Search PubMed⌕ Search

Biomedical subjects

T Sakamaki

Publications and source records attributed to T Sakamaki.

At least 109 records · Page 6Linked to original sources
PubMed1988

Plasma levels of atrial natriuretic peptide in patients with borderline and essential hypertension.

Plasma levels of atrial natriuretic peptide (ANP) were measured in outpatients with borderline hypertension (n = 15) and essential hypertension (n = 13) and in normotensive subject (n = 11). There were no significant differences among the three groups in age, serum protein, albumin, or electrolyte levels, plasma renin activity (PRA), or plasma concentrations of aldosterone and cortisol. The plasma ANP levels in the normotensive, borderline hypertensive, and essential hypertensive subjects were 36 +/- 6 pg/ml (mean +/- S.E.), 64 +/- 11 pg/ml, and 82 +/- 14 pg/ml, respectively. The levels in the essential hypertensive subjects were significantly (p less than 0.05) higher than those in the normotensives. In both borderline and essential hypertensives (n = 28), the plasma ANP levels were significantly correlated positively with systolic blood pressure (r = +0.385, p less than 0.05), and negatively with PRA (r = -0.484, p less than 0.05) and serum total calcium (r = -0.516, p less than 0.01). These results suggest that the elevation of circulating ANP in hypertensives is involved in the pathogenesis of hypertension.

Adult↗
PubMed1987

Measurement of mean arterial pressure in rats by a tail-cuff method with sensitive photoelectric sensors.

We evaluated a recently developed tail-cuff apparatus containing sensitive photoelectric sensors in the measurement of arterial pressure in rats. A total of 48 male Wistar rats were used in the study. The indirect mean arterial pressure (MPi) was determined from the cuff pressure when the pulse volume oscillations were maximal. To create sufficiently large pulse volume oscillations, we heated the rats for about 12 minutes at 38 degrees C prior to recording the pressure. The heating increased the mean arterial pressure by an average of 4 +/- 2 mmHg, as indicated by direct measurement of pressure. Three different sizes of cuffs were tested, with the result that the indirect measurements were nearly identical to those obtained directly when an appropriate cuff size was selected. The MPi was well correlated with the direct measurement of mean arterial pressure before (r = 0.918, p less than 0.001) and during (r = 0.903, p less than 0.001) elevation of arterial pressure via norepinephrine infusion. These results indicate that the MPi determined at maximum pulse volume oscillations coincides fairly well with the true mean arterial pressure.

Animals↗
PubMed1987

Role of atrial natriuretic peptide in mineralocorticoid escape phenomenon in patients with primary aldosteronism.

The withdrawal effect of spironolactone treatment on natriuresis was studied in relation to atrial natriuretic peptide (ANP) in five patients with primary aldosteronism due to adenoma. The patients had been treated with spironolactone for 2-3 months before they were admitted. After admission, blood pressure, body weight, and urinary excretion of sodium were measured daily. Venous samples were obtained twice a week for measurements of plasma levels of ANP, plasma renin activity (PRA), and plasma concentrations of aldosterone (PAC), cortisol, and deoxycorticosterone. The study was performed for 7 days during the treatment with spironolactone and for 18 days after stopping the administration. Plasma volume was determined two times, during the control period and on the 13th day after stopping spironolactone. Urinary sodium excretion decreased initially and returned to the control levels successively. Body weight and plasma volume increased, and blood pressure rose steadily. PRA and the plasma concentrations of cortisol and deoxycorticosterone decreased significantly (P less than 0.05); however, high levels of PAC did not alter significantly. Plasma ANP levels increased significantly (P less than 0.05) from 26 +/- 4 pg/ml during the control period to 195 +/- 47 pg/ml on the 13th day after stopping spironolactone. The data of the urinary sodium excretion showed the escape from sodium-retaining effect of aldosterone, and this escape could be explained by the increase in plasma ANP. Furthermore, ANP might contribute to the decrease in cortisol and deoxycorticosterone in plasma because of the direct inhibitory action of ANP on steroidogenesis.

Adult↗
PubMed1987

Retrovirus produced by a lymphoid cell line from an infant with acute lymphoblastic leukemia.

