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Biomedical subjects

N Imai

Publications and source records attributed to N Imai.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Effects of PTCR and PTCA on serial changes in left and right ventricular wall motion in acute myocardial infarction].

To evaluate the effects of early recanalization on left and right ventricular wall motion in acute myocardial infarction (AMI), we serially observed their degrees in 66 patients with AMI. The patients were categorized as Group 1:17 with spontaneous recanalization within 6 hours of onset of the chest pain; Group 2:34 with effective recanalization within 6 hours (10 by PTCR, 10 by PTCR+ PTCA, and 14 by direct PTCA), and Group 3:21 without effective recanalization. The Group 2 patients were classified in 3 subgroups according to the time intervals from onset of symptoms to recanalization; 11 patients with recanalization within 2 hours (Group 2a), 10 between 2 and 4 hours (Group 2b), and 13 between 4 and 6 hours (Group 2c). The left and right ventricular wall motion abnormality indexes (WMAI) were defined as the means of point scores for the degrees of regional wall motion abnormality at 11 segments of the left ventricle and seven segments of the right ventricle on serial two-dimensional echocardiograms. Results were as follows: 1. The LV-WMAI of Group 1 was smaller on day 1, and improved on day 28 as compared to those of the other groups (0.63 +/- 0.35 to 0.18 +/- 0.18, p less than 0.001). 2. The improvements of the LV-WMAI from days 1 to 28 in Group 2a (WMAI: 1.01 +/- 0.57 to 0.26 +/- 0.26, delta WMAI: 82 +/- 14%) and Group 2b (1.03 +/- 0.38 to 0.52 +/- 0.48, 54 +/- 36%) were greater than that in Group 2c (1.01 +/- 0.46 to 0.64 +/- 0.52, 38 +/- 47%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Stabilization of hexokinases I and II of ELD cells by binding to mitochondria.

Significance of the binding of hexokinase to mitochondria was examined with respect to stabilization of the enzyme by the binding. Stability during the incubation of the mitochondria-bound forms of hexokinases I and II, both prepared from Ehrlich-Lettre ascites hyperdiploid tumor cells (ELD cells), were compared with that of the corresponding free forms. During the incubation at pH 7.4 and 37 degrees C up to 60 min, hexokinase activities decreased gradually, and the decrease in the activity of the free form was much more marked than that of the bound form for both hexokinases. Hexokinase II was much less stable than I, and the activity of the free form of the former was almost lost by the incubation for 15 min. But, more than a half of the original activity of hexokinase II was retained even after 60 min of the incubation when the enzyme was bound to mitochondria. Addition of 50 mM glucose increased the stability of hexokinase II, but the stabilizing effect was less marked for hexokinase I. On the other hand, addition of 28 mg/ml of bovine serum albumin markedly stabilized hexokinase I to almost the same extent as was observed with mitochondria. On the contrary, the serum albumin had little stabilizing effect on hexokinase II. These findings indicate that the binding to mitochondria stabilizes the hexokinases of ELD cells, though the stability is different by nature between hexokinases I and II.

Animals↗
PubMed1989

Clinical and roentgenological studies on malalignment disorders of the patello-femoral joint. Part III: Lesions of the patellar cartilage and subchondral bone associated with patello-femoral malalignment.

This study was aimed at clarifying what mechanism of patello-femoral malalignment causes cartilage lesions and how the lesions are related to the symptoms. The study was composed of a laboratory experiment and clinical observations on 127 joints of 123 patients. In the clinical observations, cartilage lesions on the patella as well as on the groove and condyles of the femur were studied by performing either arthroscopy or open surgery. Changes of the subchondral bone of the patella were also examined through sky-line view roentgenograms to determine their relationship with cartilage lesions. From these observations, it was concluded that cartilage lesions are caused by shearing stresses produced by the abnormal motion of the patella due to malalignment, often accompanied by open or closed (to the joint cavity) subchondral lesions. The experiment showed that various types of cartilage-bone damage could be brought about depending on various combined factors of velocity and energy of the stressing force. Based on our theory, a reasonable treatment is presented.

Animals↗
PubMed1988

Interactions between cations in modifying the binding of hexokinases I and II to mitochondria.

