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Biomedical subjects

T Kamada

Publications and source records attributed to T Kamada.

At least 613 records · Page 34Linked to original sources
PubMed1989

Role of alpha 1-adrenoceptor activity in progression of cardiac hypertrophy in guinea pig hearts with pressure overload.

To elucidate the role of alpha 1- and beta-adrenergic activities in pressure overload hypertrophy, changes of alpha 1- and beta-adrenoceptors were measured by radioligand binding assay, and the preventive effects of alpha 1- and beta-adrenoceptor blockade on cardiac hypertrophy were assessed in guinea pigs after aortic banding. Five days after banding, dry weight of left ventricle had not increased, though wet weight increased due to marked intercellular oedema. In this period, the maximum binding capacity of [3H] prazosin increased to 31.1 (SEM 2.2) fmol.mg-1 from (sham operation) 17.0(2.1) fmol.mg protein-1, p less than 0.01, whereas the maximum binding capacity of [3H]dihydroalprenolol did not increase: 143(16) fmol.mg-1 (banded) v 153(13) fmol.mg-1 (sham). Three weeks after aortic banding, the maximum binding capacity of both ligands increased to 45.6(5.5) fmol.mg-1 and 232(21) fmol.mg-1, respectively, accompanied by a significant increase in left ventricular dry weight, from 0.46(0.02) mg.g-1 (sham) to 0.62(0.08) mg.g-1 (banded), p less than 0.01. Continuous subcutaneous administration of the alpha 1-blocker bunazosin (0.1 mg.kg-1.d-1) significantly attenuated the increase in left ventricular dry weight whereas the beta-blocker propranolol (5 mg.kg-1.d-1) did not: 0.55(0.03) v 0.66(0.04) mg.g-1 respectively, after 3 weeks. These results show that pressure overload elicited an increase in myocardial alpha 1-adrenoceptors before the onset of cardiac hypertrophy, and that an alpha 1-blocker could prevent the development of hypertrophy in the pressure overloaded heart.

Adrenergic alpha-Antagonists↗
PubMed1989

Role of free radicals and neutrophils in canine myocardial reperfusion injury: myocardial salvage by a novel free radical scavenger, 2-octadecylascorbic acid.

To define the role of oxygen free radicals and neutrophil involvement in evolving myocardial reperfusion injury, we evaluated the effect of 2-octadecylascorbic acid (CV-3611), a novel free radical scavenger, on neutrophil function and the extent of myocardial damage resulting from 90 min of ischaemia followed by 5 h of reperfusion in an experimental model of myocardial infarction. Dogs were randomly assigned to receive CV-3611 (5 mg.kg-1.[5 min]-1, intravenously) just before the onset of reperfusion. Infarct size, as a percent of area at risk, was reduced by 60% in CV-3611 treated group as compared with control, at 16.7(SEM 3.1)% v 41.5(4.5)%, p less than 0.01. Administration of CV-3611 markedly reduced function of neutrophils isolated from peripheral circulation during reperfusion ex vivo as estimated by free radical generation (ferricytochrome c reduction and luminol enhanced chemiluminescence), chemotactic activity, and aggregation induced by A23187. Under these conditions, the enhancement in neutrophil infiltration and free radical generation (luminol enhanced chemiluminescence) in myocardium within area at risk, especially in the border zone between viable and irreversible injured myocardium, was markedly reduced. Haemodynamic profiles were similar between control and CV-3611 treated group. These results suggest that activated neutrophils, especially their generation of oxygen free radicals, contribute to reperfusion induced myocardial injury.

Animals↗
PubMed1989

An increase in myocardial beta-adrenoceptors to compensate for postischaemic dysfunction following coronary micro-embolisation in dogs.

