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Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 109 records · Page 6Linked to original sources
PubMed1989

Role of right ventricular asynergy and tricuspid regurgitation in hemodynamic alterations during acute inferior myocardial infarction.

To elucidate the role of right ventricular asynergy and tricuspid regurgitation (TR) in hemodynamic alterations occurring during right ventricular infarction, left and right ventriculography with pressure measurements were performed in 22 patients with acute inferior myocardial infarction. Twelve patients with a proximal right coronary artery (RCA) occlusion (Group I) had elevated right atrial pressure (16 +/- 4 vs 8 +/- 5 mmHg, p less than 0.01), low cardiac output (2.5 +/- 0.7 vs 3.5 +/- 0.6 l/min/m2, p less than 0.05) and a greater degree of TR, compared with 10 patients with a distal RCA occlusion (Group II). Inferoposterior wall asynergy of the right and left ventricles was similar in Groups I and II. In Group I, there was an additional asynergy of the anterolateral free wall of the right ventricle. Cardiac output in those patients was not related to the left ventricular ejection fraction (EF) but to the right ventricular EF. A greater degree of TR was found in association with a lower right ventricular EF. The decrease in cardiac output was closely related to the extent of TR. These results indicate that right ventricular asynergy and TR due to proximal RCA occlusion may play important roles as causes of hemodynamic alterations seen during the acute phase of inferior myocardial infarction.

Aged↗
PubMed1989

Noninvasive assessment of left ventricular diastolic filling in coronary artery disease by Doppler dipyridamole-stress testing.

To evaluate left ventricular diastolic function during dipyridamole-provoked myocardial ischemia, transmitral flow was studied in 73 patients with coronary artery disease and 8 normal subjects using pulsed Doppler echocardiography. Coronary vasodilating agents like dipyridamole can provoke myocardial ischemia in patients with coronary artery disease. The peak flow velocity of left ventricular rapid filling (R), that of atrial contraction (A) and the ratio of A to R (A/R) in each cardiac cycle were measured. The rapid filling phase was divided into two subphases at the point of R. The integral of the two subphases and atrial contraction were computed and designated IR1, IR2 and IA. The time intervals of the two subphases of rapid filling were designated TR1 and TR2. Of the 73 patients with coronary artery disease, 41 patients developed ischemia (positive responder = PR) and 32 patients did not (negative responder = NR) after dipyridamole infusion. In PR, A/R increased (p less than 0.05), IR2 decreased (p less than 0.01) and TR2 shortened (p less than 0.01) significantly. In NR and normal subjects, these indices remained unchanged. We observed mitral regurgitation (MR) in 13 PR patients during acute myocardial ischemia. A/R increased in patients without MR but A/R remained unchanged in patients with MR. These results suggest that in acute myocardial ischemia, changes in Doppler indices (A/R, IR2 and TR2) reflect a left ventricular diastolic abnormality, and that the masking of the diastolic abnormality was ascribed to the presence of MR.

Blood Flow Velocity↗
PubMed1989

Effects of propranolol on coronary vasculature and cardiac performance in dogs with fixed and dynamic coronary stenosis.

The coronary hemodynamic effects of propranolol (0.1 mg/kg, i.v.) were examined in anesthetized dogs with flow-limiting dynamic and fixed coronary stenosis of the left circumflex coronary artery. During fixed coronary stenosis created by external application of an occluder device, propranolol significantly decreased coronary blood flow (CBF) by 6.8 +/- 2.7% (mean +/- SEM, p less than 0.05) and increased mean distal coronary pressure (DCP) by 7 +/- 2.1 mmHg (p less than 0.05). This resulted in a decrease in stenosis resistance (SR) by 26 +/- 3.1% (p less than 0.01) due to oxygen demand reduction. By contrast, during dynamic coronary stenosis produced by an intraluminal microballoon occluder, propranolol decreased CBF by 68 +/- 3.4% (p less than 0.01) and mean DCP by 36 +/- 4.2 mmHg (p less than 0.01), resulting in an increase in SR by 694 +/- 109% (p less than 0.01). This increase in SR was attenuated by pretreatment with an alpha-adrenergic receptor antagonist phentolamine (0.5 mg/kg, i.v.), or by holding heart rate constant at the pretreatment level. These results suggest that propranolol ameliorated the severity of stenosis during fixed coronary stenosis and exacerbated the severity during dynamic coronary stenosis. This increase in SR appears to be related to vasoconstriction of the large stenosed coronary artery, mediated both by alpha-adrenergic receptors in the coronary artery and by myocardial oxygen demand reduction.

