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Biomedical subjects

I Tikkanen

Publications and source records attributed to I Tikkanen.

At least 91 records · Page 5Linked to original sources
PubMed1989

Vasodilator properties of atrial natriuretic factor: a comparison with nitroglycerin, nitroprusside, and phentolamine during cardiopulmonary bypass.

Thirty-five patients scheduled for coronary artery surgery were studied during hypothermic cardiopulmonary bypass (CPB) to compare the arteriolar and venodilator properties of a bolus dose of atrial natriuretic factor (ANF), 100 micrograms, with those of nitroglycerin, 200 micrograms, sodium nitroprusside, 120 micrograms, phentolamine, 3 mg, and placebo. A decrease observed in mean arterial pressure was used as an indicator of a decrease in systemic vascular resistance (arteriolar dilation), while a decrease in reservoir blood volume of the CPB circuit was considered to indicate an increase in venous capacitance (venodilation). All vasodilators decreased mean arterial pressure, and there was no difference in the maximal decrease of the pressure between the drugs. However, the decrease caused by ANF appeared later than that caused by the other vasodilators and lasted longer than with nitroglycerin and sodium nitroprusside. Nitroglycerin and sodium nitroprusside decreased reservoir blood volume, while ANF and phentolamine had no effect. It is concluded that ANF is an arteriolar dilator with a time profile of its effect differing from those of nitroglycerin, sodium nitroprusside, and phentolamine. ANF seems to have no venodilator activity in patients undergoing hypothermic CPB.

Atrial Natriuretic Factor↗
PubMed1989

Attenuated diuretic and natriuretic effects of atrial natriuretic peptide in rats with heart failure.

Plasma levels of atrial natriuretic peptide (ANP) and renal responses to ANP were examined in rats with chronic cardiac failure produced by coronary artery ligation and in sham-operated controls. Plasma ANP levels were elevated in the rats with severe cardiac failure as compared with the controls (P less than 0.001). ANP injections at the doses of 1, 5, 25 and 50 micrograms/kg increased water and sodium excretion significantly at all but the lowest dose in the controls; only the two largest doses caused clear diuresis and natriuresis in the heart failure group. The diuretic and natriuretic effects of ANP were significantly weaker at the doses of 5 and 25 micrograms/kg in the rats with heart failure as compared with the controls. We conclude, that natriuretic and diuretic effects of ANP are attenuated in this chronic heart failure mode.

Animals↗
PubMed1989

Effects of licorice on plasma atrial natriuretic peptide in healthy volunteers.

Ingestion of licorice, 100 g daily for 8 weeks, caused a rise in 81% in plasma atrial natriuretic peptide (ANP) concentration in 12 healthy subjects. Mean body weight increment (1.6 kg) correlated with the increase in plasma ANP (r = 0.59; P less than 0.01). The plasma concentrations of antidiuretic hormone, aldosterone, and plasma renin activity decreased. All these hormonal effects, reflecting retention of sodium and fluid volume, were probably due to the known mineralocorticoid properties of licorice. Blood pressure increased transiently and two subjects developed reversible hypertension. The rise in plasma ANP concentration during ingestion of licorice may be considered a physiological response to prevent fluid retention and development of hypertension.

Adult↗
PubMed1989

Beneficial effects of erythropoietin on haematological parameters, aerobic capacity, and body fluid composition in patients on haemodialysis.

Eleven patients on haemodialysis were treated with erythropoietin (EPO), 50-200 U kg-1 once to three times a week, for up to 1 year. After outset of EPO all patients became transfusion-independent. Four patients did not reach the target haemoglobin (Hb) level 100 g l-1 in 5 months. These patients had higher serum concentrations of aluminium (225 +/- 87 micrograms l-1, mean +/- SD) than the responding patients (55 +/- 56 micrograms l-1). Addition of desferrioxamine to treatment with EPO resulted in a rapid rise in Hb values in these patients. Thus, aluminium may inhibit EPO responsiveness. All patients were iron overloaded. Serum ferritin levels declined in all but one patient with secondary haemochromatosis. In exercise tests the aerobic capacity and oxygen uptake increased during EPO therapy. Peak oxygen consumption (Vo2 peak), oxygen pulse, oxygen uptake at anaerobic threshold (AT) and total work output (W max) increased 19%, 36%, 26% and 24%, respectively. Lean body mass (LBM) increased by 8%. Taken together, all clinical EPO effects measured appeared clinically favourable.

