Search PubMed⌕ Search

Biomedical subjects

S Minatoguchi

Publications and source records attributed to S Minatoguchi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Marked expression of plasma brain natriuretic peptide is a special feature of hypertrophic obstructive cardiomyopathy.

OBJECTIVES: We examined whether plasma brain natriuretic peptide levels are abnormally elevated in hypertrophic obstructive cardiomyopathy compared with other cardiac diseases. BACKGROUND: We previously reported that plasma brain and atrial natriuretic peptide levels were elevated in hypertrophic cardiomyopathy. METHODS: We compared plasma concentrations of brain and atrial natriuretic peptide and hemodynamic and echocardiographic data in 50 patients with hypertrophic obstructive cardiomyopathy (n = 15, mean [+/-SD] intraventricular pressure gradient 37 +/- 16 mm Hg), hypertrophic nonobstructive cardiomyopathy (n = 15), aortic stenosis (n = 10, mean pressure gradient 41 +/- 18 mm Hg) and hypertensive heart disease (n = 10, mean systolic/diastolic blood pressure 203 +/- 16/108 +/- 11 mm Hg, respectively) and 10 normal subjects. RESULTS: Plasma brain natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group (397.1 +/- 167.8 pg/ml*) than in the hypertrophic nonobstructive cardiomyopathy (60.0 +/- 48.1 pg/ml*), hypertensive heart disease (53.9 +/- 31.4 pg/ml*), aortic stenosis (75.4 +/- 54.3 pg/ml*) and normal groups (9.8 +/- 6.4 pg/ml [*p < 0.05 vs. normal group, p < 0.05 vs. hypertrophic obstructive cardiomyopathy group]). Although plasma atrial natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group than the other patient groups, the brain/atrial natriuretic peptide ratio in the hypertrophic obstructive cardiomyopathy group was higher (4.5 +/- 2.3) than those in the other three patient groups (1.1 to 1.4) and the normal group (0.7 +/- 0.5). Left ventricular end-diastolic pressure and left ventricular end-diastolic volume index were similar among the four patient groups. The interventricular septal thickness and the ratio of interventricular septal thickness to left ventricular posterior wall thickness were similar between the hypertrophic obstructive and nonobstructive cardiomyopathy groups. CONCLUSIONS: Abnormal elevations of plasma brain natriuretic peptide levels are difficult to explain on the basis of hemodynamic and echocardiographic data and are a special feature of hypertrophic obstructive cardiomyopathy.

Adult↗
PubMed1996

[Sarcoidosis in a patient with autoimmune hemolytic anemia].

A 65-year-old woman was admitted to our hospital because of severe anemia. A skin biopsy was done in January 1994 and sarcoidosis was diagnosed. Diffuse reticular shadows were seen in both lung fields on a chest X-ray film and mediastinal lymph node swelling was seen on a chest CT scan. She was followed as an outpatient and was not treated. She suddenly experienced vertigo and general fatigue in March 1995. Laboratory findings on admission were as follows: Hb 6.2 g/dl, MCV 115.9 fl, Ret 198%, LDH 732 IU/L, I-Bil 1.9 mg/dl, and Coombs' test was positive. Autoimmune hemolytic anemia was diagnosed, and she was treated with prednisolone (1 mg/kg). As of the time of this writing, she has no relapse of hemolytic anemia though prednisolone was discontinued 6 months ago.

Anemia, Hemolytic, Autoimmune↗
PubMed1996

Highly sensitive ELISA for soluble Fas in serum: increased soluble Fas in the elderly.

We have developed and characterized a highly sensitive ELISA for soluble Fas (sFas) in the serum. The linearity of calibrator range was 0.06-2.00 micrograms/L and the detection limit was 0.01 microgram/L. The average within- and between-run CVs were 3.9% and 3.8%, respectively. The recovery of added sFas to serum was 93-118%. The effects of possible interferences (tryglyceride, hemoglobin, bilirubin) were negligible. We determined serum sFas in 155 healthy subjects, ages 20-69. The mean value of sFas in men (2.50 +/- 0.63 micrograms/L, n = 78) was significantly higher than that in women (2.01 +/- 0.53 micrograms/L, n = 77) (P < 0.001). Furthermore, there was a significant correlation between serum sFas concentration and age (men, r = 0.397, P < 0.001; women, r = 0.569, P < 0.001). Although the concentrations of sFas tended to increase with aging, it remains to be clarified how Fas-mediated apoptosis relates to aging.

