio increased. In 15 patients who had a VI ratio of over 0.75, the CI correlated inversely with the VI ratio (r = -0.70; p less than 0.01). Three of four patients who had the VI ratio of 1.0 died of congestive heart failure. Although there was positive correlation between the CI and VI ratio in patients without effective atrial contraction, there was inverse correlation in patients with effective atrial contraction. It is suggested that the VI ratio could be a good indicator of cardiac pump function.

Adolescent↗

PubMed1987

Evaluation of aortic wall distensibility by aortic pressure-dimension relation: effects of nifedipine on aortic wall.

The relation between aortic pressure and dimension was studied before and after nifedipine infusion in eight anaesthetised dogs. An electromagnetic flowmeter was positioned in the proximal ascending aorta and one pair of ultrasonic dimension gauges attached to the thoracic aorta. A Millar micromanometer was positioned just below the dimension gauges. A constrictor was placed around the thoracic aorta distal to the dimension gauges to produce an abrupt rise in aortic pressure for 15 s. After complete recovery nifedipine (0.75 micrograms.kg-1.min-1) was infused for 10 min and the same procedure repeated. The ratio (delta D:delta P) of the difference (delta D) between maximum and minimum dimensions (D) to the pulse pressure (delta P) and the percentage distensibility (delta D/delta P/minimum D) were decreased significantly after aortic constriction (0.037(0.013) to 0.019(0.004) mm.mmHg-1 and 0.247(0.075) to 0.121(0.033)%.mmHg-1, p less than 0.01, respectively), suggesting that these indices depend on afterload. Beat to beat mean pressure-dimension relations during the release of aortic constriction showed a convex upward curve and was fitted by an exponential function with a high correlation coefficient (r = 0.99). The slope of this relation was significantly reduced after nifedipine compared with before nifedipine (379(83) to 330(119) mmHg.cm-1, p less than 0.05), suggesting an increase in aortic distensibility by nifedipine. When mean aortic pressure or stroke volume before and after nifedipine was compared at the same mean dimension, which was reduced by 5% of the control mean dimension, stroke volume increased to 128%(p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