A lymphoid cell line CK-a was established from peripheral blood of an infant with acute lymphoblastic leukemia of non-T, non-B cell type with mediastinal tumor. The CK-a cells were positive for surface immunoglobulins, Epstein-Barr virus-specific nuclear antigen, HLA-DR and Leu 12 antigens, and negative for sheep erythrocyte-rosette-receptor, and Leu 1, 2, 3 and 4 antigens. Budding particles were detected in electron micrographs of ultrathin sections of the CK-a cells. In the culture media of CK-a cells, particles with a buoyant density of 1.16 g/ml and labeled with [3H]uridine and [35S]methionine but not with [3H]thymidine were found to carry reverse transcriptase activity which preferred Mg2+ to Mn2+. Enveloped particles of 80 to 120 nm in diameter were detected in the fractions at 1.16 g/ml by electron microscopy. Thus, the particles had properties compatible with a definition of Retroviridae, and were tentatively named CK virus (CKV). The genome size of CKV RNA determined by agarose-acrylamide composite gel electrophoresis was 6.1 +/- 0.2 kb. Immune electroblotting assay detected antibody reactive with a CKV protein with a molecular weight of 67,000 in the serum of the patient, but not in sera of an adult T cell leukemia patient and healthy controls. No syncytia were formed by mixed cultures of CK-a and XC cells.

Antibodies, Viral↗
PubMed1987

[Assessment of perfusion defects by intracoronary myocardial contrast echocardiography].

Myocardial contrast echocardiography has developed rapidly in the last few years. This paper is a review of this method based on our previous studies performed in 43 closed chest dogs. An injection of 2 ml of an agitated saline-Renografin mixture into the left main coronary artery provided contrast opacification of the entire circumference of the left ventricular myocardium. Contrast injection into the left anterior descending or the circumflex artery resulted in contrast opacification of localized regions of the left ventricle. Contrast injection into the left main coronary artery after a selective coronary artery occlusion resulted in a "negative" contrast outline of the corresponding area indicating the underperfused myocardium. The physiological and hemodynamic effects of the intracoronary injection of the contrast material appeared minor and brief. Perfusion defects after coronary artery occlusion assessed by myocardial contrast echo correlated well with those in equivalent sections by monastral blue dye injected into the left ventricle. Furthermore, the extent of myocardial necrosis after five hours of coronary occlusion assessed by myocardial contrast echo correlated well with the area of necrotic myocardium in equivocal slabs. Myocardial contrast washout index (T1/2) measured by digital intensity analysis of successive end-diastolic images was found to be significantly changed in dogs with varying degrees of coronary stenosis. Thus, the measurement of T1/2 appears to be feasible for evaluating degree of coronary stenosis, however, numerous technical problems remain to be clarified.

Animals↗
PubMed1986

Enhanced responses to pressor stimuli by intracerebroventricular infusions of angiotensin II in conscious rats.

Effects of the intracerebroventricular (IVT) infusion of a subpressor dose (3 ng/kg/min) of angiotensin II (ang II) on the pressor responses to intravenous (IV) infusions of ang II and to IV bolus injections of norepinephrine (NE) were studied in conscious rats. This study was undertaken to determine whether activations of the brain renin-angiotensin system alter pressor responsiveness to IV infusions of ang II and IV injections of NE in the conscious state. Pressor responses to IV infusions of ang II and IV injections of NE were potentiated by the concurrent IVT infusion of the subpressor dose of ang II. Plasma renin activity (PRA), plasma corticosterone (B), and plasma prolactin concentration (PRL) were also measured before and during the IVT infusion of the subpressor (3 ng/kg/min) or the pressor (50 ng/kg/min) dose of ang II in order to determine the mechanisms for this pressor hyperresponsiveness to vasoconstrictor substances. The IVT subpressor dose of ang II increased PRA, but did not significantly change B and PRL. The IVT pressor dose of ang II decreased PRA and increased B, but did not significantly change PRL. These results suggest that the brain renin-angiotensin system plays an important role in pressor responsiveness to IV ang II and NE. Although the mechanisms are not fully understood, pressor hyperresponsiveness to IV ang II and NE by an intracerebroventricularly administered subpressor dose of ang II may be related to increased sympathetic outflow, because of the increment in PRA.

Angiotensin II↗
PubMed1984

Regional differences in left ventricular response to atrial pacing in the dog: mapping of segmental function by two-dimensional echocardiography.