Animals↗
PubMed1989

Decreased cytosolic free calcium concentration in lymphocytes of magnesium-supplemented DOCA-salt hypertensive rats.

The effect of magnesium supplementation on blood pressure and lymphocyte cytosolic free calcium concentration (L-[Ca2+]i; nM) was examined in DOCA salt hypertensive rats (DSR). Magnesium was administered for 4 weeks with a standard diet in the form of 1% MgO (850 mg magnesium/100 g). In magnesium-supplemented DSR (DS-Mg), the elevation of systolic blood pressure (SBP; mmHg) was significantly attenuated (136.7 +/- 23.0 vs 180.6 +/- 23.4, p less than 0.005) and the L-[Ca2+]i was significantly lower (70.5 +/- 7.0 vs 84.5 +/- 7.1, p less than 0.005) than in DSR which were fed the standard rat diet. Lymphocyte magnesium content (nEq/mg protein) in DSR was lower than in control rats (160.6 +/- 18.3 vs 182.3 +/- 13.9, p less than 0.05) and approximately the same as in DS-Mg (164.9 +/- 6.9, p less than 0.05 vs control). Plasma magnesium concentration was slightly higher in DS-Mg than DSR (2.53 +/- 0.35 vs 2.21 +/- 0.26). We observed a significant positive correlation between SBP and L-[Ca2+]i in DS-Mg and in DSR as a whole. These findings suggest that oral magnesium supplementation can attenuate the elevation of blood pressure and simultaneously decrease the cytosolic free calcium concentration in DOCA salt hypertensive rats.

Animals↗
PubMed1989

Role of serotonin, histamine, and thromboxane A2 in platelet-induced contractions of coronary arteries and aortae from rabbits.

The present study was undertaken to clarify the underlying mechanisms responsible for contractions of isolated coronary arteries and aortae from rabbits in response to thrombin-stimulated autologous platelets. Thrombin-stimulated platelets evoked potent contractions of both arteries in a platelet concentration-related manner. Pretreatment of platelets with aspirin, which almost completely inhibited thromboxane A2 synthesis but not the release reaction of biologic monoamines from platelets, caused only slight suppression of platelet-induced contractions of both arteries. Ketanserin as well as methysergide markedly inhibited aortic contractions to platelets. In contrast, the contractile responses of coronary arteries to platelets were suppressed by methysergide but not by ketanserin. Pretreatment of the arteries with diphenhydramine did not inhibit the aortic responses to platelets, but significantly suppressed coronary arterial contractions induced by higher concentrations of platelets. Phentolamine had no inhibitory effects on the responses of either artery to platelets. Pretreatment of arteries with aspirin did not affect the contractile responses of either artery to platelets. The contractile responses of aortae to exogenously administered serotonin were competitively antagonized by ketanserin, but those of coronary arteries were not. Coronary contractions to serotonin were competitively inhibited by methiothepin and significantly suppressed by methysergide. The contractile responses of both arteries to histamine were antagonized by diphenhydramine but not by cimetidine. On the basis of our results obtained from studies in organ chamber, we conclude that a major role of thromboxane A2 was not demonstrated in platelet-induced contractions of the arteries, and that those of aortae were mainly mediated by platelet-derived serotonin at S2 receptor and those of coronary arteries at S1-like receptor. The contractions of coronary arteries in responses to higher concentrations of platelets were partly mediated by histamine at H1 receptor.

Animals↗
PubMed1989

[Influence of preload alteration on the transmitral flow velocity in patients with old myocardial infarction: effects of nitroglycerin and lower body negative pressure].

