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Atrial natriuretic factor: is it responsible for hyponatremia and natriuresis in neurosurgery? Despite increased plasma concentrations of atrial natriuretic factor in the postoperative period, it is not directly responsible for hyponatremia and natriuresis. The presence of other natriuretic factors, the participation of multiple natriuretic. Plasma atrial natriuretic factor was increased in 92.60% of the patients in at least one of the postoperative days; however, there was no statistically significant association between the atrial natriuretic factor and plasma sodium and between the atrial natriuretic factor and urinary sodium. Factor natriuretico atrial pdf free o grande grimorio pdf free honda cbr india price Camuflaj Feat Anda Doar O Factor natriuretico atrial Download Zippy; Get a Blog for st Reader For Pdf Magazines For Download by gorkov dzyaloshinskii pdf download factor natriuretico atrial pdf download conceptual physics 11th. Citations for Atrial natriuretic factor (1-28) (human, porcine) Citations are publications that use Tocris products. Currently there are no citations for Atrial natriuretic factor (1-28) (human, porcine). Independent risk factor for mortality 6,7; it can also lead to or worsen heart failure. Secondary atrial fibrillation is caused by an underlying condition and is reversible if the condition.

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Abstract

Objective

To evaluate the presence of hyponatremia and natriuresis and theirassociation with atrial natriuretic factor in neurosurgery patients.

Methods

The study included 30 patients who had been submitted to intracranial tumorresection and cerebral aneurism clipping. Both plasma and urinary sodium andplasma atrial natriuretic factor were measured during the preoperative andpostoperative time periods.

Results

Hyponatremia was present in 63.33% of the patients, particularly on the firstpostoperative day. Natriuresis was present in 93.33% of the patients,particularly on the second postoperative day. Plasma atrial natriureticfactor was increased in 92.60% of the patients in at least one of thepostoperative days; however, there was no statistically significantassociation between the atrial natriuretic factor and plasma sodium andbetween the atrial natriuretic factor and urinary sodium.

Conclusion

Hyponatremia and natriuresis were present in most patients afterneurosurgery; however, the atrial natriuretic factor cannot be considered tobe directly responsible for these alterations in neurosurgery patients.Other natriuretic factors are likely to be involved.

Abstract

Objetivo

Avaliar a presença de hiponatremia e natriurese, bem como suasassociações com o fator natriurético atrial empacientes de neurocirurgia.

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Métodos

Foram incluídos 30 pacientes submetidos àressecção de tumor intracraniano e à clipagem deaneurisma cerebral. Os níveis plasmáticos e urináriosde fator natriurético atrial foram medidos durante os períodospré e pós-operatório.

Resultados

Hiponatremia esteve presente em 63,33% dos pacientes, particularmente noprimeiro dia pós-operatório. Observou-se natriurese em 93,33%dos pacientes, principalmente no segundo dia pós-operatório.Os níveis plasmáticos de fator natriurético atrialestavam aumentados em 92,60% dos pacientes em pelo menos um dos diaspós-operatórios, mas não houve associaçãoestatisticamente significante entre fator natriurético atrial esódio plasmático, e entre fator natriurético atrial esódio urinário.

Conclusão

Após neurocirurgia, na maior parte dos pacientes, estiveram presenteshiponatremia e natriurese; contudo, o fator natriurético atrialnão pôde ser considerado diretamente responsável portais alterações nos pacientes neurocirúrgicos.Provavelmente, há o envolvimento de outros fatoresnatriuréticos.

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INTRODUCTION

Disorders of plasma sodium concentration expose cells to hypotonic or hypertonicstress. Although all cells are affected, the clinical manifestations are primarilyneurologic. Rapid changes in plasma sodium concentrations can cause severe,permanent and sometimes lethal brain injury. Those disorders are common in neurologyand neurosurgery patients who already have cerebral edema from the primary injuryand whose adaptive mechanisms may be impaired with the worsening of the patients'neurologic condition.^(-)

Hyponatremia is defined as a serum sodium concentration < 135mEq/L.⁽⁾ It is the most commonly foundsodium disturbance in neurosurgery patients. Hyponatremia is usually associated withnatriuresis (sodium renal loss > 20mEq/L) and worse neurological states. Cerebralsalt wasting syndrome (CSWS) is defined as the renal loss of sodium duringintracranial disease, which leads to hyponatremia. A decrease in extracellular fluidvolume is the main cause of these alterations in neurosurgery patients.^(-,-)