Adult↗
PubMed1989

No effect of short term angiotensin II infusion on plasma renin substrate levels in man.

We studied the effect of angiotensin II (A-II) infusion (4 ng/kg BW.min) on plasma renin substrate (RS) levels and PRA in five normal men during normal, diuretic-stimulated, and enalapril-interrupted function of the renin-angiotensin system. A-II infusion increased (15-25%) both systolic and diastolic blood pressure in the normal state and during angiotensin-converting enzyme inhibition, whereas the increase during diuretic-stimulated renin-angiotensin system function was less. The plasma RS concentration was measured by both direct and indirect RIA. The mean basal plasma RS levels, measured with direct assay, were 1516 +/- 150 (SE) in the normal state, 1566 +/- 150 after diuretic administration, and 1650 +/- 133 nmol/L after enalapril administration. The corresponding mean basal plasma RS levels measured with the indirect assay were 1073 +/- 100, 1031 +/- 57, and 902 +/- 78 nmol/L, respectively. Plasma RS levels did not change during or after the A-II infusions, whereas PRA decreased significantly in all experimental conditions. The results suggest that A-II exerts no direct stimulatory effect on hepatic release of RS. Thus, A-II appears not to be important in the short term regulation of plasma RS levels.

Adult↗
PubMed1989

A deficient response of atrial natriuretic peptide to volume overload in Gordon's syndrome.

Gordon's syndrome was diagnosed in a 19-year-old woman who had hypertension, hyperkalemia and hyperchloremic acidosis. In family screening, hyperkalemia and hyperchloremic acidosis were also found in the patient's mother and brother. The proband and her brother were studied and showed normal glomerular function with normal renal sodium conservation and urine acidification mechanisms. The levels of plasma aldosterone were normal in both subjects. The renin activity was low in the proband but normal in the brother. Both the basal and the volume-stimulated plasma concentration of atrial natriuretic peptide was low in the two patients. As compared with controls, the kaliuretic response to infusion of sodium chloride was not decreased in the patients. Hydrochlorothiazide promptly corrected the acidosis and the hyperkalemia as well as normalized the raised blood pressure of the proband. We suggest that a deficiency of atrial natriuretic peptide rather than an unusual avidity for sodium chloride reabsorption by the renal tubules plays a significant pathogenetic role in Gordon's syndrome.

Acid-Base Equilibrium↗
PubMed1989

[Endothelin].

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Animals↗
PubMed1988

Atrial natriuretic peptide in congestive heart failure.

Release of atrial natriuretic peptide (ANP) appears to be a compensatory response in congestive heart failure (CHF) that may counterbalance the adverse effects of stimulated renin-angiotensin and sympathetic nervous systems. We observed increased plasma ANP concentrations in CHF patients in New York Heart Association functional classes II to IV. The fact that such responses already become evident when a patient is in New York Heart Association class II supports the concept that ANP release may counteract the detrimental effects of stimulation of renin and the sympathetic nervous system even in the early phases of heart failure by promoting diuresis and natriuresis, as well as vasodilatation, thus reducing both pre- and afterload. When CHF is severe, however, the counterbalancing effects of ANP may be offset by vasoconstriction and fluid and sodium retention.

Atrial Natriuretic Factor↗
PubMed1988

Hemodynamic effects of alpha-human atrial natriuretic peptide in healthy volunteers.

