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Biomedical subjects

T Natsume

Publications and source records attributed to T Natsume.

At least 73 records · Page 4Linked to original sources
PubMed1988

Ouabain inhibits intracellular pH recovery from acidosis in cultured mouse heart cells.

Myocardial ischaemia induces cytosolic acidification, which promotes cardiac damage, dysfunction or arrhythmia. In this study, we investigated the effect of ouabain on the intracellular pH (pHi) in cultured mouse ventricular cells, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The average resting pHi in myocytes was 7.19. After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange. Ouabain inhibited this pHi recovery dose-dependently with half-maximal inhibition at 3 X 10(-5) M, but did not suppress the ionophore monensin-induced pHi elevation. The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump. Above results demonstrate the possibility that digitalis promotes intracellular acidosis or inhibits the pHi recovery from acidosis in ischaemic myocardium.

Acidosis↗
PubMed1988

Combination therapy with diltiazem and nifedipine in patients with effort angina pectoris.

The antianginal effects of diltiazem and nifedipine alone and in combination were evaluated in a double-blind, randomized, placebo-controlled trial in 11 patients (nine men and two women, 57 +/- 8 years old) with stable effort angina. Each patient received placebo, 30 mg of diltiazem, 10 mg of nifedipine, and 30 mg of diltiazem plus 10 mg of nifedipine four times daily for 1 week each. Antianginal efficacy was assessed by means of a treadmill exercise test. The exercise tolerance time was significantly prolonged from 235.1 +/- 52 (placebo period) to 342.2 +/- 101 sec by diltiazem (p less than .01) and to 325.6 +/- 73 sec by nifedipine (p less than .01). The drug combination further prolonged exercise time to 451.1 +/- 103 sec, which was significantly longer than the interval attained with either diltiazem (p less than .01) or nifedipine (p less than .01) alone. The plasma concentration of diltiazem was unaffected by the addition of nifedipine, whereas the plasma nifedipine concentration was significantly increased from 34.8 +/- 11 to 106.4 +/- 37 ng/ml (p less than .001) by the concomitant administration of diltiazem. These data suggest that exercise tolerance in patients with effort angina is increased by the concomitant administration of diltiazem and nifedipine associated with an increase in the nifedipine plasma concentration.

Adult↗
PubMed1988

Long-term survival of a patient with Lutembacher's syndrome.

An elderly woman with Lutembacher's syndrome remained asymptomatic until the age of 55, when she was treated for exertional dyspnea with digitalis and diuretics. She died of gastrointestinal hemorrhage and hepatic failure at the age of 69. The autopsy revealed a large atrial septal defect and mitral stenosis without rheumatic changes. This patient is the oldest reported survivor of Lutembacher's syndrome with nonrheumatic mitral stenosis.

Aged↗
PubMed1987

Evaluation of diseased coronary arterial branches by polar representations of thallium-201 rotational myocardial imaging.

The perfusion territories in polar representations of stress Tl-201 rotational myocardial imaging in patients with angina pectoris who had one diseased coronary segment were analyzed. The lesions proximal or distal to the first major septal perforator in left anterior descending arteries were detected by the presence or absence of defects at the base of the anterior septum. Right coronary artery lesions were detected by the presence of defects at the basal posterior septum, in contrast to the preservation of myocardial uptake at this portion in lesions of the left circumflex artery. The specific defect patterns were detected in cases with lesions at the first diagonal, obtuse marginal, and posterolateral branches. Recognition of these defects in the polar maps allows detailed detection of diseased coronary arterial branches.

Adult↗
PubMed1987

Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats.

Age-related changes in circulatory responses to short-term shaker stress were investigated in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Hemodynamics (microspheres) were measured at 8, 24, 48, and 96 weeks of age, and plasma catecholamines were measured at 8 and 96 weeks. At rest, elevated mean arterial pressure was associated with unaltered cardiac index and heart rate in SHR compared with WKY at all ages. Regional blood flow was largely similar in both strains, except for a reduced renal flow in 96-week-old SHR. Cardiac index and most regional blood flow tended to or did decline in both strains between 8 and 96 weeks. Plasma catecholamines were similar in both strains at 8 and 96 weeks. Shaker stress evoked responses similar to defense reactions in both strains. The incremental responses in mean arterial pressure, heart rate, cardiac index, and cerebral, skeletal muscle, and myocardial flow and the decremental responses in splanchnic, renal, and skin flow were greater in SHR than in WKY, particularly at 8 weeks. Most of these responses tended to or did decline between 8 and 96 weeks in both strains. The plasma catecholamine responses were also greater in SHR at 8 and 96 weeks, and they did not differ in either strain between these ages. Thus, circulatory and sympathoadrenal reactivity to acute stress were enhanced in SHR compared with WKY, independently of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1986

Atriopeptin III does not alter cardiac performance in rats.