This study examined whether beta-adrenoceptors increase in number during recovery from prolonged myocardial stunning and whether they compensate for lack of physiological response to beta-adrenergic stimulation in this abnormality. The left coronary artery was embolished in anaesthetised dogs with non-labelled microspheres (15 +/- 1 micron; 1.2 X 10(6).kg-1 body weight). Haemodynamic studies were performed before (control) and 24 h and 1 week after embolisation, in the conscious state. Myocardial noradrenaline content, plasma catecholamine concentrations and the density of beta-adrenoceptors (Bmax) were also assessed at three study intervals. At 24 h after embolisation, both systolic and diastolic cardiac function was significantly depressed. The inotropic response to isoprenaline was preserved, but the response to forskolin was markedly depressed. One week after embolisation, resting systolic function was restored to control levels and histological examination showed absence of myocardial necrosis. Although plasma noradrenaline concentration had returned to normal, myocardial noradrenaline content had decreased by 36% and the density of beta-adrenoceptors had increased by 48%. Myocardial relaxation was still impaired and the inotropic response to forskolin was also still depressed, whereas the response to isoprenaline was normal. Moreover, the down regulation of the increased beta-adrenoceptors by isoprenaline infusion for 24 h unmasked the latent systolic dysfunction. These results indicate that the density of beta-adrenoceptors increases during the recovery process from prolonged myocardial stunning and that this increase may compensate, at least in part, for impairment of the inotropic mechanism distal to the beta-adrenoceptors.

Animals↗
PubMed1989

Prediction of arterial oxygen partial pressure from intrapulmonary venous admixture.

A short program was developed to predict the PaO2 at a given FIO2 by using arterial and mixed venous blood gas data obtained at an FIO2 of 1.0. Our program resolves Adair's equation and the shunt equation inversely, on the assumption that intrapulmonary venous admixture and the arteriovenous oxygen content difference remain constant during the study. The study was conducted on 19 patients with respiratory failure who were intubated and mechanically ventilated. According to linear regression analysis, regression coefficients of 0.91 and 0.97 were obtained between the measured PaO2 values and those estimated by the arterial/alveolar oxygen tension ratio (PaO2/PaO2) and our program, respectively (n = 23). The PaO2 values were predicted more accurately by our program than those calculated by PaO2/PaO2. Because our program is simple enough to be carried out with a pocket computer, it may be helpful in a bedside decision of lowering FIO2, especially in patients who require a high FIO2 level to maintain sufficient arterial oxygenation.

Blood Gas Analysis↗
PubMed1989

Alpha 2-adrenoceptor stimulation can augment coronary vasodilation maximally induced by adenosine in dogs.

To determine whether alpha 2-adrenoceptor stimulation can augment adenosine-induced coronary vasodilation, 34 open-chest dogs were studied. When a small dose of clonidine (up to 0.24 micrograms.kg-1.min-1 ic) was administered under beta-adrenoceptor blockade, coronary blood flow [312 +/- 16 (SE) ml.100 g-1.min-1] maximally induced by intracoronary infusion of adenosine was further increased (P less than 0.05) by 66 +/- 16 ml.100 g-1.min-1, despite no significant changes in coronary perfusion pressure, myocardial oxygen consumption, and coronary venous adenosine concentration. However, when a larger dose of clonidine (0.36-0.60 micrograms.kg-1.min-1) was infused, adenosine-induced flow progressively decreased. This biphasic action of the alpha 2-adrenoceptor activity was also observed when the dose of norepinephrine was increased during alpha 1-adrenoceptor blockade with prazosin. Norepinephrine up to 0.24 micrograms.kg-1.min-1 (ic) further increased adenosine-induced coronary blood flow by 24 +/- 5% (P less than 0.001), whereas hyperemic flow was decreased by a larger dose of norepinephrine. In contrast to the alpha 2-adrenoceptor stimulation, the alpha 1-adrenoceptor stimulation (norepinephrine with yohimbine) progressively decreased coronary blood flow. Furthermore, with a small dose of clonidine, reactive hyperemic flow significantly increased compared with that without clonidine (303 +/- 13 vs. 355 +/- 13 ml.100 g-1.min-1, P less than 0.001), but a larger dose of clonidine adversely reduced reactive flow (254 +/- 18 ml.100 g-1.min-1, P less than 0.001). Adenosine release during reactive hyperemia with and without intracoronary infusions of clonidine were not altered significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Adenosine-induced hyperemia attenuates myocardial ischemia in coronary microembolization in dogs.