The hemodynamic effects of synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were evaluated in a double-blind, placebo-controlled study with echocardiography and systolic time intervals in 11 healthy volunteers. During an infusion of alpha-hANP for 30 min, when plasma ANP concentration increased to a peak level of approximately 300 pg/ml, an increase occurred in diuresis (+174%, p less than 0.01 vs. placebo) and natriuresis (+148%, p less than 0.05). Heart rate increased (+10%, p less than 0.05), but the mean arterial pressure remained unchanged. The left ventricular end-diastolic diameter was reduced (-3%, p less than 0.01), as was the left ventricular end-systolic diameter (-11%, p less than 0.001). Total peripheral resistance (-12%, p less than 0.05) and midsystolic circumferential wall stress (-16%, p less than 0.05) decreased, while cardiac output increased (+15%, p less than 0.05), as did fractional shortening (+15%, p less than 0.001). Within 30 min postinfusion, all differences between the ANP and placebo treatments had disappeared. No significant difference between the treatments was observed in preejection period or preejection period/left ventricular ejection time ratio. In conclusion, when administered as a short infusion, alpha-hANP causes peripheral arterial vasodilation and thus, by reducing left ventricular afterload, improves the pump function of the heart. Venous vasodilating effect of alpha-hANP may contribute to the decrease in left ventricular preload, but a diuresis-induced reduction in circulating intravascular volume may also be influenced.

Adult↗
PubMed1988

Plasma atrial natriuretic peptide in cardiac transplant recipients. A prospective study.

Cardiac transplantation in 10 patients with congestive heart failure resulted in reduction of high plasma concentrations of atrial natriuretic peptide (ANP), preoperatively five-fold above normal, to a level two-fold above normal, which was maintained throughout a 12-week follow-up period. Cardiac function was normalized in all patients. Transient increases in plasma ANP, in four cardiac recipients 3-10-fold their basal levels, could neither be related to rejection episodes nor to cardiac dysfunction, but rather to signs of fluid and sodium retention. High plasma ANP levels in cardiac transplant recipients suggest that the capacity to secrete ANP is preserved in the transplanted heart.

Adolescent↗
PubMed1988

Atrial natriuretic peptide and atrial pressures in newborns with transposition of the great arteries.

The relation of atrial pressure to atrial plasma concentration of atrial natriuretic peptide (ANP) was studied in four newborns undergoing catheterization because of transposition of the great arteries. In three patients, mean left atrial pressure clearly exceeded right atrial pressure (12 +/- 7 vs. 2 +/- 3 mmHg; mean +/- SD). In one patient mean atrial pressures were identical (4 mmHg). In all patients the ANP concentration in the left atrium exceeded that of the right (833 +/- 464 vs. 415 +/- 366 pg/ml; mean +/- SD). There was a significant (r = 0.97; p less than 0.01) correlation between pressure and ANP concentration in the left atria. In the right atria, no linear correlation existed between pressure and ANP concentration. ANP concentration in the left atrium decreased after a lowering of the left atrial pressure by atrial septostomy. In these patients, the left atrium seems to be the main source of circulating ANP.

Atrial Natriuretic Factor↗
PubMed1987

Haemodynamic effects of atrial natriuretic peptide in rats with heart failure.

Plasma atrial natriuretic peptide (ANP), a hormone secreted by the heart, is elevated in cardiac failure. In the aim to study the role of ANP in cardiac failure, the haemodynamic response to ANP was examined in rats with chronic heart failure produced by coronary artery ligation. Plasma ANP was clearly elevated in all infarcted rats before ANP injection as compared with controls. ANP lowered the blood pressure and impaired cardiac contractility, as measured by the maximal positive value of the first derivative of the pressure signal, in a dose-dependent manner. The blood pressure lowering effects of ANP were attenuated in rats with cardiac failure. We conclude that rats with experimentally induced heart infarct are partially resistant to the haemodynamic effects of ANP.

Animals↗
PubMed1987

Elevated plasma atrial natriuretic peptide in rats with myocardial infarcts.

We measured atrial natriuretic peptide (ANP) plasma levels in rats with experimental heart failure caused by left coronary artery ligation. ANP levels were clearly higher in infarcted rats (409 +/- 59 pg/ml; mean +/- S.E.M.) than in sham-operated controls (39 +/- 6 pg/ml). Moreover, plasma ANP levels increased progressively with the severity of cardiac dysfunction and size of infarct. Increased release of ANP in post-infarction heart failure appears to be a meaningful compensatory response to control rising preload. Our results are in keeping with evidence from human studies showing increased plasma concentration of ANP in patients with congestive heart failure. This model is a useful tool to further explore the role of ANP in heart failure.