The effects of atriopeptin III (APIII) on systemic haemodynamics were examined in 12 anaesthetized rats. Five minutes following intravenous injection (i.v.) of 10 micrograms/kg APIII, cardiac output CO, measured by electromagnetic flowmetry, stroke volume and mean arterial pressure (MAP) decreased by 14, 13 and 8% (P less than 0.05), respectively, and total peripheral resistance (TPR) increased by 10% (P less than 0.05). Heart rate (HR) and left ventricular end-diastolic pressure (LVEDP) did not change. In order to examine cardiac performance, whole blood was infused into three groups of 12 rats each receiving either no injection, APIII (10 micrograms/kg i.v.) or APIII (10 micrograms/kg i.v.) plus a continuous infusion of phenylephrine to increase MAP to pre-injection levels. Cardiac performance curves did not differ among the three groups. These data indicate that the immediate decreases in MAP and CO produced in rats by a maximum natriuretic bolus dose of APIII were not mediated by a negative myocardial inotropic effect.

Animals↗
PubMed1986

Hemodynamic effects of atrial natriuretic hormone.

The atrial natriuretic hormone (ANH) alters cardiovascular function independent of changes in body fluid volume. Most investigators agree that ANH decreases mean arterial pressure (MAP). However, although some investigators have observed a decrease in total peripheral resistance in association with the decrease in MAP, a more frequent observation has been decreased cardiac output (CO). The mechanism whereby ANH decreases CO is unknown, but does not appear to be the result of direct myocardial depression, reductions in intravascular or cardiopulmonary volumes, or venodilation. Alterations in skeletal muscle and splanchnic blood flow have been reported by some but not all investigators. Although increases in renal blood flow have been reported, they are transitory and have not been consistently observed by all researchers. The cardiovascular effects of ANH appear to be influenced not only by the dose, but also by the cardiovascular control mechanisms that operate at the time of ANH administration. Non-renin-dependent hypertensive models exhibit a decrease in MAP associated with decreased CO, whereas in renin-dependent animals this hypotension is associated with a decrease in total peripheral resistance.

Animals↗
PubMed1985

Hemodynamic effects of prolonged treatment with diltiazem in conscious normotensive and spontaneously hypertensive rats.

To determine systemic and regional hemodynamic effects of prolonged treatment with the calcium antagonist diltiazem (30 mg/kg twice daily by gastric gavage, for 3 weeks), data from 12 Wistar-Kyoto (WKY) and 10 spontaneously hypertensive (SHR) rats were compared with those obtained from 11 WKY and 10 SHR controls treated with the vehicle. Systemic and regional hemodynamics were determined in the conscious, unrestrained state using the reference sample microsphere method. Mean arterial pressure (MAP) decreased in SHR by 9% (183 +/- 4 to 167 +/- 4 mm Hg; p less than 0.05) but remained unchanged in WKY, while cardiac index (CI) tended to decrease in both strains; heart rate fell by 15% only in WKY (481 +/- 10 to 354 +/- 13 beats/min; p less than 0.05). Total peripheral resistance index (TPRI) tended to decrease in SHR but to increase in WKY. Organ blood flow in SHR decreased in skin and splanchnic organs, while organ vascular resistance decreased in brain and increased in splanchnic organs. In contrast, organ blood flow increased in heart and decreased in kidneys and skin of the WKY, while organ vascular resistance decreased in heart and increased in kidneys and skin. Thus, diltiazem produced nonuniform and different hemodynamic effects in the two strains. Further, diltiazem did not alter the cardiac mass in either rat strain. We therefore conclude that diltiazem demonstrated a mild hypotensive effect in SHR that was associated with slight reductions in CI and TPRI, the latter being nonuniformly distributed in the component organ circulations.

Animals↗
PubMed1985

Alterations in renal Na+K+ATPase activity and [3H]ouabain binding in Goldblatt hypertensive rabbits.