We have recently reported that coronary microembolization sustains myocardial ischemia with hyperemic response of coronary blood flow (CBF) induced by massive release of adenosine from the ischemic myocardium. In this study, we tested the hypothesis that this hyperemic flow caused by released adenosine improves myocardial ischemia. In eight dogs (control), microspheres (5.0 X 10(4)/ml of base-line CBF) were repetitively injected until CBF decreased toward zero, and the changes in CBF, fractional shortening, lactate extraction ratio (LER), and adenosine release were studied. In 15 other dogs, an identical procedure was done with an intracoronary infusion of prazosin (4 micrograms.kg-1.min-1, n = 8) or theophylline (0.1 mg.kg-1.min, n = 7) to elucidate the effect of adenosine, since prazosin inhibits release of adenosine from ischemic myocardium and theophylline blocks adenosine receptors. In 16 other dogs, hemodynamic and metabolic parameters were examined with and without these drugs after a single injection of microspheres (1.0 X 10(5)/ml of base-line CBF). In the control group, CBF increased to 170 +/- (SE) 14% of the base-line CBF at 16-30% of maximal embolization. In contrast, intracoronary infusion of prazosin markedly attenuated adenosine release and hyperemic response and significantly deteriorated both fractional shortening and LER. Theophylline also significantly attenuated the hyperemic response and tended to decrease both fractional shortening and LER. A salutary effect of adenosine release was further confirmed by the improvement of ischemic changes in the same dog after withdrawal of prazosin and theophylline associated with an increase in CBF. Thus we conclude that adenosine released from ischemic myocardium improves ischemia in microembolization through the hyperemic response.

Adenosine↗
PubMed1989

Furosemide accelerates gentamicin accumulation in cultured renal cells (LLC-PK1 cells).

Furosemide is known to potentiate gentamicin nephrotoxicity. The mechanism of potentiation is unclear. In our previous studies, we demonstrated that furosemide enhanced gentamicin accumulation in rabbit renal tissues when injected as a bolus [Kidney int. 33:363, 1988] or repeatedly subcutaneously [Diuretics II, Elsevier, New York 1987, pp.693]. In this study, we evaluated the effects of furosemide on gentamicin accumulation in cultured renal cells (LLC-PK1) and hepatoma cells (H4IIE). Thus, we excluded effects secondary to furosemide-elicited hemodynamic changes. Seven days after seeding, the culture medium was exchanged for medium containing 1 mM gentamicin alone [G] or 1 mM gentamicin +1 mM furosemide [GF]. In LLC-PK1 cells, gentamicin concentration in [GF] was significantly higher than that in [G], while gentamicin was not detected in H4IIE cells with or without furosemide. We conclude that furosemide can accelerate gentamicin accumulation in renal tissues and potentiate gentamicin nephrotoxicity.

Animals↗
PubMed1989

Visualization of subendocardial myocardial ischemia with myocardial contrast echocardiography in humans.

Previous studies indicate the degree of myocardial echo contrast enhancement may be related to regional myocardial perfusion. In this study, myocardial contrast echocardiography was used to characterize changes in the transmural myocardial blood flow distribution that were provoked by rapid atrial pacing in 11 patients with one-vessel coronary artery disease. Ten patients without coronary artery disease served as controls. Myocardial contrast echocardiography was performed by intracoronary injection of 2 ml hand-agitated amidotrizoate sodium meglumine (Urografin-76) and by imaging a short-axis view of the left ventricle with two-dimensional echocardiography before and during injection of the contrast agent. The two-dimensional echocardiographic images at end diastole, before and after injection of the contrast agent, were digitized off-line into a 512 x 512 pixel matrix with 256 gray levels/pixel to quantify the degree of the enhancement of the peak gray level after injection. Transmural myocardial blood flow distribution was evaluated by measuring the ratio of the enhanced gray level in the endocardial half (endo) to that in the epicardial half (epi) (endo:epi gray level ratio) in the anteroseptal, posterolateral, and inferior segments before and just after rapid atrial pacing in each patient. In patients without coronary artery disease, there were no differences in the endo:epi gray level ratio between any of the three segments both before and after pacing. Mean values of the three segments were 0.95 +/- 0.08 before pacing and 0.90 +/- 0.13 after pacing, respectively. In contrast, in patients with coronary artery disease, the endo:epi gray level ratio for the segment supplied with stenotic coronary artery decreased after pacing (0.40 +/- 0.21 vs. 0.93 +/- 0.18, p less than 0.01), probably reflecting subendocardial myocardial ischemia, whereas that for the segment supplied with nonstenotic coronary artery remained unchanged (0.88 +/- 0.20 vs. 0.99 +/- 0.23, NS). Thus, changes in transmural myocardial blood flow distribution with rapid pacing, which may be due to transient subendocardial ischemia, are visualized with myocardial contrast echocardiography.