Interactions between cations in modifying the binding of hexokinases I and II to mitochondria was examined with reference to the intracellular condition. Mitochondria-binding of either of hexokinases I and II, both prepared from mouse ascites ELD cells, was markedly increased by Mg2+ as has been known well. However, even in the absence of Mg2+, marked binding was attained by 100 mM K+ alone especially for hexokinase I, which seemed generally more ready to bind to mitochondria. On the other hand, the effect of Mg2+ to increase the binding was reduced by the addition of K+, and the decreasing effect of K+ was much more marked for hexokinase II than I. These results indicate that, in addition to Mg2+, monovalent cations as represented by K+, also have marked effect on the binding, and the effect is different for each hexokinases I and II, which may be responsible for the difference in the intracellular distribution between these hexokinases.

Animals↗
PubMed1988

Effects of naloxone on systemic and regional hemodynamic responses to exercise in dogs.

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.

Adrenocorticotropic Hormone↗
PubMed1988

Comparative effects of nitroprusside and pinacidil on myocardial blood flow and infarct size in awake dogs with acute myocardial infarction.

The effect of nitroprusside in limiting myocardial infarct was compared with that of pinacidil, a new antihypertensive agent with potent coronary vasodilator properties, in instrumented awake dogs subjected to 4 hr of left anterior descending coronary artery occlusion and 20 hr of reperfusion. Dogs were randomly assigned to receive intravenous normal saline, nitroprusside, or pinacidil beginning 40 min after the onset of coronary artery occlusion and continuing throughout the occlusion and the first hour of reperfusion. Nitroprusside and pinacidil were titrated to decrease mean aortic pressure by 25 mm Hg; normal saline had no effect on mean aortic pressure. Other systemic hemodynamic variables were not significantly altered by normal saline or nitroprusside, and myocardial blood flow did not change during normal saline infusion in normal and ischemic myocardium. In contrast, nitroprusside increased the blood flow and the endocardial/epicardial flow ratio in ischemic myocardium. This increase in ischemic myocardial blood flow was accompanied by a significant reduction in infarct size (40 +/- 3% of region at risk vs 58 +/- 4% in the normal saline group; p less than .05). Pinacidil increased heart rate, cardiac output, and the peak rate of rise of left ventricular pressure. Furthermore, despite causing a threefold to fourfold increase in normal myocardial blood flow, pinacidil had no effect on either blood flow to ischemic myocardium or infarct size (57 +/- 5%). The data indicate that the marked coronary vasodilator effect of pinacidil does not cause an increase in ischemic blood flow or a reduction in infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure.

Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. Vasopressin inhibition increased cardiac output and left ventricular dP/dt and dP/dt/P, and it decreased total peripheral vascular resistance, whereas mean aortic pressure did not change significantly. Simultaneously, blood flow increased to skeletal muscle, kidneys, skin, and right and left ventricular myocardium. Plasma catecholamines also increased. Pretreatment with propranolol and prazosin abolished the increases in cardiac output and left ventricular function produced by vasopressin inhibition. Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.

Animals↗
PubMed1987

Specific inhibitors of tyrosine-specific protein kinase, synthetic 4-hydroxycinnamamide derivatives.

Several newly synthesized 4-hydroxycinnamamide derivatives such as 3-(3',5'-di-isopropyl-4'-hydroxybenzylidene)-2-oxindol (ST 280), 3-(3',5'-di-methylthiomethyl-4'-hydroxybenzylidene)-2-oxindole (ST 458), alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamide (ST 638) and 3-(3'-ethoxy-4'-hydroxy-5'-phenylthiomethylbenzylidene)-2-pyrol idinone (ST 642) were found to inhibit tyrosine-specific protein kinase activity of the epidermal growth factor (EGF) receptor with IC50 values of 0.44 microM, 0.44 microM, 0.37 microM and 0.85 microM, respectively. None of them showed inhibitory effect on the enzyme activities of serine- and/or threonine-specific protein kinases such as cAMP-dependent protein kinase, Ca2+/phospholipid-dependent protein kinase C, casein kinase I and casein kinase II. In addition, none of them had effect on Na+/K+-ATPase or 5'-nucleotidase. The results suggest that the compound ST 280, ST 458, ST 638 and ST 642 are potent and specific inhibitors of tyrosine-specific protein kinase.

