B型利鈉利尿胜肽在心臟衰竭之臨床應用

Clinical Application of B-type Natriuretic Peptide in Heart Failure

B型利鈉利尿胜肽（BNP）是由心室肌細胞分泌。隨著心臟衰竭病程進展，生理、病理會產生系列性的代償變化，例如交感神經活化、體液容積過多等。這些變化最終都對心臟衰竭的病程進 展不利。BNP隨著心臟衰竭的生理病理變化被釋放出，BNP對系列性代償機轉具有對抗作用：在腎臟系統，BNP會收縮出球動脈、擴張入球動脈，使腎絲球過濾率增加，達到排泄鈉、水，改善體液滯留和組織充血的功能；在心血管系統，BNP有血管擴張作用，使血壓下降和減輕前負荷； 在神經系統，BNP有抑制交感神經活性作用，使心跳過快改善。BNP是可用來檢測心臟衰竭的新型生物標誌。目前BNP廣泛應用於心臟血管疾病的臨床實務和相關研究。此報告藉由文獻回顧闡述心臟衰竭和BNP的關係，以提供照顧心臟衰竭的資訊。

B-type natriuretic peptide (BNP) is a new biomarker expressed from the myocytes located in the ventricle. When heart failure (HF) progresses, the change of compensatory mechanisms that result in the pathophysiological process of HF develops such as sympathetic stimulation and volume overload. Those changes in pathophysiological responses finally become detrimental as HF progresses. The release of BNP results in a variety of physiological changed that confront the compensatory mechanisms. BNP is a counter-regulatory hormone. In the kidneys, BNP increases glomerular filtration rates via efferent arteriolar vasoconstriction and afferent arteriolar vasodilatation. This results in diuresis and sodium loss, which ameliorate fluid balance and congestion. In the cardiovascular system, BNP causes a decrease in blood pressure and preload by causing vasodilatation. In the nervous system, there is a suppression of sympathetic activity as a result of BNP release, resulting in improvement in heart rate with reduction of tachycardia. BNP is now widely used in cardiovascular clinical practice and research throughout the world. This report reviews the relationship between heart failure and BNP for providing information in the care of heart failure.