Adult↗
PubMed1989

Beneficial effects of alpha 2-adrenoceptor activity on ischemic myocardium during coronary hypoperfusion in dogs.

We have previously reported that alpha 2-adrenoceptor stimulation enhances adenosine-induced coronary vasodilation. In the present study, we tested the hypothesis that alpha 2-adrenoceptor activity exerts beneficial effects on myocardial ischemia through augmentation of vasodilatory effects of released adenosine. In open-chest dogs, the left anterior descending coronary artery was perfused through an extracorporeal bypass tube from the carotid artery. Propranolol was infused into the bypass tube to exclude the metabolic effects of norepinephrine. When clonidine (0.24 micrograms/kg/min i.c.) was infused for 10 minutes after reduction of coronary blood flow by partial occlusion of the bypass tube, coronary blood flow was increased by 43% from 27 +/- 1 ml/100 g/min despite no changes in coronary perfusion pressure (38 +/- 5 mm Hg) and a slight decrease in adenosine release. Both fractional shortening and lactate extraction ratio of the perfused area were significantly improved (fractional shortening, 1.8 +/- 1.0 to 10.9 +/- 1.5%, p less than 0.001; lactate extraction ratio, -57.8 +/- 6.5 to -31.9 +/- 2.4%, p less than 0.005). Identical results were observed in the denervated hearts, indicating that the beneficial effect of clonidine is not attributed to the prevention of norepinephrine release from the sympathetic nerve terminals. The beneficial effects of clonidine were prevented by yohimbine, an alpha 2-adrenoceptor blocking agent. An adenosine receptor antagonist, 8-phenyltheophylline, also prevented the beneficial effects of clonidine, indicating that these beneficial effects are mediated by effects of adenosine. Furthermore, the extent of augmentation of coronary flow in the ischemic heart was coincided with that of augmentation of exogenous adenosine-induced hyperemic flow (40%) by clonidine. Production of cyclic AMP in the coronary artery during myocardial ischemia was augmented by clonidine. In 12 other dogs, myocardial ischemia was produced by intracoronary embolization of microspheres (15 microns in diameter). Clonidine enhanced (39%) the hyperemic coronary flow and improved both fractional shortening and lactate extraction ratio. Thus, we conclude that alpha 2-adrenoceptor stimulation can ameliorate myocardial ischemia mainly due to enhancement of vasodilatory effects of adenosine released from the ischemic myocardium.

Acidosis↗
PubMed1989

Portosystemic collaterals in portal hypertension: visualization by using blood-pool SPECT imaging.

Single-photon emission CT (SPECT) was performed with technetium-99m autologous RBCs in 11 patients with chronic hepatitis and in 46 cirrhotic patients with portal hypertension to determine the value of the procedure for identifying portosystemic collateral blood flow. Twenty millicuries (740 MBq) of 99mTc-RBCs, labeled by an in vivo technique, were given IV, and tomographic imaging of the intraabdominal vascular blood pool was performed. Fourteen patients with cirrhosis also had arterial portography, and 37 had scintiphotosplenoportography. In 38 of 46 patients with cirrhosis, SPECT images showed portosystemic collaterals. The coronary vein was seen in 52% of the patients, the short gastric vein in 11%, the gastrorenal or splenorenal shunt in 24%, the umbilical vein in 11%, and the anterior abdominal wall vein in 17%. Portosystemic collaterals were not shown in any of the patients with chronic hepatitis. Collaterals were identified on SPECT images in 10 of 11 patients in whom collaterals were documented by arterial portography and in all 28 patients in whom collaterals were shown by scintiphotosplenoportography. Furthermore, SPECT clearly showed a patent portal vein in three patients and the coronary vein in two patients, when these veins were not identified by means of scintiphotosplenoportography. This experience suggests that SPECT is useful for the noninvasive identification of portosystemic collaterals in patients with portal hypertension.

