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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure. 153 81

The specific binding sites for atrial natriuretic peptide (ANP) were present in cultured vascular smooth muscle cells (VSMC) from stroke-prone spontaneously hypertensive (SHRsp) and Wistar-Kyoto(WKY) rats with a Bmax of 3.65 +/- 0.13 and 1.89 +/- 0.09 pmol/mg pr. and a Kd of 72.0 +/- 10.2 and 42.1 +/- 4.8 x 10(-12) mol/L, respectively. The basal levels of cGMP of the two strains showed no statistical difference. After treatment with ANP (1.67 x 10(-7) mol/L) for 5 min, the cGMP levels of VSMC were increased by 139 folds in SHRsp and 271 folds in WKY rats, i.e., cGMP levels were significantly lower in the former (P less than 0.01). Therefore, the cultured VSMC of SHRsp had higher ANP receptor density but lower affinity and responsiveness to ANP than that of WKY rats. After incubation of VSMC in the medium containing high NaCl (2-folds of normal) at 37 degrees C for 24 h, the number of ANP binding sites decreased to 34.8 +/- 8.2% in SHRsp and to 38.6 +/- 9.4% in WKY rats (P less than 0.01) with a parallel decrease of cGMP, while the affinity of ANP receptor did not change. It is suggested that the lower responsiveness of ANP receptor to ANP in SHRsp might result in a diminution of vasorelaxation to ANP and thus an increase of arterial pressure. In addition, the more down-regulation of ANP receptor by high NaCl in cultured VSMC from SHRsp implicates that it is one of the mechanisms that high dietary intake of NaCl might enhance high blood pressure.
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PMID:[Regulation of atrial natriuretic peptide receptor in cultured aortic vascular smooth muscle cells from stroke-prone spontaneously hypertensive and Wistar-Kyoto rats]. 166 42

We examined the effect of atrial natriuretic peptide on cerebral edema in 96 rats. Forty-four rats were given 30 (n = 11), 120 (n = 26), or 150 (n = 7) micrograms/kg of the peptide intravenously over 24 hours after occlusion of the left middle cerebral artery to induce cerebral ischemia. We then measured the brain water content, the brain sodium and potassium contents, the in vitro proton nuclear magnetic resonance longitudinal (T1) and transverse (T2) relaxation times, and the area of the edematous regions. Compared with saline treatment (n = 39), peptide treatment decreased the brain water content in a dose-dependent manner and decreased the brain sodium content significantly (p less than 0.05). Peptide treatment also suppressed the lengthening of both T1 and T2 in edematous tissue (p less than 0.05 and p less than 0.01, respectively) and reduced the area of the edematous regions observed by magnetic resonance imaging (p less than 0.01). Atrial natriuretic peptide appears to have a pharmacological effect on ischemic brain edema, possibly by suppressing the elevation of water content through regulation of electrolyte transport in the brain.
Stroke 1991 Jan
PMID:Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method. 182 2

Right heart overload is one of the most important prognostic factors in patients with chronic lung diseases. To clarify hemodynamic and therapeutic significance of atrial natriuretic peptide (ANP) in pulmonary circulation, plasma ANP concentrations were measured during right heart catheterization (RHC) in patients with chronic lung diseases under static and dynamic conditions. 1) Mixed venous, arterial and venous plasma ANP levels in 45 patients were significantly different one another (p less than 0.01). Significant relationships were also seen between ANP concentrations, and mean pulmonary arterial pressure (PPA; r = 0.85, p less than 0.01), right ventricular systolic pressure (r = 0.91, p less than 0.01), mean right atrial pressure (PRA; r = 0.48, p less than 0.01), and pulmonary vascular resistance (r = 0.84, p less than 0.01). 2) Arterial ANP levels were measured before and after 28% supplemental oxygen inspiration and administration of intravenous aminophylline (5 mg/kg) in patients with chronic obstructive pulmonary disease (COPD). Plasma ANP levels were significantly reduced concomitantly with the reduction of PRA after oxygen, and stroke volume, PRA, pulmonary capillary wedge pressure (Pcw) after aminophylline, respectively. 3) Plasma ANP levels were markedly elevated during both exercise with and without aminophylline (5 mg/kg), but the degree of elevation was significantly less with aminophylline. The reductions of PPA, Pcw and PRA were also observed during aminophylline exercise compared with control exercise, whereas plasma catecholamine levels increased similarly in both studies. These findings suggest that plasma ANP levels reflect the state of right heart load in patients with chronic lung diseases and that its levels are useful to evaluate therapeutic value as for right heart overload.
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PMID:[Hemodynamic and therapeutic significance of plasma atrial natriuretic peptide in chronic lung diseases]. 182 35

