atrial-natriuretic-factor and Cerebral-Infarction

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the pathogenetic mechanism of the hyponatremia was assessed based on the therapeutic effect obtained. The subjects were 14 patients (6 with subarachnoid hemorrhage, 3 with hypertensive intracerebral hemorrhage, 2 with cerebral infarct and 3 with head injury) who developed hyponatremia, as a complication during their hospital stay for their intracranial lesions from April to December 1992. Patients with serum Na levels below 135 mEq/l for more than 2 days with no other discernible etiology were defined as having hyponatremia of central origin. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. When improvements occurred within 3 days, in 3 to 7 days, or 8 days or more efficacy was rated "excellent", "good" or "poor", respectively. The mean interval until the onset of hyponatremia was 10.4 days, its mean duration was 5.7 days, and the mean minimum serum sodium level was 129.5 mEq/l. The dose of fludrocortisone administration was 0.1 mg/day except for one patient who was treated with 0.3 mg/day. The mean period of administration was 3.7 days (range: 3 to 6 days), and the route was via a stomach tube in 5 cases and oral in 9 cases. The therapeutic effect was excellent in 9 cases, good in 3 cases and poor in 2 cases, the efficacy rate being 86%. None of the patients manifested side effects. Plasma atrial natriuretic peptide levels were above 100 pg/ml in 2 patients and 50-100 pg/ml in 8 patients and neither of the former 2 patients exhibited "excellent" efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Brain Diseases; Cerebral Hemorrhage; Cerebral Infarction; Female; Fludrocortisone; Humans; Hyponatremia; Male; Middle Aged; Sodium; Subarachnoid Hemorrhage

The plasma levels of endothelin-1 (ET-1) and atrial natriuretic peptide (ANP) have been measured in 37 patients with acute ischemic stroke, on admission and 3 and 7 days thereafter. The plasma ET-1 levels at the onset of symptoms were about two-fold those observed in age-matched normal volunteers (3.5 +/- 2.26 v 1.54 +/- 0.9 pg/mL, respectively; P < .001). These levels remained significantly elevated during the 7-day study period. The neurologic deficit was assessed daily by Mathew's modified scale (MS). A significant correlation was found between neurologic status on admission and ET-1 plasma values; patients with worse neurologic status (MS < 45 points) had higher ET-1 plasma values than those with better neurologic status (MS > 45 points) (5.4 +/- 2.34 v 3.05 +/- 2.04 pg/mL, respectively, P < .05). The plasma ET-1 values did not correlate either with the site of the infarction or with its primary cause (cardioembolic, lacunar, or atherothrombotic). No significant differences were seen in plasma ET-1 concentrations between patients who eventually died and those who survived the acute event. The plasma ANP were about 18-fold higher in ischemic stroke patients on admission than in controls at admission (110.9 +/- 29.5 v 5.84 +/- 3.96 pg/mL, respectively, P < .01). These values remained significantly elevated on days 3 and 7. There was no correlation between the ANP plasma values and the neurologic status, the site or mechanism of the stroke, or the plasma ET-1 levels. In conclusion, ischemic stroke is associated with marked acute and long-duration increases of ET-1 and ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Brain Ischemia; Cerebral Infarction; Cerebrovascular Disorders; Endothelins; Female; Humans; Male; Middle Aged; Neurologic Examination

The maternal system is challenged with many physiological changes throughout pregnancy to prepare the body to meet the metabolic needs of the fetus and for delivery. Many pregnancies, however, are faced with pathological stressors or complications that significantly impact maternal health. A shift in this paradigm is now beginning to investigate the implication of pregnancy complications on the fetus and their continued influence on offspring disease risk into adulthood. In this investigation, we sought to determine whether maternal hypertension during pregnancy alters the cerebral response of adult offspring to acute ischemic stroke. Atrial natriuretic peptide gene-disrupted (ANP(-/-)) mothers exhibit chronic hypertension that escalates during pregnancy. Through comparison of heterozygote offspring born from either normotensive (ANP(+/-WT)) or hypertensive (ANP(+/-KO)) mothers, we have demonstrated that offspring exposed to maternal hypertension exhibit larger cerebral infarct volumes following middle cerebral artery occlusion. Observation of equal baseline cardiovascular measures, cerebrovascular structure, and cerebral blood volumes between heterozygote offspring suggests no added influences on offspring that would contribute to adverse cerebral response post-stroke. Cerebral mRNA expression of endothelin and nitric oxide synthase vasoactive systems demonstrated up-regulation of Et-1 and Nos3 in ANP(+/-KO) mice and thus an enhanced acute vascular response compared to ANP(+/-WT) counterparts. Gene expression of Na(+)/K(+) ATPase channel isoforms, Atp1a1, Atp1a3, and Atp1b1, displayed no significant differences. These investigations are the first to demonstrate a fetal programming effect between maternal hypertension and adult offspring stroke outcome. Further mechanistic studies are required to complement epidemiological evidence of this phenomenon in the literature.