Adult↗
PubMed1989

The effect of DQ-2511, a newly synthesized anti-ulcer drug, on the gastric mucosal hemodynamics and ulceration in rats.

DQ-2511, which is a dopamine derivative, is a newly synthesized anti-ulcer drug. Pretreatment with DW-2511 in the hemorrhagic shock-reperfusion model in rats significantly prevented the decreases of gastric mucosal blood volume, mucosal blood oxygenation index and the ulcer formation. The decrease in gastric mucosal blood oxygenation index in hemorrhagic shock state has a linear correlation with the size of the mucosal ulcers both in DQ-2511 and control groups. The results suggested that DQ-2511 exerts its anti-ulcer activity by improving mucosal hemodynamics in hemorrhagic shock-reperfusion rat model.

Animals↗
PubMed1989

Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics. Effect of glucagon infusion.

The effect of glucagon on hepatic regional hemodynamics was investigated in patients with chronic liver disease during peritoneoscopy with reflectance spectrophotometry. When glucagon was infused intravenously in patients with a non-cirrhotic liver, the regional hepatic tissue oxygen consumption, as estimated spectrophotometrically, increased significantly, whereas the index of hepatic tissue blood volume did not change appreciably, and consequently, the oxygen saturation of hemoglobin in the hepatic tissue blood decreased. In contrast, the administration of glucagon in patients with liver cirrhosis resulted in a significant increase in the index of hepatic tissue blood volume and produced a minor increase in hepatic tissue oxygen consumption. The oxygen saturation of hepatic blood hemoglobin tended to increase in the cirrhotics. The result suggests the presence of functional vasoconstriction at the presinusoidal and/or sinusoidal vessels in the cirrhotic liver, possibly due to a decreased vasomotor activity and/or an abnormal regulatory function of vasoactive substances, which are released by glucagon.

Adult↗
PubMed1989

Enhancement of gentamicin-induced inhibition of phosphatidylinositol hydrolysis in rabbit renal proximal tubular brush-border membrane by furosemide.

Gentamicin inhibited phosphatidylinositol (PI) hydrolysis catalyzed by rabbit renal phospholipase C in a dose-dependent manner. The inhibition was potentiated by furosemide in a dose-dependent manner. Furosemide may enhance gentamicin nephrotoxicity by potentiating the inhibitory effect of gentamicin on brush-border membrane PI degradation.

Animals↗
PubMed1989

[Evaluation of function of human collateral coronary arteries using myocardial contrast echocardiography].

The morphology of collateral vessels can be imaged by coronary angiography, but no method has been available for evaluating their function. This is a report of the use of regional myocardial perfusion to visualize collateral flow by means of myocardial contrast echocardiography in 28 patients with old myocardial infarction. Myocardial contrast echocardiography was accomplished by the intracoronary injection of two ml agitated amidotrizoate sodium meglumine. Short-axis images of the left ventricle were recorded on video tape. Those images were digitized off-line into a 512 x 512 pixel matrix. Using coronary angiography, the morphology and function of the collateral vessels were evaluated, then classified as poor, moderate or good. Myocardial perfusion was evaluated using the enhanced gray level after contrast injection, and the level was compared with the morphology and degree of collateral development. The enhanced gray level was evaluated arbitrarily as 3 +/- 2 U (mean +/- S.D.) in the "poor" group; 13 +/- 6 U in the "moderate" group; and 20 +/- 11 U in the "good" group (p less than 0.01 vs the "poor" group; NS vs the "moderate" group). Regional myocardial perfusion via the collateral vessels was generally proportional to the morphology. However, there were a few discrepancies between these two parameters.

Aged↗
PubMed1989

[Estimation of myocardial viability in left ventricular regions with akinetic wall motion by postextrasystolic potentiation using list-mode radionuclide ventriculography in an interesting case with silent ischemia and with premature ventricular complexes (quadrigeminy)].