Adult↗
PubMed1995

Modulation of noradrenaline release through presynaptic alpha 2-adrenoceptors in congestive heart failure.

Stimulation of presynaptic alpha 2-adrenoceptors inhibits the release of noradrenaline from sympathetic nerve endings; however, the extent to which it operates in patients with congestive heart failure is still unknown. To investigate the degree of negative feedback to the release of noradrenaline via presynaptic alpha 2-adrenoceptors at sympathetic nerve endings, we measured plasma noradrenaline levels before and after the injection of phentolamine (i.e., plasma noradrenaline concentration at rest, plasma noradrenaline concentration after phentolamine injection [NAph], and the phentolamine-induced increase in plasma noradrenaline [delta NAph]). Plasma noradrenaline concentration at rest, NAph, and delta NAph increased in a stepwise manner from New York Heart Association class I to class III. A positive correlation was found between the plasma noradrenaline at rest and delta Naph (n = 123, r = 0.697, p < 0.001). These results suggest that the enhanced release of plasma noradrenaline is substantially buffered by the mechanism of noradrenaline release-inhibitory presynaptic alpha 2-adrenoceptors in patients with congestive heart failure, and this buffer serves to protect organs such as the heart from excess sympathetic stimulation.

Aged↗
PubMed1995

Plasma adrenaline modulates alpha 1-adrenoceptor mediated pressor responses and the baroreflex control in patients with borderline hypertension.

Plasma level of adrenaline has been reported to be elevated in borderline hypertension. However, its role in developing and maintaining hypertension is still not completely understood. This study aimed to estimate the role of plasma adrenaline in developing hypertension. Ten patients with borderline hypertension (BHT) and 10 age-matched normotensive subjects were included. We infused at least three graded doses of phenylephrine, an alpha-adrenoceptor agonist, into the antecubital vein of subjects lying quietly in a supine position. Mean blood pressure was measured continuously through the right radial artery. Cardiac output was measured by the thermodilution method before and after the administration of each dose of phenylephrine infusion. We obtained dose-response curves for mean blood pressure and total peripheral resistance to phenylephrine. Baroreflex sensitivity was calculated by plotting the longest R-R intervals against the elevated peak mean blood pressure after the infusion of each dose of phenylephrine. Plasma noradrenaline and adrenaline concentrations at rest were measured by high performance liquid chromatography coupled with trihydroxyindole fluorimetric detection. The plasma adrenaline level at rest was higher in patients with BHT than in normotensive subjects. With graded infusion of phenylephrine, both the pressor responses and the changes in total peripheral resistance were greater in patients with BHT than in normotensive subjects. The plasma adrenaline level was positively correlated with the slope of dose response curves for the increments of mean blood pressure to phenylephrine (r = 0.60, p < 0.01). Baroreflex sensitivity was reduced in patients with BHT as compared with normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Modulation of norepinephrine release in adriamycin-induced heart failure in rabbits: role of presynaptic alpha 2-adrenoceptors and presynaptic angiotensin II receptors.

In congestive heart failure (CHF), sympathetic neurotransmitter release is enhanced. We investigated the possibility that this is due in part to alterations in activation of either release-inhibiting alpha 2-adrenoceptors or release-enhancing angiotensin II (AII) receptors at postganglionic sympathetic nerve endings. CHF was induced in rabbits by adriamycin [1 mg/kg intravenously (i.v.), twice weekly for 8 weeks] and was characterized by reduced cardiac output (CO) and enhanced norepinephrine (NE) release rate in pentobarbital-anesthetized rabbits. After pithing and stimulation of the spinal sympathetic outflow, there was no difference in NE release rate between the two groups, suggesting that the enhanced NE release rate observed in adriamycin-treated anesthetized rabbits was of central origin. The alpha 2-adrenoceptor-blocking drug yohimbine (1 mg/kg, i.v.) enhanced NE release rate, which is an indication of feedback inhibition of NE release through presynaptic alpha 2-adrenoceptors. In anesthetized rabbits, this effect of yohimbine was greater in adriamycin-treated than in vehicle-treated animals. However, in pithed rabbits with electrically stimulated sympathetic outflow, there was no difference in the facilitative effect of yohimbine between the two groups, suggesting that inhibitory presynaptic alpha 2-adrenoceptors are activated to a greater extent in heart failure due to the increased transmitter release. Removing inhibitory alpha 2-adrenoceptor input has a functional consequence in that yohimbine increased heart rate (HR) in adriamycin-treated but not in vehicle-treated anesthetized rabbits. Captopril (1 mg/kg, i.v.) decreased NE release rate in pithed rabbits with stimulated sympathetic outflow but had no effect on NE release rate in anesthetized rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1993

Modulation of noradrenaline release via activation of presynaptic beta-adrenoceptors in rabbits with adriamycin-induced cardiomyopathy.