Animals↗
PubMed1987

Competitive inhibitor binding assay (CIBA) of captopril and other ACE inhibitors.

We describe a new principle for measuring concentrations of pharmacologically active captopril or other angiotensin-converting enzyme (ACE) inhibitors in blood. Serum is incubated with 125I-labelled ACE inhibitor (351A, a p-hydroxy-benzamidine derivative of N-(1-carboxy-3-phenylpropyl)-L-lysyl-L-proline) in a nonequilibrated system, in which label and ACE inhibitor compete for binding to added serum ACE. Free label is separated by adsorption to coated charcoal. Sensitivity for captopril is 2 ng/ml, and for other tested ACE inhibitors 0.25-5 ng/ml. Results in healthy volunteers showed rapid absorption of captopril with maximal concentration of active drug within 1 h, and fast disappearance within 2.5 h. Stability of captopril was improved by immediate 1:100 dilution of blood samples with assay buffer. In spite of this precaution, analysis should be performed within two days to avoid loss of active drug due to polymerization and protein binding. Samples of other tested ACE inhibitors can be frozen and later analyzed at convenience. The new principle is simple, sensitive, and specific.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Plasma atrial natriuretic peptide concentrations during induction of anesthesia and acute volume loading in patients undergoing cardiac surgery.

Induction of anesthesia with fentanyl for coronary artery bypass grafting decreased (P less than .05) plasma atrial natriuretic peptide (ANP) concentrations from awake values in twelve patients. During a steady state of anesthesia before surgery, isotonic saline solution (10 mL/kg) was infused simultaneously with the elevation of the lower extremities in six patients, while six subjects served as controls receiving no volume loading and having no leg raising. The ANP levels returned to the awake values in the volume-loaded patients, while plasma ANP remained at anesthetized baseline levels in the control subjects (P less than .01 between the groups). Ten minutes after the end of the loading procedure, plasma ANP had begun to decrease again towards the postinduction level in the loaded group, but a significant (P less than .05) difference was still observed between the groups. These changes in ANP levels paralleled those of cardiac filling pressures. In conclusion, the results suggest that the degree of distention of the atria regulates the secretion of atrial natriuretic peptide into the circulation in patients anesthetized with fentanyl.

Anesthesia, Intravenous↗
PubMed1987

Plasma atrial natriuretic peptide in health and disease.

The plasma concentration of atrial natriuretic peptide (ANP) in 16 healthy subjects on a free diet was 41 +/- 23 pg ml-1 (mean +/- SD) when upright and 58 +/- 27 pg ml-1 in the supine position (P less than 0.05), which confirms the concept that the supine position raises plasma ANP. Water immersion to the neck for 2 h caused a brisk diuresis, natriuresis and raised plasma ANP in 8 healthy subjects, suggesting that ANP is a mediator of diuresis and natriuresis during immersion. Dynamic exercise (50-200 W per 4 min) on a bicycle ergometer caused a gradual increase in plasma ANP in 6 healthy males, with a close correlation between the increases in plasma ANP and heart rate (r = 0.96). Thus, plasma ANP levels are increased in healthy subjects by stimuli causing an increased preload and possibly by tachycardia itself. Markedly raised plasma levels of ANP were found in patients with congestive heart failure, and upright posture caused a further rise of plasma ANP which correlated with the increase in heart rate (r = 0.87). High plasma ANP concentrations were also found in 25 patients with end-stage renal failure maintained on haemodialysis. When these patients were subdivided into those with concomitant heart failure and those with normal cardiac function, changes in plasma ANP correlated with predialysis weight gain and weight loss during dialysis, but only in patients without heart failure. In 9 infants treated by operative or pharmacological closure of persistent ductus arteriosus, high pre-treatment plasma ANP values were lowered by successful therapy, and plasma ANP correlated with the degree of left atrial distension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