Topics: Adult Children; Animals; Atrial Natriuretic Factor; Cerebral Infarction; Disease Models, Animal; Endothelins; Female; Humans; Hypertension, Pregnancy-Induced; Mice; Nitric Oxide Synthase; Pregnancy; Prenatal Exposure Delayed Effects

Greater change of postural blood pressure (BP) is often seen in elderly hypertensives and is recognized as a risk factor for cognitive decline and poorer cerebrovascular outcome, but its clinical significance still remains to be clarified. We performed a head-up tilting test, ambulatory BP monitoring, and brain MRI in 59 hypertensives and 27 normotensive subjects. We measured plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels at rest to assess cardiac burden. The 59 hypertensive patients were classified into 3 groups: an orthostatic hypertension (OHT) group with orthostatic increase in systolic BP (SBP) > or = 10 mmHg (n=16); an orthostatic hypotension (OHYPO) group with orthostatic SBP decrease < or = -10 mmHg (n=18); and an orthostatic normotension (ONT) group with neither of these two patterns (n=25). A group of 27 normotensive subjects (NT) was also included as a control. Plasma BNP (72 +/- 92 vs. 29 +/- 24 pg/ml, p < 0.05) and BNP/ANP ratio (4.6 +/- 3.3 vs. 2.4 +/- 1.5, p < 0.05) were significantly higher in the OHYPO than in the NT group. The BNP/ANP ratio was also higher in the OHT than in the NT group (5.1 +/- 3.9 vs. 2.4 +/- 1.5, p < 0.01). The number of silent cerebral infarct (SCI), prevalence of SCI and number of multiple SCIs was the highest in the OHT group, followed in order by the OHYPO, ONT and NT groups. Blood pressure and left ventricular mass index were not significantly different among the 3 hypertensive groups. In conclusion, hypertensive patients with greater change of postural BP (OHT and OHYPO) were shown to have increased risk of advanced silent brain lesions and greater cardiac burden.

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Blood Pressure; Cerebral Infarction; Female; Humans; Hypertension; Hypertrophy, Left Ventricular; Hypotension, Orthostatic; Magnetic Resonance Imaging; Male; Middle Aged; Natriuretic Peptide, Brain; Stroke Volume; Ventricular Dysfunction, Left

Cortical spreading depression (CSD) is characterised by slowly propagating waves of cellular depolarization and depression and involves transient changes in blood flow, ion balance and metabolism. In cerebral ischaemia, peri-infarct CSD-like depolarization potentiates infarct growth, whereas preconditioning with a CSD episode protects against subsequent ischaemic insult. Thus, many of the long-lasting molecular changes that occur in CSD-affected tissue are presumed to be part of a 'neuroprotective cascade.' 3',5'-Cyclic guanosine monophosphate (cGMP) has been shown to be a neuroprotective mediator and the nitric oxide system, which increases cGMP production by soluble guanylate cyclase, is up-regulated by CSD. Atrial and C-type natriuretic peptide (ANP/CNP) are present in cerebral cortex and their actions are mediated via particulate guanylate cyclase receptors and cGMP production. Therefore, in further efforts to characterise the role of cGMP-related systems in CSD and neuroprotection, this study investigated possible changes in cortical natriuretic peptide expression following acute, unilateral CSD in rats. Using in situ hybridisation, significant 20-80% increases in ANP mRNA were detected in layers II and VI of ipsilateral cortex at 6 h and 1-14 days after CSD. Ipsilateral cortical levels were again equivalent to control contralateral values after 28 days. Assessment of cortical concentrations of ANP immunoreactivity by radioimmunoassay revealed a significant 57% increase at 7 days after CSD. Despite using a sensitive signal-amplification protocol, authentic ANP-like immunostaining was readily detected in subcortical nerve fibres, but was not reliably detected in normal or CSD-affected neocortex, suggesting the presence of very low levels, and/or active or differential processing of the peptide. Cortical CNP mRNA levels are not altered by CSD, indicating the specificity of the observed effects.Overall, these novel findings demonstrate a prolonged increase in cortical ANP expression after an acute episode of CSD. The overlap between the described time course of CSD-induced protection against ischaemic insult and demonstrated increases in ANP levels, suggest that ANP (like nitric oxide) may contribute to CSD-induced neuroprotection, via effects on cGMP production and other signal-transduction pathways.