We investigated the role of beta-adrenoceptors at postganglionic sympathetic nerve endings in noradrenaline release in rabbits with cardiomyopathic congestive heart failure produced by adriamycin (1 mg/kg, I.V., twice a week for 8 weeks). Plasma noradrenaline levels were measured before, 30 min after, and 60 min after the start of continuous intravenous administration of adrenaline (0.06 micrograms/kg/min) in adriamycin-treated and vehicle-treated rabbits in anesthetized condition and pithed condition with electrically stimulated sympathetic outflow (3 Hz, 1 ms square wave pulse, 90 V). In both the anesthetized and pithed conditions, adrenaline increased plasma noradrenaline levels in vehicle-treated rabbits. However, in the adriamycin-treated rabbits, adrenaline had no effect on the plasma noradrenaline level. Pretreatment with propranolol (0.2 mg/kg, bolus I.V. + 0.1 mg/kg/hr, continuous infusion) almost completely abolished the rise in plasma noradrenaline associated with adrenaline infusion in vehicle-treated rabbits. These results suggest that in rabbits with adriamycin-induced cardiomyopathy, the noradrenaline release from the sympathetic nerve endings via the activation of presynaptic beta-adrenoceptors is reduced. This might be due to down-regulation of presynaptic beta-adrenoceptors caused by the elevated plasma noradrenaline due to cardiac failure. However, other possibilities such as reduced affinity or impaired signal transduction cannot be excluded.

Animals↗
PubMed1992

Enalapril decreases plasma noradrenaline levels during the cold pressor test in human hypertensives.

1. The effects of the angiotensin-converting enzyme (ACE) inhibitor enalapril on the responses of blood pressure and plasma catecholamine levels to the cold pressor test in human hypertensives were examined. 2. Systolic and diastolic blood pressure decreased significantly after treatment with enalapril (5 mg/day for 4 weeks) as did the resting level of plasma noradrenaline. 3. The cold pressor test induced a rise in blood pressure and plasma noradrenaline levels. After 2 and 4 weeks enalapril treatment, the rises in the plasma noradrenaline level and systolic and diastolic pressure due to cold pressor test were reduced significantly. 4. These results suggest that ACE inhibition has a sympatho-inhibitory effect. One possible explanation is that enalapril reduces angiotensin II formation thus decreasing the activation of release-enhancing angiotensin II receptors on postganglionic sympathetic nerve endings.

Blood Pressure↗
PubMed1992

A comparison of guanfacine, bunazosin, atenolol and nadolol on blood pressure and plasma noradrenaline responses to cold pressor testing.

1. The role of the presynaptic adrenoceptor subtypes in man was investigated based on observation of the changes in blood pressure (delta BP) and plasma noradrenaline concentration (delta NA) with the cold pressor test (CPT). 2. The CPT was well reproducible for BP and NA when performed at a 2 week interval in patients with mild hypertension. 3. After administration for 4 weeks, guanfacine (Gf; alpha 2-adrenoceptor agonist) decreased the delta NA response to CPT. 4. After administration for 2 or 4 weeks, bunazosin (Bu; alpha 1-adrenoceptor antagonist) atenolol (At; beta 1-adrenoceptor antagonist) and nadolol (Nd; non-selective beta-adrenoceptor antagonist) did not affect the delta NA response to CPT. 5. Both Gf and Bu decreased the systolic blood pressure response (delta SBP) to CPT after 4 weeks of the administration. Neither At nor Nd significantly changed the delta SBP response to CPT. 6. It is likely that Gf stimulated the presynaptic alpha 2 adrenoceptors at the sympathetic nerve endings as well as the central alpha 2 adrenoceptors, inhibiting the release of noradrenaline. It is unlikely that Bu, At and Nd exerted any clearly defined action on the presynaptic adrenoceptors in human hypertensive subjects.

