Value of Brain Natriuretic Peptide in Diagnosis and Control of Hyperthyroid Patients

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Sara Osama badr ◽  
mohamed kamer ◽  
Hazem Ashmawy ◽  
amal gharib ◽  
Ekhlas Hussein
2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Aviva Peleg ◽  
Yonathan Hasin

Background: Contrast media (CM) administrated during percutaneous coronary intervention (PCI) is associated with endothelial dysfunction (ED) and systemic vascular injury. Brain natriuretic peptide (BNP) administration 24 hours post PCI decreases ED. Aims: To evaluate 1.The ability of human BNP (hBNP) infusion during PCI, to prevent ED in acute coronary syndrome's (ACS) patients post the PCI. 2. The effect of CM on human coronary microvascular endothelial cells (HCMEC).3. Explain ED by invitro study. Methods and results (in vivo): Non-ST elevation ACS patients who underwent PCI (111) were randomized into 2 groups: an hBNP group who received hBNP infusion during the procedure (n=44), and control group who received nitroglycerin (n=67). Flow mediated dilatation (FMD) (by ≥2.5%), BNP, corin, serum creatinine (sCr) and estimate Glomerular Filtration Rate (eGFR), before and 24 hr after operative were recorded, starting with the same baseline. The post PCI FMD and eGFR were significantly reduced in the control group (p=0.05, 0.002) but not in the hBNP group (p=0.16, 0.4). BNP, corin and sCr increased significantly in the control group (p=0.001, 0.003, 0.0002 respectively) but not in hBNP group (p=0.09, 0.07, 0.18). Methods and results (in vitro): HCMEC were treated with CM (10%) in the presence and absence of BNP. eNOS, corin and cGMP levels were measured by ELISA and the results were compared to untreated cells. In both treatments eNOS was significantly reduced (p=0.001) and corin was significantly increased (p=0.002). cGMP was not affected by CM treatment (p=0.278), but was increased significantly (p=0.001) by hBNP combination. cGMP immuno-flourescence staining of HCMEC showed distorted cellular cGMP appearance by CM treatment, that was corrected in the combination with hBNP with accentuated subsarcolemmal staining. Conclusions: CM reduces eNOS level in HCMEC. Therefore, reduced in NO-cGMP pathway's products, probably is the mechanism that induces ED in-vivo. BNP treatment reduces FMD diminution and kidney injury post PCI. A compensatory rise in corin that increases BNP as well as the hBNP administration, invivo and invitro, maintains cytosolic cGMP via NP-cGMP pathway, and compensates for NO-cGMP loss, (reduced sGC) and thus prevents ED.


1999 ◽  
Vol 96 (1) ◽  
pp. 5-15 ◽  
Author(s):  
Kaare T. JENSEN ◽  
Hans EISKJÆR ◽  
Jan CARSTENS ◽  
Erling B. PEDERSEN

The effect of a continuous infusion of human brain natriuretic peptide, 2 ;pmol·min-1·kg-1, during 60 ;min was studied in nine patients with congestive heart failure and in 10 healthy control subjects. Brain natriuretic peptide increased from 1.6 to 101 ;pmol/l in control subjects and from 25 to 173 ;pmol/l in congestive heart failure during infusion. Urinary sodium excretion increased significantly in both congestive heart failure (60%) and control subjects (71%), but the absolute increase was significantly lower in congestive heart failure (27 ;μmol/min) than in control subjects (190 ;μmol/min). Urinary flow rate did not change. The lithium clearance technique was used to evaluate the segmental tubular function; the distal fractional reabsorption of sodium decreased significantly less in congestive heart failure (DFRNa: -0.8%) than in control subjects (DFRNa: -3.7%). Baseline values for glomerular filtration rate and renal plasma flow were reduced in congestive heart failure, but brain natriuretic peptide induced no significant changes between congestive heart failure and control subjects. Brain natriuretic peptide induced the same absolute increase in secondary messenger cGMP in plasma and urine in both patients and healthy subjects. It is concluded that the natriuretic response to brain natriuretic peptide infusion was impaired in patients with congestive heart failure compared with healthy subjects, and it is likely that the impaired natriuretic response was caused by a reduced responsiveness in the distal part of the nephron.


2021 ◽  
pp. 45-46
Author(s):  
Shahrukh Khilji ◽  
Bushra Fiza ◽  
Shehreen Akhtar ◽  
Jai Prakash ◽  
Maheep Sinha

INTRODUCTION: Congestive Heart Failure is a complex physiological syndrome caused from structural or functional alterations to the myocardium. Lactate is produced by anaerobic metabolism and is secreted by the Brain-Natriuretic peptide heart ventricles in response to left ventricular stretching or wall tension. AIM: The aim of the study was to evaluate Brain-Natriuretic Peptide, Lactate levels and Blood pressure in Congestive Heart Failure patients and compared them with healthy individual. MATERIALS AND METHODS: Total 80 participants who fullled the inclusion and exclusion criteria were enrolled in the study. They were divided into two group i.e., case and control group. Case group included 40 patients of Congestive Heart Failure, age between 18-65 years and control group comprised of 40 healthy individuals with similar age range. Blood sample were drawn and analyzed for the evaluation of Serum lactate and Brain-Natriuretic Peptide. Blood Pressure was also measured in both the groups. RESULT: The present study has demonstrated that the level of Brain-Natriuretic Peptide and lactate were signicantly high in Congestive heart failure patients when compared with control group. Systolic and Diastolic blood pressure were also higher among patients group. CONCLUSION: The results of the study suggested that the levels of Lactate and Brain-Natriuretic Peptide were high in Congestive heart failure patients when compared with healthy individual. Systolic and Diastolic blood pressure were also higher among patients group. Elevated lactate and Brain-Natriuretic Peptide level can be recommended as useful indicator of poor prognosis and hence can be helpful in early identication of patients at risk.


2004 ◽  
Vol 171 (4S) ◽  
pp. 399-400
Author(s):  
Ramaswamy Manikandan ◽  
Calvin Nathaniel ◽  
Ravi Gullipalli ◽  
Adebanji Adeyoju ◽  
Stephen C.W. Brown ◽  
...  

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