5'-Nucleotidase↗
PubMed1987

Possible processing of mitochondria-bindable hexokinase to the nonbindable form by a lysosomal protease in rat liver.

As a possible mechanism for the absence of mitochondria-bindable hexokinase in the liver, the presence of a protease similar in action to chymotrypsin, which specifically eliminates the binding ability of the bindable hexokinase without changing its catalytic properties, was investigated in rat liver. The lysosomal fraction prepared from the liver converted the bindable hexokinase prepared from rat brain to the nonbindable form with little change in catalytic activity. The activity of such a "processing protease" was much lower in rat brain, where the bindable form is predominant. The processing activity cosedimented with lysosomal marker enzyme activities in the subcellular fractionation of livers from normal and Triton WR-1339-injected rats. A fair portion of the activity was detected in the lysosomes without disruption. The activity was maximal at pH 6.0-7.0, inactivated almost completely by tosylphenylalanine chloromethyl ketone, tosyllysine chloromethyl ketone, leupeptin, antipain, and chymostatin, and dependent on dithiothreitol and mercaptoethanol. These results suggest that a protease, properties of which are fairly similar to those of cathepsin M, may be involved in the post-translational processing of original bindable hexokinase to the nonbindable form in rat liver.

Animals↗
PubMed1987

Characterization of two types of histone H2B genes from macronuclei of Tetrahymena thermophila.

Two histone H2B gene clones were isolated from macronuclei of Tetrahymena thermophila. Nucleotide sequences of the two clones were highly homologous within the coding region but not in the noncoding region. Comparison of the deduced amino acid sequences between the two clones showed three differences in a total of 121 amino acids. Each of the two clones contained a TAA triplet within the coding region, which appeared to code for a glutamine residue. To demonstrate the existence of histone mRNA containing UAA triplet, nuclease P1 protection mapping using total cellular RNA and nucleotide sequencing of primer extension products were carried out. The results clearly indicated that two cloned histone H2B genes were transcribed, giving rise to the major histone H2B mRNAs with a UAA triplet sequence in frame. The tentative 5'- and 3'-ends of histone H2B mRNAs were determined.

Amino Acid Sequence↗
PubMed1987

Selective pharmacological effects of triprolyl and pentasarcosyl angiotensin II.

Among the various biological effects of angiotensin II (AII), both pressor activity and aldosterone stimulation appear to be mediated by functionally different receptors. With this in mind, we compared pressor and aldosterone-stimulating activities of AII with those of triprolyl [(Pro)3] AII and pentasarcosyl [(Sar)5] AII. In conscious male Wistar rats (Pro)3 AII and (Sar)5 AII produced 48 and 46% of the pressor activity of AII. After intravenous infusion (conscious unrestrained rats, 125 pmol/kg/min for 30 min), plasma aldosterone concentrations were not significantly different from those of control rats which were infused with saline. However, when the rats were infused with AII (125 pmol/kg/min for 30 min), plasma aldosterone concentrations increased significantly (1,306 +/- 80 pg/ml). This study indicates that (Pro)3 AII and (Sar)5 AII may prove to be useful tools to elucidate biological actions of AII.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1987

Effects of milrinone on systemic hemodynamics and regional circulations in dogs with congestive heart failure: comparison with dobutamine.

Milrinone is a new bipyridine inotropic agent with direct vasodilator properties. To determine the role of the vasodilator action in mediating systemic and regional hemodynamic responses to milrinone, we administered two equipotent inotropic doses of either milrinone or dobutamine to dogs with chronic congestive right heart failure produced by tricuspid avulsion and pulmonary artery stenosis. Similar increases in cardiac output, right and left ventricular dP/dt, and left ventricular dP/dt/P were produced by milrinone and dobutamine; however, heart rate increased and mean aortic pressure decreased only with milrinone infusion. In addition, while total peripheral vascular resistance decreased with both agents, the decrease was greater with milrinone. Regional blood flows were measured by a radioactive microsphere method. Milrinone and dobutamine produced similar increases in myocardial blood flow and left ventricular oxygen consumption. Dobutamine infusion decreased quadriceps muscle vascular resistance and had no effect on renal and splanchnic circulations. In contrast, milrinone infusion increased vascular resistance in quadriceps muscle and decreased it in renal and splanchnic beds. Thus, when milrinone was used in inotropic doses similar to those of dobutamine, the responses in systemic and regional hemodynamics in congestive heart failure differed. Milrinone produced a greater decline in total peripheral, renal, and splanchnic vascular resistances, probably resulting from its direct vasodilator action.