Adrenergic alpha-Antagonists↗
PubMed1992

The effects of phentolamine and nitroglycerin on right-sided hemodynamics in cardiac patients can be explained by a shift of the systemic venous return curve and right-ventricular output curve.

The present study investigated the effects of phentolamine (PH) and nitroglycerin (NG) on the hemodynamics of the right heart in patients with cardiac disease. The patients were divided into a well-functioning left heart group (W group, n = 15) and a poorly-functioning left heart group (P group, n = 15). Right cardiac hemodynamic parameters and plasma noradrenaline (NA) and adrenaline (A) concentrations were measured before and after administering PH (0.1 mg/kg, i.v.) or NG (0.6 mg, sublingual). In a parallel animal study we obtained a systemic venous return curve by measuring mean circulatory pressure (MCP), mean right atrial pressure (RAP) and cardiac output, before and after administering PH (0.1 mg/kg, i.v.) or NG (12.5 micrograms/kg, i.v.) to anesthetized open-chest dogs (n = 14). We used MCP data (W group: 7.5 mmHg, P group: 10 mmHg) obtained in a separate series of human studies in our laboratory. We constructed the venous return curve by connecting the MCP point on abscissa with the cardiac index (CI)-RAP plot obtained in the clinical study. We also constructed the right ventricular output curve by connecting the point of -2 mmHg on the abscissa with the CI-RAP plot. We obtained the following results: (1) PH shifted the CI-RAP plot to the left and upwards, while NG shifted the CI-RAP plot to the left almost horizontally on the CI-RAP plane, where CI was plotted on ordinate and RAP on abscissa. The length [formula: see text] C = control point, PH = point after PH) of the shift of CI-RAP plot due to PH was greater in the P group than in W group, while there was no difference in the length [formula: see text] C = control point, NG = point after NG) of the shift of CI-RAP plot due to NG between P and W groups. (2) Both PH and NG significantly elevated plasma NA and A concentrations in both the W and P groups. In the P group, PH increased the plasma NA concentration significantly more than did NG, but both drugs increased plasma A concentration to a similar extent. (3) Both PH and NG significantly decreased the mean pulmonary arterial pressure with NG doing so significantly more than PH.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1991

Milrinone inhibits sympathetic-mediated tachycardia by a postjunctional action independent of cyclic AMP.

In pithed rats with stimulated sympathetic outflow, the phosphodiesterase inhibitor milrinone (0.3 mg/kg, i.v.) decreased the peak tachycardiac response produced by both sympathetic nerve stimulation (15 s at 0.5-3 Hz) and norepinephrine administration (0.3-5 micrograms/kg, i.v.). However, another phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX, 0.5 mg/kg, i.v.) had no effect on the peak tachycardic response to sympathetic stimulation. Similarly, in isolated rat atria, milrinone (9 mumol/L) inhibited the tachycardia produced by norepinephrine, whereas IBMX (1 mumol/L) had no effect. The inhibitory effect of milrinone on sympathetic responses was not due to changes in norepinephrine release since milrinone (9 mumol/L) increased norepinephrine release in isolated rat atria incubated with [3H]norepinephrine. When the duration of the tachycardia (rather than the peak tachycardic response) produced by sympathetic nerve stimulation was measured, it was found to be prolonged by both milrinone and IBMX, suggesting that in this case cyclic AMP was involved. Furthermore, in contrast to its inhibitory effects on norepinephrine-induced tachycardia in rat atria, milrinone enhanced the tachycardia produced by the adenylate cyclase activator forskolin. These results suggest that milrinone has complex actions on sympathetic control of heart rate and that beta-adrenoceptor tachycardia occurs by mechanisms dependent on and independent of cyclic AMP.

1-Methyl-3-isobutylxanthine↗
PubMed1990

[Plasma noradrenaline response to phentolamine in "latent" left-sided heart failure].