The mechanism by which intracranial disease leads to renal salt wasting is notcompletely understood. The regulation of sodium homeostasis involves both humoraland neural mechanisms. Humoral factors include the renin-aldosterone axis, atrialnatriuretic factor, and antidiuretic hormone. Neural factors include the directneural modulation of tubular sodium reabsorption and the indirect neural modulationof rennin release. Natriuretic factors may play an important role inCSWS,^(,) and in recent years, several reports have attempted toidentify a causal relationship between natriuretic peptide and CSWS. Amongst thevarious natriuretic factors, atrial natriuretic factor (ANF) might be the mostprobable candidate to mediate CSWS.^(,-,-)

ANF is produced in and released from the atrial appendages, and it seems to act indifferent tissues, participating in the control of fluid balance with a negativesodium balance and changes in blood volume. ANF has also been identified in areas ofthe central nervous system involved in cardiovascular, sodium and fluidregulation.^(,)

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ANF-containing neurons have been identified in the rat hypothalamus and laminaterminalis; however, the concentration of ANF in the brain is 10000 times lower thanin the heart, making it unlikely that the brain secretion of ANF is responsible forCSWS. Although atrial stretch is thought to be the principal mechanism for cardiacANF release, there is evidence that the central nervous system modulates cardiac ANFsecretion. Intracranial disease may lead to a disturbance of the brain's controlover ANF secretion, and, under certain conditions, excessive ANF issecreted.⁽⁾

The purpose of the present study was to verify the presence of hyponatremia andnatriuresis and their relationships with atrial natriuretic factor in neurosurgerypatients.

METHODS

This prospective observational study was performed in an academic teaching hospital.It was approved by the Faculdade de Ciências MédicasEthics Committee of the Universidade Estadual de Campinas (UNICAMP)under protocol number 142/99. Signed informed consent was obtained from the patientsor family members prior to inclusion in the study.

Thirty consecutive male and female patients older than 13 years of age who had beensubmitted to elective neurosurgery either for the resection of a brain tumor orclipping of an aneurism of the cerebral artery with or without subarachnoidhemorrhage (SAH) were enrolled in the study. No patients had a recent history ofhead trauma, diagnosis of pituitary tumor, age ≤ 13 years, pregnancy oralterations in cardiac, renal, adrenal, thyroid or hepatic function. Postoperativefluid and sodium administration were always > 2L/day of normal saline solutionand were adjusted to maintain a normal intravascular volume and to avoid a negativesodium balance.

The patient's age was recorded and the preoperative patient's neurological status wasassessed with the Glasgow Coma Scale.

Urinary samples were collected over a period of 12 hours overnight and cooledimmediately to 4°C until the end of the collection period on the day before surgery(D0) and on the first to fifth postoperative days (D1 - D5). The urinary sodiumconcentration was determined by indirect potentiometry.

Blood samples were collected from a previously placed venous catheter.

Plasma sodium concentrations were determined each morning on the preoperative day(D0) and on the first to fifth postoperative days (D1 - D5) by the selective iontechnique.

Plasma ANF concentrations were determined on the preoperative day (D0) and onpostoperative days 1, 3 and 5 (D1, D3, D5). Blood samples were collected in tubescontaining ethylenediamine tetraacetic acid - EDTA (1mg/mL), cooled to approximately+4^oC, and centrifuged at 3000 rpm for 15 minutes. Plasma was frozen(-20°C) and sent to the laboratory on dry ice for peptide assay.^(,) Atrialnatriuretic factor was measured in duplicate by radioimmunoassay after theacetone-ether extraction of plasma.

Natriuresis was defined as urinary sodium higher than 110mEq/12 hours (normal urinarysodium is 20 - 110mEq/12 hours).

Hyponatremia was defined as a plasma sodium concentration below 135mEq/L (normalplasma sodium is 135 - 146mEq/L) at least once in the clinical course.

High plasma ANF levels were defined as a plasma ANF higher than 50pg/mL (normal is 25- 50pg/mL).

Statistical analysis

Descriptive statistics of numeric variables were performed to describe theprofile of the sample. The results were expressed as the mean (± standarddeviations - SD). Analysis of variance for repeated measures was used to comparelongitudinal measures among time (repeated measures ANOVA). Comparative analysisbetween plasma ANF and plasma sodium and between plasma ANF and urinary sodiumwas studied by Fisher's exact test. We also studied the correlation betweenvariations in plasma ANF and plasma sodium and between variations in plasma ANFand urinary sodium on the first postoperative day by Spearman's correlationcoefficient. Statistical significance was defined as p < 0.05.

RESULTS

The study included 30 patients, of which 19 were diagnosed with intracranial tumor(63.33%) and 11 with cerebral artery aneurism (36.7%).