Topics: Animals; Atrial Natriuretic Factor; Brain Ischemia; Cell Survival; Cerebral Cortex; Cerebral Infarction; Cortical Spreading Depression; Cyclic GMP; Gene Expression; Ischemic Preconditioning; Male; Neurons; Potassium Chloride; Rats; Rats, Sprague-Dawley; Reaction Time; RNA, Messenger; Signal Transduction; Up-Regulation

To determine the potential role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the pathogenesis of cerebral salt wasting.. Clinical case report.. Regional pediatric intensive care unit.. A 3-yr-old boy with a cerebral infarct secondary to traumatic carotid artery dissection who developed hyponatremia associated with weight loss and excessive renal sodium excretion on the sixth day after hospitalization.. Plasma concentrations of ANP, BNP, antidiuretic hormone, and renin were determined serially and compared with concentrations measured in a group of eight healthy children undergoing elective surgical procedures. Compared with controls, ANP and BNP plasma concentrations on the eighth day after hospitalization were increased 1.9-fold and 7.7-fold, respectively. Thereafter, the course of ANP and BNP paralleled that of sodium and H2O excretion and remained elevated until the 14th (BNP) and 16th (ANP) days after hospitalization. Serum antidiuretic hormone and renin concentrations were within normal ranges during the entire observation period.. Cerebral salt wasting is associated with elevated plasma concentrations of ANP and BNP. Natriuretic peptides may play a role in the pathogenesis of this syndrome.

Topics: Atrial Natriuretic Factor; Carotid Artery, Internal, Dissection; Cerebral Infarction; Child; Child, Preschool; Humans; Hyperpituitarism; Hyponatremia; Male; Natriuretic Peptide, Brain; Renin; Vasopressins

Atrial natriuretic peptide (ANP) is a powerful hormone with hypotensive, natriuretic, diuretic, and many other beneficial effects. Direct infusion of ANP in therapeutics has limited success because of its short half-life in the circulation. Our previous studies have shown that ANP gene delivery attenuates hypertension, cardiac hypertrophy, and renal injury in Dahl salt-sensitive (Dahl-SS) rats. To investigate the potential therapeutic value of ANP gene delivery on salt-induced stroke and cerebrovascular disorders, an adenovirus harboring the human ANP gene (Ad.RSV-cANP) was injected into Dahl-SS rats on a high salt diet. A single intravenous injection of the ANP gene caused a significant reduction of blood pressure that lasted for more than 3 weeks. A maximal blood pressure reduction of 28 mm Hg was observed 2 weeks after gene delivery as compared with that of control rats injected with adenovirus harboring the LacZ gene under the control of the Rous sarcoma virus promoter (Ad.RSV-LacZ). Immunoreactive human ANP can be detected in the heart, lung, kidney, and brain of rats after gene delivery. The stroke mortality rate of Dahl-SS rats was significantly decreased (from 54% to 17% at 3 weeks and from 70% to 50% at 4 weeks after ANP gene delivery as compared with rats injected with control virus). ANP gene delivery also significantly attenuates salt-induced aortic hypertrophy as evidenced by reduced thickness of the aortic wall. This is the first study to demonstrate the potential of ANP gene delivery in reducing the mortality rate caused by cerebrovascular disorders and stroke. Successful application of this technology may have potential value in treating individuals with a high risk of stroke.

Topics: Adenoviridae; Animals; Atrial Natriuretic Factor; Avian Sarcoma Viruses; Blood Pressure; Cerebral Infarction; Cerebrovascular Disorders; Genetic Therapy; Genetic Vectors; Humans; Male; Rats; Rats, Inbred Dahl; Simian virus 40

Plasma atrial natriuretic peptide (ANP) was measured with radioimmunoassay in 39 patients with acute stroke. The mean level was 144.3 +/- 8.7 pg/ml; this was significantly higher in comparison with those in normal controls (55.8 +/- 4.7 pg/ml, n = 20) and hypertension patients (87.7 +/- 8.0 pg/ml, n = 15). Serial measurement of ANP level in 6 patients showed that it was elevated on the first day of the stroke, reached to its peak on the second or third day and returned to normal after two weeks. Five patients had hyponatremia following the attack of stroke and the plasma ANP level was further elevated. It is suggested that elevated plasma ANP level might be a pathogenetic factor of the accompanying hyponatremia in stroke.

Topics: Aged; Atrial Natriuretic Factor; Cerebral Hemorrhage; Cerebral Infarction; Female; Humans; Hyponatremia; Male; Middle Aged; Radioimmunoassay