To study synthesis, storage, and secretion of brain natriuretic peptide (BNP) in the heart, we have measured BNP mRNA and BNP concentrations in the hearts of Wistar-Kyoto rats and also have investigated its secretion from the isolated perfused heart. The atrium expressed the BNP gene at a high level, and a considerable amount of BNP mRNA also was present in the ventricle, which corresponded to approximately 40% of the atrial BNP mRNA concentration. When tissue weight was taken into account, the total content of BNP mRNA in the ventricle was approximately threefold larger than that in the atrium, although the atrial natriuretic peptide (ANP) mRNA content in the ventricle was only 7% of that in the atrium. By contrast, the BNP concentration in the ventricle was 4.07 +/- 0.97 pmol/g, which was less than 1% of that in the atrium (451 +/- 86 pmol/g). The basal secretory rate of BNP from the isolated perfused whole heart was 49.3 +/- 6.1 fmol/min, approximately 60% of which was maintained even after atrial removal, whereas the secretory rate of ANP was reduced to less than 5%. We also studied age-matched spontaneously hypertensive rats-stroke prone. The rank order of the BNP mRNA concentration in the hearts of these rats was left ventricle greater than right ventricle greater than right atrium = left atrium, and the total BNP mRNA content and BNP secretory rate in the ventricle were twice as large as in Wistar-Kyoto rats. These results demonstrate that BNP is a novel cardiac hormone in rats and is predominantly synthesized in and secreted from the ventricle. This is in striking contrast to ANP, which occurs mainly in the atrium. The results also suggest possible pathophysiological roles of BNP in certain cardiovascular disorders.
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PMID:Natriuretic peptides as cardiac hormones in normotensive and spontaneously hypertensive rats. The ventricle is a major site of synthesis and secretion of brain natriuretic peptide. 183 May 18

Cardiovascular and endocrine responses were evaluated in 12 adult patients over a 5-day period following 30% to 66% burn injury. Heart rate, mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance, and stroke volume were measured. Plasma concentrations of angiotensin II, atrial natriuretic peptide, vasopressin, neuropeptide Y, norepinephrine, and epinephrine were measured. On the day of burn injury, systemic vascular resistance was markedly elevated, and stroke volume and cardiac output were low, but all normalized by day 3, and cardiac output and stroke volume increased by day 5 without significant changes of central venous pressure or pulmonary capillary wedge pressure. Mean arterial pressure and heart rate did not change significantly over the 5-day period. Vasopressin, angiotensin II, neuropeptide Y, norepinephrine, and epinephrine concentrations in plasma were elevated on admission. Vasopressin concentrations were elevated 50 times normal on admission and returned to normal levels by days 4 to 5. Plasma atrial natriuretic peptide concentrations were normal on admission and increased significantly on days 3 to 5. The reciprocal relationship between systemic vascular resistance and cardiac output and between vasopressin and atrial natriuretic peptide correlate with each other and the observed physiologic events that occurred following burn injury and resuscitation. All of these changes in cardiac performance occurred without significant alterations in preload or afterload as measured by central venous pressure, pulmonary capillary wedge pressure, and mean arterial pressure. Increases in plasma levels of atrial natriuretic peptide correlated with the increased stroke volume and cardiac output observed in these patients. The results of this study are consistent with the conclusion that the extreme elevations of plasma vasopressin levels contribute to the vascular complications of increased systemic vascular resistance and decreased cardiac output and contractility seen following burn injury.
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PMID:Cardiovascular and neurohumoral responses following burn injury. 197 29

We evaluated the responses to 90 minutes and 8 days of therapy with a new long-acting vasodilator flosequinan in ten patients with moderate chronic congestive heart failure in an open, uncontrolled study. Acute administration of 100 mg orally resulted in a decrease of preload, with a reduction of left ventricular end-diastolic volume, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, and right atrial pressure. Following the acute administration, we found no significant changes of heart rate, cardiac index, stroke volume, peripheral vascular resistance, ejection fraction, and dp/dt. Chronic application for 8 days (100 mg/day) showed persistent effects on preload, with a significant decrease of pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. After 8 days of treatment, cardiac index was significantly increased from 2.2 +/- 0.2 l/min/m2 to 2.8 +/- 0.2 l/min/m2 (p = 0.013) and stroke volume from 57 +/- 10 ml to 74 +/- 9 ml (p = 0.022). Peripheral vascular resistance decreased by ml (p = 0.022). Peripheral vascular resistance decreased by 28%. After 8 days, bicycle exercise capacity increased significantly from 383 +/- 44 sec to 422 +/- 43 sec (p = 0.01) and the patients were able to increase their walking distance over a 6-minute exercise test from 426 +/- 46 m to 477 +/- 33 m (p = 0.007), with a concomitant decrease of dyspnea (p = 0.013). Plasma renin concentration showed only a rise 90 minutes after the acute administration on day 8 of the study, and atrial natriuretic peptide and 6-keto-prostaglandin F1-alpha decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise capacity, hemodynamic, and neurohumoral changes following acute and chronic administration of flosequinan in chronic congestive heart failure. 198 May 98