To estimate the pumping function of the left-sided heart in patients with "latent" left-sided heart failure due to heart disease which primarily affected the left-side of the heart (former NYHA class I and II), we measured (i) the increase of peripheral venous pressure in response to supine mild leg exercise (delta VP), and (ii) the increase of plasma noradrenaline (NA) concentration due to phentolamine (PH) injection (delta NAPH). We divided the patients into well-functioning left-sided heart group (delta CI/delta PAW greater than 0.180 L.min-1.M-2.mmHg-1) and poorly-functioning left-sided heart group (delta CI/delta PAW less than or equal to 0.180 L.min-1.M-2.mmHg-1) on the basis of a ratio (delta CI/delta PAW), relating the increase in cardiac index (delta CI) in response to exercise to the concomitant increase in mean pulmonary artery wedge pressure (delta PAW). This diving line (delta CI/delta PAW = 0.180 L.min-1.M-2.mmHg-1) correlated with delta VP (diving line: delta VP = 35 mmH2O) and with delta NAPH (diving line: delta NAPH = 0.353 ng/ml). Our results suggest that delta VP and delta NAPH reflected the pumping function of the left-sided heart with considerable accuracy.

Cardiac Output, Low↗
PubMed1989

Differential vasodilator effect of nitroglycerin on systemic capacitance and resistance vessels in anesthetized dogs, and the mechanism of its action--a study by measuring mean circulatory pressure and total peripheral resistance.

The aim of our studies was to examine if the baroreceptor reflex induced by intravenous injection of nitroglycerin (NG) nearly nullifies the vasodilator action of NG on the systemic capacitance vessels in dogs anesthetized with pentobarbital. We performed total spinal anesthesia (TSA) in open-chest dogs to eliminate the baroreceptor reflex. Dogs in which mean blood pressure (MBP) was maintained at about 100 mmHg by continuous intravenous infusion of epinephrine formed the TSA 100 group, and those in which MBP was maintained at about 70 mmHg formed the TSA 70 group. Dose-response curves relating 5-6 different doses (0.8 to 200 micrograms/kg) of intravenous NG, to changes in mean circulatory pressure (% delta MCP) and to changes in total peripheral resistance (% delta TPR), were constructed. These data were compared with those from untreated dogs. In addition, we also studied plasma catecholamine (CA) concentrations before and after the intravenous injection of NG. (1) There was no significant difference in the dose-response curves of NG for % delta TPR between the 3 groups. (2) There was no significant difference in the dose-response curves for % delta MCP between the 2 TSA groups. However, there was significant difference in the dose-response curves for % delta MCP between the TSA groups and the untreated dogs. The dose-response curves for % delta MCP in the TSA groups shifted upwards as compared with that of the untreated dogs. (3) In the TSA 100 group, there was no significant increase in the plasma CA concentrations with 100 micrograms/kg of NG. In the untreated group, intravenous injection of 12.5 micrograms/kg and 100 micrograms/kg of NG caused a dose-related fall in MBP and a dose-related rise in the plasma norepinephrine and epinephrine concentrations. Our results suggest that the vasodilator action of NG on the systemic capacitance vessels in the untreated dogs was counterbalanced partly by the vasoconstriction produced by the baroreceptor reflex, with its direct vasodilator effect masked when the hypotensive doses of NG were given acutely.

Anesthesia, Spinal↗
PubMed1989

Increase in plasma noradrenaline concentration after the administration of phentolamine in the patients with "latent" left-sided heart failure.

We measured increments of peripheral venous pressure induced by dynamic leg exercise (delta VP) in 10 healthy subjects (Group C) and 70 patients with heart diseases which primarily affect the left-side of the heart. None of the subjects showed apparent symptoms of left- or right-sided heart failure. The patients were divided into 2 groups on the basis of delta VP, namely, Group N (delta VP less than 35 mmH2O, n = 30, normal reaction) and Group H (delta VP greater than or equal to 35 mmH2O, n = 40, abnormal reaction). We measured the increments of plasma concentrations of noradrenaline (delta NAPH) and adrenaline (delta APH) with infusion of phentolamine (PH). Parallel studies with nitroglycerin and prazosin supplied strong evidence that delta NAPH was brought about mainly by the blockade of alpha 2-receptors at the sympathetic nerve terminals. Thus, we estimated the degree of sympathetic nerve activity from the central nervous system by opening using PH the negative feed-back loop for noradrenaline (NA) release at the sympathetic nerve terminals, and this degree of sympathetic nerve activity was compared with the degree of delta VP. The results obtained were 1) there was a rough overall correlation between delta VP and delta NAPH in the subjects of Groups C, N and H, and 2) delta NAPH was significantly higher in Group H than in Groups C and N. These results suggest that much reliance can be placed on the measured increment of plasma NA concentration in response to the administration of PH in assessing the degree of enhanced sympathetic nerve activity in the patients with "latent" left-sided heart failure.