Animals↗
PubMed1987

The role of endogenous opioids in congestive heart failure: effects of nalmefene on systemic and regional hemodynamics in dogs.

We studied the role of endogenous opiates and their interrelationships with the sympathetic nervous system in an experimental preparation of right-sided congestive heart failure (CHF) produced by surgical tricuspid avulsion and progressive pulmonary arterial constriction. Three groups of dogs with CHF and one group of sham-operated dogs were studied. One group of dogs with CHF was given normal saline as pretreatment, while the other two groups were pretreated with either propranolol alone (beta-blockade) or propranolol plus prazosin (alpha- plus beta-blockade). CHF was characterized by weight gain, ascites, elevated right atrial pressure, tachycardia, and reduced cardiac output. Compared with sham-operated animals, animals with CHF exhibited significantly higher baseline levels of plasma beta-endorphin and cortisol. Furthermore, only the animals with CHF responded to the opiate receptor-antagonist nalmefene with significant increases in plasma beta-endorphin, cortisol, and adrenocorticotropic hormone. Administration of nalmefene increased aortic blood pressure, cardiac output, left ventricular dP/dt and dP/dt/P, and blood flow to the myocardium, skeletal muscle, and kidneys in dogs with CHF, but had no appreciable effects in sham-operated dogs. beta-Receptor blockade abolished the increase in cardiac output, left ventricular performance, and blood flow produced by nalmefene, but had no effect on the pressor response to nalmefene. The increase in mean aortic pressure in the beta-blockade group was accompanied by an increase in skeletal muscle vascular resistance. Addition of prazosin in the alpha- plus beta-blockade group abolished the increases in mean aortic pressure and skeletal muscle vascular resistance, suggesting that the changes after propranolol probably resulted from unmasking of alpha-receptor-mediated vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Effects of percutaneous transluminal coronary angioplasty on segmental left ventricular function in patients with acute myocardial infarction.

In order to investigate the usefulness of percutaneous transluminal coronary angioplasty (PTCA) on subsequent left ventricular (LV) function in patients with acute myocardial infarction (AMI), regional ejection fraction (REF) was calculated from the left ventriculogram and compared in the acute and chronic phases (4 weeks after infarction) in 19 successful cases of PTCA (group A). In addition, 15 successful cases of intracoronary thrombolysis (PTCR) (group R) and 14 unsuccessful cases (group U) were also analyzed in this study. From the results, the following points were elucidated. (1) REF of group A in the chronic phase showed a significant increase compared to that in the acute phase (10 +/- 18% vs 20 +/- 19%, p less than 0.01), and this was similar to that observed in group R (9 +/- 19% vs 21 +/- 16%, p less than 0.01). (2) All cases in group A showed a significant increase in REF (p less than 0.02), if recanalization occurred within 3 hours after the onset of AMI. Some cases in the 3-6 hour recanalization group showed a decrease in REF. (3) In group A, only patients with subtotal occlusion on the initial coronary angiogram showed a significant increase in REF 4 weeks later (p less than 0.01), whereas patients with total occlusion on the initial coronary angiogram showed no significant increase in REF. (4) In group A, only patients recanalized between 3 and 6 hours showed a severe degree of prolonged contrast staining immediately after successful recanalization following PTCA. Thus, chronic phase regional wall motion was markedly improved by PTCA in those cases with residual flow. In contrast, abrupt recanalization after PTCA might causally decrease regional wall motion due to hemorrhagic infarction, if it is performed in cases with total occlusion.

Angioplasty, Balloon↗