The benzimidazol analogue BM14.478 is a phosphodiesterase inhibitor with both vasodilator and positive inotropic properties. Hemodynamic parameters and plasma hormone levels of 8 patients (1 female, 7 male) with chronic congestive heart failure NYHA Classes II-IV (1 patient with coronary artery disease, 7 patients with primary dilated cardiomyopathy) were assessed before and until 6 h after the intravenous application of 1.0 mg BM14.478. There was a significant decrease of mean pulmonary artery pressure (28 +/- 11 vs. 23 +/- 11 mmHg; p less than 0.05), mean right atrial pressure (8.6 +/- 5.2 vs. 5.0 +/- 4.7 mmHg; p less than 0.02), and systemic vascular resistance (1651 +/- 484 vs. 1206 +/- 252 dynes.s.cm-5; p less than 0.05) as early as 10 min after injection of BM14.478. Pulmonary vascular resistance also was reduced (128 +/- 86 vs. 61 +/- 39 dynes.s.cm-5, 30 min after injection; p less than 0.02). Simultaneously there was a significant increase of cardiac index (2.3 +/- 0.7 vs. 3.1 +/- 0.8 l.min-1.m-2, 10 min after injection; p less than 0.02), and stroke volume index (28.8 +/- 11.7 vs. 33.9 +/- 8.5 ml.min-1.m-2; 30 min after injection; p less than 0.05). Although mean heart rate did not change significantly, some patients reacted with a transient increase. There was also a slight but insignificant increase of the double product. No serious side effects were observed. The hemodynamic improvement was followed by a delayed reduction of plasma levels of epinephrine (51 +/- 20 vs. 41 +/- 21 pg/ml; p less than 0.02; 30 min after injection) and atrial natriuretic peptide (229 +/- 283 vs. 121 +/- 168 pg/ml; p less than 0.05; 1 h after injection). Mean levels of plasma norepinephrine, however, did not change significantly and individual responses showed large variations, which could not be predicted by the behavior of the hemodynamic parameters. Three of eight patients (2 of these with elevated baseline filling pressures) even showed a marked increase of plasma norepinephrine levels after BM14.478. Response of plasma renin activity and plasma vasopressin levels to BM14.478 also was heterogeneous. According to the results of this study, acute administration of the phosphodiesterase inhibitor BM14.478 has an immediate beneficial hemodynamic effect in patients with severe congestive heart failure by reducing both preload and afterload, and by increasing cardiac index and stroke volume. However, this improvement of hemodynamic parameters is not necessarily accompanied by a favorable short-term response of plasma hormones, and therefore does not allow any conclusions on survival of these patients.
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PMID:Hemodynamic and neuroendocrine response to acute administration of the phosphodiesterase inhibitor BM14.478 in patients with congestive heart failure. 204 89

Brain natriuretic peptide is a recently discovered neuropeptide. We used an antiserum against porcine brain natriuretic peptide to identify a system of immunoreactive innervation of the cerebrovascular tree in the rat. The internal carotid artery and the proximal portions of the middle and anterior cerebral and posterior communicating arteries were the most intensely innervated by immunoreactive fibers. The density of innervation decreased distally along the anterior, middle, and posterior cerebral arteries and the basilar and vertebral arteries. Brain natriuretic peptide and the related atrial natriuretic peptide are known to cause dilatation of cerebral arteries. Our findings suggest that brain natriuretic peptide may serve as a vasodilatory neuromodulator in the cerebral circulation.
Stroke 1990 Nov
PMID:Brain natriuretic peptide-like immunoreactive innervation of the cerebrovascular system in the rat. 223 76

Hemodynamic and hormonal effects of captopril were prospectively studied in 12 children (median age 5.8 years, range 4 weeks to 15 years) with dilated cardiomyopathy. A mean dose of 1.83 mg captopril/kg body weight was administered in three or four single doses depending on age. Left ventricular volume, ejection fraction (EF), cardiac index (CI), and systemic vascular resistance (SVR) were noninvasively determined by two-dimensional (2D) and Doppler echocardiography before and 2 days and 3 months after the onset of treatment. Blood pressure and heart rate were recorded as well. Additionally, on the day hemodynamic measurements were made, plasma renin activity (PRA), serum aldosterone, and plasma atrial natriuretic peptide (ANP) concentrations were determined. Plasma catecholamines were measured before and 2 days after captopril treatment. Concomitant medication was kept constant during the short-term phase of captopril treatment. During long-term therapy, diuretics were reduced according to the clinical status. Stroke volume (SVI) (-7%), end-systolic (ESVI) (-31%), and end-diastolic (EDVI) (-21%) volume indexes were significantly reduced (p less than 0.05) during short- and long-term therapy. The remaining hemodynamic parameters showed only minor, statistically not significant, changes. During short-term therapy, median serum aldosterone levels fell from 138-88.5 pg/ml (p less than 0.05), and plasma ANP decreased from 144-94 pg/ml (p less than 0.05). After 3 months these effects were less marked and statistically no longer significant. Changes in PRA and plasma catecholamines were not statistically significant at any time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril in children with dilated cardiomyopathy: acute and long-term effects in a prospective study of hemodynamic and hormonal effects. 240 5


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