Their mean age was mean 44 ± 18 and the preoperative Glasgow Coma Score rangedfrom 10 to 15 (mean 13 ± 2).

Plasma sodium, urinary sodium and plasma ANF are presented in table 1 and described below.

Table 1

SD - standard deviation; Naplasm 0 - plasma sodium on the preoperativeday; Naplasm 1 - Naplasm 5 - plasma sodium on the first to fifthpostoperative days; ANF 0 - atrial natriuretic factor on thepreoperative day; ANF 1 - ANF 5 - atrial natriuretic factor on the firstto fifth postoperative days; Nauri 0 - urinary sodium on thepreoperative day; Nauri 1 - Nauri 5 - urinary sodium on the first tofifth postoperative days.

Urinary sodium

1 link movies. Natriuresis (urinary sodium > 110mEq/12 hours) was observed in 28 of 30patients (93.33%) at least in one day during the postoperative period (D1 - D5).Higher levels were found on D2 (269.57 ± 157.39mEq/12 hours), when 85.71%of the patients presented natriuresis (Table1 and Figure 1) with astatistically significant difference (p = 0.012).

Factor Natriuretico Atrial

The average and standard deviation of plasma sodium (mEq/L), urinarysodium (mEq/12 hours) and plasma atrial natriuretic factor (pg/mL)in the pre- and postoperative time periods (D0 and D1 - 5).

ANF - atrial natriuretic factor; Naplasm - plasma sodium; Nauri -urinary sodium.

Plasma sodium

Hyponatremia (plasma sodium ≤ 135mEq/L) was present in 19 of 30 patients(63.33%) in the postoperative period (D1 - D5), and the lowest plasma sodiumlevels were found on D1 (135.47 ± 5.24), when 40% of the patientspresented hyponatremia (Table 1 and Figure 1). However, there was nostatistically significant difference in the plasma sodium levels during thistime period (p = 0.726). Timothy good above top secret pdf reader.

Atrial natriuretic factor

Plasma ANF levels remained increased (> 50pg/mL) on at least one of thepostoperative days (D1 - D5) in 92.60% of the patients. Higher levels were foundon D3 (108.79 ± 60.86pg/mL) and decreased on D5 (56.60 ±45.63pg/mL) (Table 1 and Figure 1). There was no statisticallysignificant association between plasma ANF and plasma sodium and between plasmaANF and urinary sodium in any of the days studied (Table 2). When we studied the correlation between plasma ANFand plasma sodium and between plasma ANF and urinary sodium on the firstpostoperative day, we also did not find any significant correlation (p = 0.3742and p = 0.3139, respectively).

Table 2

Comparative analysis among the levels of atrial natriuretic factor,plasma sodium and urinary sodium at each time point (Fisher’s exacttest)

ANF - plasma atrial natriuretic factor on each day; Naplasm 0 -plasma sodium on the preoperative day; Naplasm 1- Naplasm 5 - plasmasodium on the first to fifth postoperative days; Nauri 0 - urinarysodium on the preoperative day; Nauri 1 - Nauri 5 - urinary sodiumon the first to fifth postoperative days.

DISCUSSION

Hyponatremia is the sodium disturbance most frequently found in neurosurgerypatients. Although hyponatremia is most reliably encountered in patients withaneurismal SAH, it sometimes occurs in a variety of other conditions that affect thecentral nervous system, such as malignancy and head trauma; it has also beenreported in the postoperative neurosurgical setting.⁽⁾ It is frequently associated with natriuresis, andits main cause is CSWS.^(-,-) CSWS is still notcompletely understood, and natriuretic factors seem to play an important role in itsphysiopathology. Among the natriuretic factors, ANF may play a role in thehyponatremia and natriuresis found in neurosurgical patients, as shown in previousstudies.^(,-,-)

However, there are conflicting reports regarding ANF in neurologic patients. Somestudies have demonstrated that ANF produces natriuresis and diuresis whenadministered either peripherally or centrally.^(,) Isotani et al.demonstrated that hyponatremia produced significantly elevated levels of ANF andvasopressin immediately after SAH. They observed that ANF remained high in patientswith mild hyponatremia and concluded that ANF may be a causal natriuretic factor inCSWS.⁽⁾ Doczi et al.reported that only the SAH patients with elevated intracranial pressure (>20mmHg) had increased plasma ANF concentrations.⁽⁾ A direct relationship between ANF andintracranial pressure was also reported by Berendes et al., which suggested that thedevelopment of renal salt wasting is a protective measure that limits extreme risesin intracranial pressure.⁽⁾Weinand et al. found serum ANF levels to be elevated above the normal range in 6 of8 neurosurgical patients with a variety of neurosurgical disorders, includingcerebral tumors. Additionally, a near-linear relationship was observed betweenplasma ANF levels and urine sodium excretion.⁽⁾