Two-dimensional echocardiography was applied in 10 closed-chest dogs to evaluate, in several left ventricular (LV) short-axis cross sections and subsegments, the regional contractile response to right atrial pacing. Compared with sinus rhythm (81 +/- 10 beats/min), which exhibited a moderate 7.2 +/- 12.0% (mean +/- standard deviation) base-to-apex increment in function, this gradient was significantly augmented to 34 +/- 12% by pacing at a heart rate of 180 beats/min. Measurements of wall thickening and perimeter shortening exhibited similar trends. Differences also were observed in subsegments of individual cross sections: in sinus rhythm the base-to-apex difference in function was relatively minor in the anterior and lateral aspects of the left ventricle (-9.1 +/- 18% and -1.9 +/- 19%), whereas a significant increase was noted in posterior and midseptal zones (18 +/- 17% and 22 +/- 30%). In response to pacing, the anterior and lateral wall base-to-apex gradients were significantly augmented (25 +/- 8% and 35 +/- 34%), but there was no further change in the posterior or septal regions. In conclusion, apical regions of the canine left ventricle responded to right atrial pacing with significant augmentation of contractile function, whereas more basal levels showed little response. Circumferentially, response to atrial pacing was most pronounced in the anterior and lateral segments.

Animals↗
PubMed1984

Verification of myocardial contrast two-dimensional echocardiographic assessment of perfusion defects in ischemic myocardium.

Myocardial contrast two-dimensional echocardiography was used in 21 closed chest dogs to assess its ability to delineate the extent of underperfused acutely ischemic myocardium. An agitated saline-Renografin echocardiographic contrast agent was injected into the left main coronary artery after left anterior descending coronary artery occlusion, and the size of the contrast echo-free area characterizing the perfusion defect was outlined in short-axis cross sections of the left ventricle. In 13 dogs, monastral blue dye was injected after 45 minutes of coronary artery occlusion and before sacrifice to provide anatomic delineation of underperfused zones in equivalent sections. Perfusion defects assessed by contrast two-dimensional echocardiography correlated well with those delineated by monastral blue dye (r = 0.91). Contrast echocardiographic study was also performed in eight other dogs at 5 hours of occlusion, after which infarct size was measured with triphenyl-tetrazolium-chloride. Contrast echocardiographic outline of the perfusion deficiency correlated but slightly overestimated the extent of necrosis (r = 0.88). It is concluded that contrast two-dimensional echocardiography can detect and outline the underperfused "risk area" during acute coronary artery occlusion, and may also permit assessment of the extent of myocardial infarction.

Animals↗
PubMed1984

Correlation of myocardial echo contrast disappearance rate ("washout") and severity of experimental coronary stenosis.

The relation between experimental coronary stenosis and myocardial contrast echo disappearance rate ("washout") was investigated in anesthetized closed chest dogs. Of 13 dogs, 8 had serial contrast echographic studies with two successive degrees of coronary stenosis (50 and 70%) produced by threading stenotic plugs into the proximal left circumflex coronary artery. Studies were repeated with complete coronary occlusion achieved by inflation of an intracoronary balloon immediately proximal to the plugs. Myocardial contrast echograms were recorded in short-axis cross sections of the left ventricle after intracoronary injection of 2 ml hand-agitated saline-Renografin solution through a catheter placed in the coronary artery. An echo contrast washout index (t 1/2) was measured by digital processing computer analysis of successive end-diastolic images obtained by two-dimensional echocardiography during myocardial contrast agent injection. The injection to injection correlation coefficient of these t 1/2 measurements was satisfactory (r = 0.87, standard error of estimate 4.8 seconds). Involved segment t 1/2 measurements were found to be significantly altered by intracoronary stenosis and occlusion, ranging from 23 +/- 6 seconds (mean +/- standard deviation) in the control state, 29 +/- 9 and 44 +/- 10 seconds for 50 and 70% stenosis, respectively, and 104 +/- 35 seconds for total occlusion. It was concluded that myocardial contrast two-dimensional echocardiographic measurement of t 1/2 appears to be a useful index of the degree of coronary stenosis.

Animals↗
PubMed1984

Effect of spironolactone on fluid volumes and adrenal steroids in primary aldosteronism.