For determining an indication of percutaneous transluminal angioplasty (PTCA), a 73-year-old-man with silent ischemia and with ventricular premature complexes (quadrigeminy) were performed cardiac nuclear studies. This case had 99% stenosis in LCX (#11) and 90% stenosis in RCA (#1), and demonstrated akinetic wall motion in left ventricular (LV) inferior and posterior regions. Exercise-redistribution Tl-201 studies indicated myocardial viability in a portion of the inferior wall but not in the posterior wall. To estimate the potential contractile function in the regions with akinesis, from the list-mode data of radionuclide ventriculography, those of postsinus beats and postextrasystolic beats were separately selected and were analyzed for investigating LV wall motion and LV ejection fraction (EF). With the post-extrasystolic potentiation, LVEF increased from 36% to 45% and the systolic wall motion was augmented in the inferior wall but not in the posterior wall. From these findings we recognized the existence of myocardial viability in a portion of the inferior wall. After PTCA for the RCA lesion, improvements of the myocardial Tl-201 distribution and LV wall motion in the inferior wall were definitely observed and hence LVEF increased by 16% to contribute to an increase in exercise performance. Thus, this case indicates that the postextrasystolic potentiation is useful for determining an indication of PTCA in patients with LV asynergy, demonstrating the myocardial viability and the potential LV function.

Aged↗
PubMed1989

[Noninvasive diagnosis of cardiac involvement by technetium-99m-pyrophosphate (Tc-99m PYP) myocardial scintigraphy in 2 cases of familial amyloid polyneuropathy and 1 case of secondary amyloidosis].

To validate the significance of technetium-99m-pyrophosphate (Tc-99m PYP) myocardial scintigraphy in diagnosing cardiac amyloidosis, 2 patients with familial amyloid polyneuropathy (FAP) and 1 patient with amyloidosis secondary to chronic rheumatic arthritis were studied. All three patients had echocardiographic abnormalities, which were increased wall thickness of the interventricular septum and the left ventricular posterior wall, and granular sparkling appearance in the septum. In 2 patients with FAP, abnormal myocardial uptake of Tc-99m PYP was diffusely detected in Tc-99m PYP SPECT. In the remaining 1 patient with secondary amyloidosis, however, Tc-99m PYP SPECT showed no abnormality, although we had confirmed the presence of myocardial amyloid deposits (type AA amyloid protein) with high amount in the histological examination. Thus, these results indicate that Tc-99m PYP scintigraphy may have a limitation in detecting cardiac involvement in secondary amyloidosis although it is useful in FAP.

Adult↗
PubMed1989

[Radial long-axis tomography: a new reconstructing algorithm for thallium-201 myocardial SPECT].

The long-axis (L-A) tomograms of the heart in thallium-201 SPECT have been conventionally reconstructed as those parallel to the midventricular vertical or horizontal L-A plane. We developed a new algorithm for reconstructing the rotated L-A tomograms around the L-A to longitudinally observe thallium-201 myocardial distribution and to provide an optimal view of the cardiac apex. After determining the orientation of the L-A and reconstructing the short-axis (S-A) tomograms using standard techniques, the coordinates of the S-A planes were transformed to the polar coordinates whose origin is located at the position of the L-A in each plane. Then, "radial L-A tomograms", i.e. midventricular L-A planes oriented at the angle of every 6 degrees to the midventricular horizontal L-A plane, were reconstructed. Also, we developed a new technique for analyzing thallium-201 distribution of the L-A tomograms. For the basal 2/3 regions, two profiles which consist of the pixels with maximum count on the upper and lower myocardial portions of the lines (spaced at 1 pitch) vertically to the L-A were computed. For the remaining apical 1/3 regions, the semi-circumferential maximum-count profile from the values of 30 radii spaced at 6 degrees interval were computed. Based on these profiles, a 2D polar representation was then generated. From the study using a cardiac phantom with an apical small infarction, the usefulness of this new tomographic method for the detection of apical myocardial ischemia was demonstrated. The application to the exercise/redistribution studies in patients with effort angina indicated that radial long-axis tomography provides precise information about the longitudinal extent of perfusion defects, particularly in the apical regions.

Algorithms↗