To evaluate the role of renal Na+K+ATPase in the presence of Goldblatt hypertension, the enzyme activity and [3H]ouabain binding were examined in cortical and medullary homogenates from two-kidney, one clip (2K1C), one-kidney, one clip (1K1C), unilaterally nephrectomized and normal rabbits. Four weeks after the surgery, systolic blood pressures (SBPs) of 2K1C and 1K1C rabbits were increased significantly to 128 +/- 3 and 129 +/- 2 mmHg, respectively. In contrast, SBPs in the normal controls and unilateral nephrectomized (1K) animals were 83 +/- 2 and 86 +/- 3 mmHg, respectively. In the 2K1C rabbits, atrophy (91%) occurred in the kidney on the ischaemic side and hypertrophy (110%) occurred in the contralateral kidney. Na+K+ATPase activity and number of [3H]ouabain binding sites were reduced in the homogenates of the ischaemic kidney of 2K1C rabbits. In the 1K1C rabbits, marked hypertrophy of the kidney (155%) occurred, and the activity of Na+K+ATPase and the number of [3H]ouabain binding sites increased slightly in the cortex and medulla, compared with the normal controls. 5'-Nucleotidase, a plasma membrane marker enzyme, remained unchanged in both groups of hypertensive rabbits. Dissociation constant (KD) values for [3H]ouabain binding did not differ significantly in the renal homogenates of of 2K1C and 1K1C, compared with findings in the normal controls. The inhibitory activity of plasma was measured by studying [3H]ouabain binding to Na+K+ATPase of renal tubular basolateral membrane vesicles purified by Percoll gradient. The inhibition was more pronounced with plasma from 2K1C, 1K1C and 1K rabbits than from the control animals. Our findings suggest that in the Goldblatt hypertensive model, changes in Na+K+ATPase activity were due to alterations in glomerular filtration rate (GFR).

Animals↗
PubMed1984

Systemic and regional hemodynamic effects of acute and prolonged treatment with urapidil or prazosin in normotensive and spontaneously hypertensive rats.

The regional and systemic hemodynamics of urapidil and prazosin were investigated after intravenous (1 mg/kg or 0.01 mg/kg, respectively) and prolonged (three weeks) oral treatment (20 mg/kg a day or 2 mg/kg a day, respectively) in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Following intravenous administration, both urapidil and prazosin decreased mean arterial pressure, mediated through a decrease in total peripheral resistance and accompanied by a transient increase in heart rate in both strains. The changes in regional circulations were more widespread after urapidil, but of longer duration after prazosin. Prolonged administration of urapidil or prazosin resulted in a significant decrease in mean arterial pressure and total peripheral resistance only in SHR. With urapidil treatment, the decrease in vascular resistance was distributed throughout all circulations, with no change in heart rate or cardiac index. Heart rate increased in WKY rats and cardiac index increased in SHR following prazosin treatment. Cardiac mass remained unchanged following treatment with either drug.

Animals↗
PubMed1983

Circadian rhythm of blood pressure in primary aldosteronism and renovascular hypertension--analysis by the cosinor method.

The circadian rhythm of blood pressure in 11 patients with primary aldosteronism (ALD) and 15 patients with unilateral renovascular hypertension (RVH) was analyzed using the cosinor method which fits a cosine function to a series of data. In ALD, both systolic (SP) and diastolic blood pressures (DP) increased in the late evening; the amplitude and acrophase of the circadian rhythm for SP were 7.3 (5.3 to 9.3, mean and 95% confidence limits) mmHg and 20:47 (19:42 to 21:52) hours, respectively, and for DP 2.6 (1.3 to 3.9) mmHg and 21:34 (19:40 to 23:28) hours, respectively. After excision of an adrenal adenoma in 6 patients, the circadian rhythm of SP and DP was abolished. In RVH, the acrophase of the circadian rhythm of SP and DP differed by about 12 hours; the amplitude and acrophase for SP were 5.7 (3.9 to 7.5) mmHg and 17:49 (16:35 to 19:02) hours, respectively, and for DP 1.5 (0.2 to 2.7) mmHg and 6:08 (2:44 to 9:31) hours, respectively. After various surgical interventions in 8 patients, the circadian rhythm of SP persisted with little change in acrophase, while that of DP disappeared. The difference in circadian rhythm suggests a difference in mechanisms of blood pressure control in ALD and RVH.

Adenoma↗
PubMed1983

Cation transport of red blood cells from hypertensive patients in Japan.

This study was performed to determine whether there is any difference in cation transport of red blood cells from normotensive subjects and hypertensive patients in Japan. Net Na+ efflux and net K+ influx rates were measured in sodium-loaded red cells from 19 normotensive subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes and the net cation flux rate were compared between these groups. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive subjects. Parameters such as age, sex, blood pressure, plasma renin activity, and plasma aldosterone concentration were also examined in 2 groups of essential hypertensive patients, divided on the basis of their Na+/K+ net fluxes. However, there is no significant difference between the groups. These results suggest that the ratio of cation flux is related to hypertension independently of these parameters.

Adolescent↗