We studied the influence of preload alteration on the pattern of transmitral flow as obtained by pulsed Doppler echocardiography. In protocol I, 14 patients with old myocardial infarction (OMI) were observed by simultaneous measurements of transmitral flow by PDE and left ventricular end-diastolic dimension (LVDd) using M-mode echocardiography during the control period and after sublingual nitroglycerin. In protocol II, eight patients with OMI were similarly observed during stepwise lower body negative pressure (LBNP: 0, -10 and -20 mmHg). The rapid filling phase was categorized in two subphases at peak R as the first half and second half phases. The integrals of each half phase and the atrial systolic phases (IR1, IR2 and IA) were measured by planimetry. After the administration of nitroglycerin, LVDd decreased significantly; whereas the mean arterial pressure decreased and heart rate increased significantly. The peak R and IR1 decreased significantly, but the peak A, IR2 and IA remained unchanged. During LBNP, LVDd decreased stepwise; whereas there was no change in the mean arterial pressure or heart rate. The changes in the peak R and IR1 paralleled the preload reduction during LBNP. The peak A, IR2, and IA remained unchanged. In conclusion, the first and second half volumes during the LV rapid filling phase can be influenced by various factors. The patterns of the transmitral flow velocity, the maximal velocity and first half volume in the LV rapid filling phase may be influenced by preload alteration.

Adult↗
PubMed1989

Evaluation with equilibrium radionuclide angiography of left ventricular systolic and diastolic function in pulmonary hypertension secondary to chronic pulmonary diseases.

To evaluate left ventricular systolic and diastolic function in patients with pulmonary hypertension secondary to chronic pulmonary diseases, 86 patients were studied using equilibrium radionuclide angiography with forward and reverse gating from the R wave. At rest left ventricular function, both in systolic and diastolic properties, in patients with pulmonary hypertension was significantly lower than in normal subjects (LVEF; P less than 0.05, PER; p less than 0.05, PFR; P less than 0.025, FF; P less than 0.025). During exercise left ventricular systolic function did not increase as much as in normals (LVEF; N.S., PER; N.S.). Left ventricular diastolic function during exercise was significantly lower than at rest (PFR; P less than 0.05, FF; P less than 0.001). The indices of left ventricular function obtained from radionuclide angiography had no close correlation with pulmonary hemodynamics or with blood gases. These results demonstrated that left ventricular dysfunction in patients with pulmonary hypertension was observed both at rest and during exercise, and might play an important role in reduced exercise tolerance.

Female↗
PubMed1989

[Myocardial perfusion assessed by dynamic computed tomography, with respect to viable muscle in the infarcted region].

To clarify the significance of regional myocardial perfusion, 31 patients of old myocardial infarction including 11 cases undergoing PTCA with a left anterior descending artery lesion were studied using dynamic transmission computed tomography with excellent time resolution. Serial one-second dynamic scans with an electrocardiographic triggering system were performed at the middle level of the left ventricle using a bolus injection of contrast medium via the inferior vena cava. The F/V (F = flow, V = volume) ratio, a parameter of perfusion per unit of myocardium, was calculated from gamma-variate fitted time density curves obtained in the myocardium and in the left ventricular cavity. The F/V ratio was significantly lower in patients not only with severe but also mild and no coronary artery stenosis (post PTCA: 185 +/- 54, 50-75% stenosis: 193 +/- 47, 90% stenosis: 181 +/- 51, 99% stenosis: 140 +/- 34, 100% stenosis: 142 +/- 27 ml/min/100 g, control value: 243 +/- 51 ml/min/100 g, post PTCA, 50-75% stenosis, 90% stenosis vs control p less than 0.05, 99%, 100% stenosis vs control p less than 0.005). The functional images depicting myocardial perfusion frequently revealed abnormal perfusion findings in patients not only with severe but also mild and no coronary stenosis. In the patients with mild or insignificant coronary stenosis, the F/V ratio was dependent on the severity of left ventricular wall motion abnormalities (hypokinesis: 192 +/- 51, akinesis or dyskinesis: 141 +/- 32 ml/min/100 g; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1989

[Evaluation of left ventricular filling dynamics by pulsed Doppler echocardiography during afterload stress in ischemic heart disease using angiotensin II infusion].