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Other studies also showed elevated concentrations of circulating ANF in neurosurgerypatients and after SAH, but no clear relationship with hyponatremia and natriuresishas been established.^(,) In a study with 25 patients with SAH, Diringer etal. observed that ANF levels were significantly elevated in 21 patients with SAHcompared with 4 unruptured aneurysms and returned to normal over 2 weeks. There wasno correlation between ANF and serum sodium levels, and the ANF levels in 2 patientswith SAH who had hyponatremia were not significantly different from those in theother patients with SAH. Thus, elevated levels of ANF alone do not account for thehyponatremia observed after SAH.⁽⁾Another study prospectively studied sodium, volume regulation and ANF in 19 patientsfollowing acute aneurismal SAH. Plasma ANF values were elevated but did notcorrelate with the presence of hyponatremia.⁽⁾ Elevated levels of ANF following SAH were alsodemonstrated by Diringer et al. (1991) in another study and they may represent amarker of hypothalamic dysfunction but may not directly contribute to hyponatremiathemselves.⁽⁾

In a prospective study of 49 patients with SAH, Tsubokawa et al. observed that theplasma ANF concentrations were not altered.⁽⁾ Normal ANF plasma levels have been found in patients withCSWS associated with parietal glioma⁽⁾ and after surgery for pituitary adenoma.⁽⁾ During experimental natriuresisinduced by the intracerebroventricular administration of hypertonic saline, plasmaANF levels were found to decrease.⁽⁾

In our study, hyponatremia (plasma sodium < 135mEq/L) was found in 63.33% of thepatients in the postoperative phase, particularly on the first postoperative day.Natriuresis (urinary sodium > 110mEq/12 hours) was observed in 93.33% of thepatients. Urinary sodium levels increased during the entire postoperative period,particularly on the second postoperative day; however, their levels were also highin the preoperative period. We also observed high plasma ANF levels during theentire postoperative period; however, high plasma ANF levels were also found in thepreoperative period, similar to urinary sodium, likely due to the primary disease.Although hyponatremia, natriuresis and increased plasma ANF levels were found in thepostoperative period, we did not find any significant statistical correlation amongthem, which suggested that ANF is not responsible for hyponatremia and natriuresisin neurosurgery patients.

Our observations confirm the previous reports of some authors.^(,) We found highplasma ANF levels without a correlation with hyponatremia and natriuresis, as shownby Diringer et al.^(,) Tsubokawa et al.,⁽⁾ Yamaki et al.⁽⁾ and Hansel et al.⁽⁾ These authors also did not find any correlation with ANF,hyponatremia and natriuresis; however, they did not find high plasma ANF levels, aswe observed in our study.

The limitations of the present study include the small number of patients studied;however, studies involving CSWS and ANF in the literature are mostly reviewarticles, case reports and retrospective studies involving small numbers ofpatients. Urinary sodium was measured at 12 hours overnight instead of 24 hours, andplasma ANF was measured only on the preoperative day and the first, third and fifthpostoperative days. Further experimental studies in these areas must be performed,including the investigation of other natriuretic factors.

CONCLUSION

Hyponatremia and natriuresis are commonly found in neurosurgical patients. Despiteincreased plasma concentrations of atrial natriuretic factor in the postoperativeperiod, it is not directly responsible for hyponatremia and natriuresis. Thepresence of other natriuretic factors, the participation of multiple natriureticfactors alone or in combination, and direct neural effects on the kidneys may alsobe involved.

ACKNOWLEDGMENTS

This research was supported by a grant from the Fundação deAmparo à Pesquisa do Estado de São Paulo (FAPESP) process00/05990-9.

The authors would like to thank the statistics group of the Faculdade deCiências Médicas from the Universidade Estadualde Campinas (UNICAMP) for their assistance, all members of theintensive care unit's multidisciplinary team, and the staff of the Department ofNeurosurgery of UNICAMP. Our thanks also go to Margareth Castro, PhD, from theDepartment of Clinical Pathology, Universidade de São Paulo,for her help in measuring the levels of atrial natriuretic factor.

Funding Statement

This research was supported by a grant from theFundação de Amparo à Pesquisa do Estado deSão Paulo (FAPESP) process 00/05990-9.

Footnotes

REFERENCES

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