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研究生:許寬立
研究生(外文):Xu, Kuan-Li
論文名稱:糖尿病之心臟功能的研究
論文名稱(外文):Study on cardiac function in diabetes mellitus
指導教授:曾淵如曾淵如引用關係陳朝峰陳朝峰引用關係
指導教授(外文):Zeng, Yuan-RuChen, Zhao-Feng
學位類別:博士
校院名稱:國立臺灣大學
系所名稱:臨床醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:1997
畢業學年度:85
語文別:中文
論文頁數:119
中文關鍵詞:非胰島素依賴性糖尿病x症候群彈性蛋白離體心臟配置最大彈性容量心肌硬度常數醫學
外文關鍵詞:Non-insulin diabetes mellitussyndrome xtitinLangendorff preparationmaximal elastancemyocardial stiffnes constantMEDICINE
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The disease entity "diabetic cardiomypathy" originated from
the findingthat cardiac function in diabetes mellitus usually is
impaired in the abscenceof coronary artery stenosis or any other
heart disease. However, the supporting evidences were from the
studies mostly with the subjects of minor group--type Idiabetes;
with the entire cardiac performance rather than myocardial
contractilitybeing assessed; and with the animal experiments
which evaluated the biochemical and functional alterations,
being by destruction of pancreas, not corresponding to the
insulin resistant condition in type II diabetes. In order to
supplement the inappropriateness mentioned above, we studied the
type II diabetic patients from two aspects: firstly, the
influence of diabetes mellitus to the cardiac function of
patients with syndrome x, whichhad evidence of myocardial
ischemia functionally, in the abscence of coronary stenosis.
Secondly the cardiac function of diabetic patients who had no
coronary stenosis or other heart diseases, and were free from
cardiac symptoms. The former study revealed that about 10%
oa patients with syndrome x developed diabetes melitus. Their
left ventricles became more hypertrophied and less compliant
along with the uration of diabetes. The detrimental effectof
hypertension to the cardiac function was more apparent than that
of diabetesand aggravated the diabetic effect furthermore. The
latter study using the relation between end-systolic wall stress
and circumferential fiber shortening evaluated the the cardiac
contractility, which was independent of heart rate and loading
conditions. It showed that in diabetic patients diastolic
function impaired earlier than systolic function. At baseline
state, patients had diastolic dysfunction but the systolic
function still kept intact and the ejection fraction of left
ventricle even increased in the patients without microvascular
complications. However, under some stress (dobutamine chalenge)
the reserve of contractility was inadequate in diabetic
patients, especiallyin those with microvascularcomplications.
In animal experiment, the Wistar rats fed with high fructose
diet and clonidinedeveloped insulin resistance, elevated blood
glucose without elevation of bloodpressure--the condition
mimicking diabetic cardiomyopathy. With langendorffpreparation,
the intrinsic myocardial mechanics of isolated heart was
assessed bymaximal elastance and constant of compliance. The
resuts showed that in rats of such condition, cardiac
performance still kept intact. Nevertheless, maximal
elastancedecreased and contant of compliance increased,
indicaing impairment of both systolicand diastolic function. The
myocardial titin content, measured by the density ratio oftitin/
actin which was read with densitometry, also decreased. In the
experimental ratswhich developed elevation of both blood glucose
and pressure, the function of systoleand diastole got more
worse. Titin is an important component of cytoskeleton in
cardiac sarcomere. Itprovides elasticity to sarcomeres and
serves as a template for newly synthesizedmyoproteins to
contruct new sarcomeres. In the experimental rats mimicking
diabeteiccardiomyopathy, the decrease in titin content made
myofibrils less stretchable andtherefore myocardial
contractility decreased according to Frank-Starling law. In
the myocardia of mildly to moderately failing heart with
hypertrophiccardiomyopathy, dilated cardiomyopathy, rheumatic
and congential heart diseases, thetitin contents were similar
among the different cardiac diseaes and positively
correlatedwith the left ventricular ejection fraction. The
decreased density ratio of titin/actin indicated early change of
myocardial damage. From the above studies, there are still
some questions remained to be solved. Firstly, is the
microvascular change in syndrome x caused by insulin resistance?
Does the cardiac function become impaired before flank diabetes
mellitus develops?secondly, is the inadequate reserve of
myocardial contractility in diabetic patient withnormal cardiac
function at baseline state improved by strict control of
siabetes, withinsulin injection or any methods to ameliorate
insulin resistance? Thirdly, doeselevated catecholamine have
different effects to IDDM and NIDDM? Fourthly, what isthe
relation among diabetes, syndrome x and cardiomyopathy? They
seem to be some branches from insulin resistance to coronary
stenosis. Fifthly, is titin influenced byhyperglycemia direatly
or by the metabolites in the polyol pathway? Sixthly, does the
titin content measured by the density ratio of titin/actin
correlate with the pathologicalpicture in myocardium? There is a
long way to go to clarify these related questions.
Hypertension usually accompanies diabetes and aggrravates the
cardiac dysfunctioncaused by diabetes. Angiotensin converting
enzyme inhibitors can lower blood pressure and make insulin
resistance and microvascular change better. It has beenreported
that the insertion/deletion polymorphism of the angiotensin
converting enzymegene is related to the possibility of
developing hypertension in the diabetic patients.next step in
our plan is to evaluate the cardiac effect of angiotensin
converting enzymeinhibitor in the diabetic patients, according
to the gene polymorphism of angiotensin converting enzyme.

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