To evaluate cardiac reserve in ischemic heart disease, we simultaneously investigated left ventricular filling parameters using pulsed Doppler echocardiography (PDE) and catheter-obtained hemodynamics before and during afterload stress (angiotensin II test) in 14 patients with ischemic heart disease. The patients were divided into two groups according to their left ventricular function, i.e., mean left ventricular ejection fraction (mLVEF): Group I (n = 7, mLVEF = 65%) and Group II (n = 7, mLVEF = 43%). The peak velocity of rapid filling (R), the peak velocity of atrial contraction (A), the ratio of the two peak velocities (A/R), flow velocity integrals of the rapid filling phase (IR) and atrial contraction phase (IA) were obtained by PDE. Results were as follows: 1. During afterload stress, blood pressure, pulmonary artery wedge pressure, and left ventricular end-diastolic pressures (LVEDP) were elevated in both groups (p less than 0.01). The stroke work index (SWI) increased (p less than 0.01) and the time constant of left ventricular isovolumic pressure decay (T) was unchanged in Group I. SWI did not increase and T was prolonged in Group II (p less than 0.05). delta SWI/delta LVEDP, the ratio of the SWI change to the LVEDP change, during afterload stress was larger in Group I than in Group II (p less than 0.02). 2. Before the infusion of angiotensin II, R and IR were larger in Group I than in Group II. The A/R in Group I was less than that in Group II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

[Genesis of systolic anterior motion (SAM) of the mitral valve in patients with aortic regurgitation].

This study was performed to evaluate the incidence and genesis of systolic anterior motion (SAM) of the mitral valve apparatus in patients with aortic regurgitation (AR). The study population consisted of 44 patients with non-rheumatic AR, without significant aortic stenosis or mitral regurgitation. The presence and location of SAM in the short-axis view were determined by M-mode echocardiography guided by two-dimensional echocardiography. The extent and direction of the regurgitant jet were decided by pulsed or two-dimensional Doppler echocardiography. SAM was observed in 21 (48%) of the 44 patients, and it was more frequently observed in patients with an etiology of aortic valve prolapse or annuloaortic ectasia than in those of other etiology (10/14 vs 10/30; p less than 0.05). Twenty-eight patients whose regurgitant jet was directed posteriorly and impinged on the mitral valve apparatus had a significantly higher incidence of SAM than did the other 16 patients (18/28 vs 3/16; p less than 0.01). In eight of 10 patients in whom the direction of the regurgitant jet could be precisely observed by two-dimensional Doppler echocardiography. SAM was observed at the place where a regurgitant jet was directed along the anterior mitral valve in the short-axis view. M-mode measurements (LVDd, LVDs, %FS, LVDd-LVDs) of the patients with SAM had greater values than those of patients without SAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Independent inhibition of DNA synthesis by protein kinase C, cyclic AMP and interferon alpha/beta in rabbit aortic smooth muscle cells.

In quiescent cultures of rabbit aortic smooth muscle cells, whole blood serum-induced DNA synthesis was inhibited markedly by protein kinase C-activating 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and phorbol-12, 13-dibutyrate (PDBu), cyclic AMP-derivatives, such as dibutyryl cyclic AMP (Bt2cAMP) and 8-bromo-cyclic AMP, and interferon alpha/beta. Neither TPA nor interferon alpha/beta elevated the cellular cyclic AMP level. Neither Bt2cAMP nor interferon alpha/beta induced the phospholipase C-mediated hydrolysis of phosphoinositides. The down-regulation of protein kinase C by prolonged treatment with PDBu abolished the antiproliferative action of TPA but did not affect that of Bt2cAMP or interferon alpha/beta. TPA and Bt2cAMP inhibited the serum-induced DNA synthesis when added within 12 h after the addition of the serum, while interferon alpha/beta was active only when added within 6 h. These results suggest that there are at least three independent signaling systems, protein kinase C- and cyclic AMP-mediated systems and an unidentified system for interferon alpha/beta, which are involved in the antiproliferative mechanisms in rabbit aortic smooth muscle cells.

Alprostadil↗
PubMed1988

Platelet-derived growth factor (PDGF)-induced phospholipase C-mediated hydrolysis of phosphoinositides in vascular smooth muscle cells--different sensitivity of PDGF- and angiotensin II-induced phospholipase C reactions to protein kinase C-activating phorbol esters.

In cultured rabbit vascular smooth muscle cells (VSMC), platelet-derived growth factor (PDGF), a potent mitogen for VSMC, induced the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates (IP1, IP2 and IP3, respectively). The doses of PDGF necessary for these reactions were similar to those for DNA synthesis. The maximal level of IP1 was comparable to, and those of IP2 and IP3 were about half of those induced by angiotensin II, a potent vasoconstrictor. However, the time courses of the PDGF-induced reactions were slower than those of the angiotensin II-induced ones. Moreover, protein kinase C-activating phorbol esters inhibited the angiotensin II-induced reactions, but did not the PDGF-induced ones. These results indicate that PDGF induces the phospholipase C reactions in VSMC but suggest that the signaling mechanism of PDGF to the phospholipase C is different from that of angiotensin II.