Plasma volume (PV) and extracellular fluid volume (ECF) were determined in 7 patients with essential hypertension (controls) and in 10 patients with primary aldosteronism, while on a high Na diet (342 mEq/day) and on a low Na diet (12 mEq/day). The volume studies were repeated in 6 of the primary aldosteronism patients during treatment with spironolactone for over 3 months. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), cortisol concentration, and serum Na and K concentrations were measured in all patients while on a Na-restricted diet (85 mEq/day) as well as on high-Na and low-Na diets. There were no significant changes in arterial pressure during different Na diets in any groups of patients with essential hypertension, or primary aldosteronism with and without spironolactone therapy. Spironolactone treatment normalized the arterial pressure in patients with primary aldosteronism at all Na intakes. These patients had greater values for PV and ECF than did those with essential hypertension. Spironolactone treatment reduced PV during the low-Na diet, but did not alter it during the high-Na diet. Spironolactone did not produce significant changes in ECF during either the high-Na or low-Na diets. Although there were no changes in PV and ECF in patients with primary aldosteronism due to changes in Na intake, both PV and ECF were significantly less in these patients during spironolactone treatment and in patients with essential hypertension during low-Na intake than during high-Na intake. With primary aldosteronism, PRA was depressed and PAC was elevated when compared to essential hypertension, these were not altered by different Na diets in the patients with primary aldosteronism as they were in those with essential hypertension. During treatment with spironolactone the PRA was restored to normal and showed normal changes with variations in dietary Na, but PAC remained elevated during spironolactone. Plasma cortisol was the same among those with essential hypertension and patients with untreated and spironolactone-treated primary aldosteronism. Serum K was less in untreated primary aldosteronism during all Na diets than in essential hypertension, but during spironolactone it was restored to normal. These results suggest that in primary aldosteronism the reduction in arterial pressure by spironolactone treatment does not occur simply by reductions in body fluid volumes. The long-term treatment of patients with primary aldosteronism with spironolactone does not inhibit the production of aldosterone, possibly because of enhanced activity of the renin-angiotensin system and an increase in serum K.

Adrenal Cortex Hormones↗
PubMed1984

Hemodynamic effects of captopril in one-kidney, one clip hypertensive rabbits.

Hemodynamic effects of captopril were examined in chronic one-kidney, one clip renal hypertensive rabbits and normotensive controls either in normal sodium or in sodium depletion. The mean arterial pressure (MAP) of hypertensive and normotensive rabbits in sodium depletion did not differ from that in normal sodium, while plasma renin activity (PRA) was elevated by sodium depletion. The cardiac output of sodium depleted groups decreased slightly. The increase in total peripheral resistance was greater in hypertensive than in normotensive groups. The MAP in all groups was decreased by acute administration of captopril irrespective of sodium intake. The decrease in MAP in the sodium-depleted hypertensive group was correlated with the control values of PRA, but no correlation was observed in other groups. Captopril significantly reduced the cardiac output of the sodium-depleted hypertensive group, but not of the other groups. These results show that: (1) the lowering effect of captopril on arterial pressure is not mediated only by blocking of the renin-angiotensin system, and (2) the decrease in cardiac output with captopril in sodium depleted hypertensive rabbits is an important factor in the reduction in the arterial pressure.

Animals↗
PubMed1983

Relation between functional response to nitroglycerin and extent of myocardial necrosis in dogs: mapping of the left ventricle by 2-dimensional echocardiography.

The relation between functional response to brief nitroglycerin infusions and extent of myocardial damage was studied sequentially in closed-chest dogs with acute occlusion of the left anterior descending coronary artery. Two-dimensional echocardiography was used to derive segmental left ventricular (LV) function (systolic fractional area change and systolic wall thickening), and this function was compared with the extent of necrosis measured 5 hours after occlusion in equivalent segments of corresponding pathologic slabs. Two-dimensional echocardiographic study before the dogs were killed indicated that remote nonnecrotic segments always responded to nitroglycerin by significant augmentation of segmental LV function. Segments in which necrosis was less than 40% showed a significant nitroglycerin-induced potentiation in segmental LV function. In contrast, segments in which necrosis was greater than 60% had no potentiation with nitroglycerin. In those segments in which eventual necrosis was 60 to 80%, significant nitroglycerin-induced augmentation in segmental LV function was observed only before and 30 minutes after the coronary occlusion. When the degree of necrosis was greater than 80%, no significant potentiation of segmental LV function was observed even as early as 30 minutes after occlusion. Thus, the degree of nitroglycerin-induced potentiation of segmental cardiac function is closely associated with the extent of myocardial necrosis in the particular ventricular segment. Two-dimensional echocardiography coupled with a nitroglycerin potentiation test might be useful for assessment of the viability of ischemic myocardium.

Animals↗