Adult↗
PubMed1988

Response of peripheral venous pressure and plasma catecholamine concentration to supine leg exercise--a study in patients with mild congestive heart failure.

We measured the peripheral venous pressure (VP) in supine leg exercise in 25 "normal" subjects and 122 patients with primarily left-sided heart diseases (NYHA class I = 68, class II = 54 cases) to determine whether or not plasma catecholamine concentration would increase in patients with mild congestive heart failure, in response to dynamic exercise. Cardiac patients (n = 122) were divided into 2 groups on the basis of VP increment (delta VP): Group N had 60 patients with delta VP less than 35 mmH2O, and Group H had 62 patients with delta VP in excess of 35 mmH2O. Plasma concentrations of noradrenaline (NA) and adrenaline (A) were measured before and during leg exercise. The relation between delta VP, NA and A, and the relation between delta VP and increments of NA (delta NA) and of A (delta A) by leg exercise were studied in both the cardiac patients and the "normal" subjects (Group C). (1) NA at rest was 0.225 +/- 0.016 ng/ml (mean +/- SE) in Group C and 0.216 +/- 0.009 ng/ml in Group N. It was 0.468 +/- 0.026 ng/ml in Group H, which was significantly higher than in Group C (p less than 0.001), or Group N (p less than 0.001). (2) delta NA was 0.051 +/- 0.009 ng/ml (mean +/- SE) in Group C, 0.067 +/- 0.007 ng/ml in Group N, and 0.249 +/- 0.019 ng/ml in Group H. There was a statistically significant difference in delta NA between Groups C and H (p less than 0.001) and between Groups N and H (p less than 0.001). (3) There was no significant difference between the three groups in A at rest, or in delta A. (4) There was a correlation between delta VP and NA at rest (r = 0.614, p less than 0.001) and between delta VP and delta NA (r = 0.708, p less than 0.001). These data suggest that sympathetic nervous activity increased in the patients with high delta VP but without overt heart failure, and that the constriction of the capacitance vessels caused by an increase in NA could be at least one of the mechanisms involved in raising the delta VP in those patients.

Adolescent↗
PubMed1987

Effects of phentolamine on response to supine leg exercise of peripheral venous pressure and plasma catecholamine concentration--a study in patients with mild congestive heart failure.

The present study examined the effects of phentolamine (PH) on the increments in peripheral venous pressure (delta VP), and of plasma noradrenaline (delta NA) and adrenaline (delta A) concentration, in response to supine leg exercise. Peripheral venous pressure and plasma catecholamine concentrations were measured at rest and during exercise, before and after intravenous injection of PH (0.1 mg/kg) in 10 healthy volunteers (Group C), and in 42 patients with primarily left-sided heart diseases but without apparent right-sided or left-sided heart failure (NYHA class I, II). These cardiac patients were divided into 2 groups on the basis of delta VP. Those with delta VP below 35 mmH2O comprised the normal group (Group N), and those with delta VP more than 35 mmH2O the abnormally high group (Group H). 1) In Group C, delta VP changed only slightly from 11.1 +/- 2.8 (mean +/- SE) to 4.9 +/- 1.7 mmH2O with an intravenous injection of PH. On the other hand, PH caused a significant decrease in delta VP from 22.2 +/- 2.3 to 10.4 +/- 2.3 mmH2O in Group N (p less than 0.001), and from 52.7 +/- 3.4 to 17.0 +/- 12.4 mmH2O in Group H (p less than 0.001). It was suggested that PH blocked the alpha-receptors of the systemic capacitance vessels, thereby inhibiting the constriction of these vessels. 2) Both NA at rest and delta NA before PH were significantly higher in Group H than those in Groups C or N. delta NA increased significantly after the PH injection in all 3 groups, i.e., from 0.038 +/- 0.013 (mean +/- SE) to 0.282 +/- 0.051 ng/ml in Group C, from 0.056 +/- 0.013 to 0.279 +/- 0.034 ng/ml in Group N and from 0.279 +/- 0.034 to 0.839 +/- 0.103 ng/ml in Group H. The increase in delta NA after PH was especially marked in Group H. It was suggested that the "sympathetic nervous activity" was increased in the patients with an impaired left ventricular pumping function. 3) PH caused a slight increase in delta A in all groups, but there was no significant difference in delta A before and after PH in the 3 groups.

Adult↗