Angiotensin II↗
PubMed1988

Phorbol ester modulates serotonin-stimulated phosphoinositide breakdown in cultured vascular smooth muscle cells.

Stimulation of cultured rabbit aortic vascular smooth muscle cells (VSMC) with serotonin (5HT) induced a rapid generation of inositol phosphates from receptor-mediated hydrolysis of inositol phospholipids. Pretreatment of these cells with 500ng/ml of pertussis toxin for 24h prior to addition of 5HT reduced 5HT-induced formation of inositol phosphates. Phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA) or phorbol-12,13-dibutyrate (PDBu), are known to activate protein kinase C (PKC), but their role on cultured VSMC stimulated by 5HT has not been defined. TPA exhibited a rapid inhibition of 5HT-stimulated phosphoinositide breakdown, although 4 alpha-phorbol-12,13-didecanoate (4 alpha PDD), an inactive phorbol ester, did not inhibit it. These data suggest that a guanine nucleotide inhibitory (Gi) protein couples 5HT receptor to phospholipase C and TPA modulates 5HT-stimulated hydrolysis of inositol phospholipids in cultured VSMC through activation of PKC.

Animals↗
PubMed1988

Angiotensin II induces expression of the c-fos gene through protein kinase C activation and calcium ion mobilization in cultured vascular smooth muscle cells.

Incubation of the serum-deprived cultures of rat vascular smooth muscle cells with angiotensin II, a potent vasoconstrictor, caused a rapid and transient increase in the c-fos mRNA level. The doses of this agonist necessary for the increase in the c-fos mRNA level coincided with those for the phospholipase C-mediated hydrolysis of phosphoinositides. Moreover, protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate and Ca2+-ionophore A23187 increased the c-fos mRNA level in an additive manner. These results suggest that angiotensin II induces expression of the c-fos gene through the activation of protein kinase C and Ca2+ mobilization in cultured vascular smooth muscle cells.

Angiotensin II↗
PubMed1988

The role of chloride in the sympathetic nervous system in DOCA-salt hypertension.

Elevation in blood pressure in the deoxycorticosterone acetate (DOCA)-treated rat with a high-sodium, normal-chloride diet was less than that in the DOCA-salt rat not on such a diet. Compared with the DOCA-salt rat, there were greater sodium concentration in the carcass, and less norepinephrine turnover rates in the heart and the spleen than in the DOCA treated rat given a high sodium normal chloride diet. Extracellular fluid volumes were similar. These results suggest that not only water and sodium retention by sodium loading but also that activation in sympathetic nervous system by the combined effect of chloride and sodium are responsible for the development of DOCA-salt hypertension.

Animals↗
PubMed1988

Effects of oral magnesium on blood pressure and red cell sodium transport in patients receiving long-term thiazide diuretics for hypertension.

Twenty patients receiving long-term (1.0 to 10.3 years) thiazide diuretic treatment for essential hypertension (Th group) received magnesium supplementation as MgO (600 mg Mg/day) for 4 weeks and placebo for another 4 weeks. Before and at the end of each period, we measured blood pressure; intraerythrocyte magnesium, sodium, and potassium (R-Mg, R-Na, and R-K); and erythrocyte ouabain (10-4 M) sensitive sodium efflux rate constant (Kos). The same measurements were also performed in 21 untreated age-matched essential hypertensives (EHT group). In the Th group, R-Mg was lower, R-Na was higher, and Kos was lower than in the EHT group before magnesium supplementation. Oral magnesium resulted in a significant increase in R-Mg (p less than 0.005) and a decrease in R-Na (p less than 0.01), together with an increase in Kos (p less than 0.005) in the Th group. During magnesium supplementation, the increased Kos was correlated negatively with the lowered R-Na (r = -0.57, p less than 0.01) and positively with the increased R-Mg (r = 0.61, p less than 0.005). Systolic, diastolic, and mean blood pressures were reduced significantly during magnesium administration by a mean of 7.5, 3.0, and 4.5 mm Hg. The results indicate that long-term diuretic treatment may give rise to an intracellular magnesium deficiency and a suppression in cell membrane active transport for sodium, with a resultant increase in intracellular sodium content.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