呋喃唑酮制备大鼠扩张型心肌病模型

目的：探讨用呋喃唑酮饲养Wistar大鼠建立扩张型心肌病（DCM）大鼠模型的可行性。 方法： 用呋喃唑酮饲养Wistar大鼠建立扩张型心肌病大鼠模型, 超声心动图检测大鼠左心室结构和功能；有创导管测压力；测量大鼠左心室内径和游离壁厚度，HE染色观察大鼠心肌细胞形态学变化,V-G和免疫组化染色检测心肌胶原纤维并计算胶原容积分数(CVF)。 结果： ①DCM组大鼠饲养12周后诱发呋喃唑酮扩张型心肌病（Fz-DCM）总成功率为66.6%(20/30)。② DCM组大鼠左室舒张期末内径、左室收缩末内径、右房压、左室内径、心脏重量/体重比值均明显大于NC组，左室内径缩短率、左室射血分数、左室游离壁厚度均明显小于NC组（均P<0.05）。③DCM大鼠心肌细胞肥大、变性，间质胶原纤维增生，Ⅰ、Ⅲ型胶原纤维及CVF明显增加。 结论： 呋喃唑酮能成功诱发DCM大鼠模型；Fz-DCM大鼠出现左室扩大、心室壁变薄，间质纤维组织增生等病理改变，并且左室收缩功能下降，提示Fz-DCM大鼠模型能反映扩张型心肌病的病理生理特征。     

Norepinephrine-induced cardiac hypertrophy of the cat heart.

Norepinephrine administration causes progressive hypertrophy of the mammalian heart as measured by myocardial mass. The purpose of this study was to determine the growth response of the myocardial tissue components as well as the myocardial cell itself to norepinephrine. Young, adult cats were given low doses of norepinephrine in dextrose or dextrose alone twice daily for 15 days. On day 16, there were no changes in the animals body weight, right ventricular systolic pressure, right ventricular end-diastolic pressure, heart rate, cardiac index, or blood pressure. However, the right ventricle/body weight, the left ventricle/body weight and the total heart weight/body weight were increased significantly in the norepinephrine treated animals. The increase was on the order of 40%. The cardiac muscle cell was also significantly increased in size and both the right and left ventricular cardiac muscle cells exhibited a dramatic increase in size as measured by cross sectional area. Upon stereological examination it was found that the amount of hypertrophy as seen in the cardiac muscle cells was paralleled by the hypertrophy seen in the other tissue components of the myocardium. The volume density of the muscle cells, the interstitial components, as well as the blood vessel compartment were identical in the control and in the norepinephrine-treated groups. In conclusion, this study demonstrates that the response of the myocardium to norepinephrine is similar to that seen in response to a volume overload rather than that seen in response to pressure overload.     

Norepinephrine-induced cardiac hypertrophy of the cat heart

Norepinephrine administration causes progressive hypertrophy of the mammalian heart as measured by myocardial mass. The purpose of this study was to determine the growth response of the myocardial tissue components as well as the myocardial cell itself to norepinephrine. Young, adult cats were given low doses of norepinephrine in dextrose or dextrose alone twice daily for 15 days. On day 16, there were no changes in the animals body weight, right ventricular systolic pressure, right ventricular end-diastolic pressure, heart rate, cardiac index, or blood pressure. However, the right ventricle/body weight, the left ventricle/body weight and the total heart weight/body weight were increased significantly in the norepinephrine treated animals. The increase was on the order of 40%. The cardiac muscle cell was also significantly increased in size and both the right and left ventricular cardiac muscle cells exhibited a dramatic increase in size as measured by cross sectional area. Upon stereological examination it was found that the amount of hypertrophy as seen in the cardiac muscle cells was paralleled by the hypertrophy seen in the other tissue components of the myocardium. The volume density of the muscle cells, the interstitial components, as well as the blood vessel compartment were identical in the control and in the norepinephrine-treated groups. In conclusion, this study demonstrates that the response of the myocardium to norepinephrine is similar to that seen in response to a volume overload rather than that seen in response to pressure overload.     

Early morphological alterations of pressure-overloaded cat right ventricular myocardium

Pressure overload of the right ventricle results in an increase in ventricular mass. It also results in abnormal in vitro contractile function in advance of the onset of congestive heart failure as determined in papillary muscles removed from these ventricles. To correlate these functional abnormalities with any early underlying morphological changes, a band was placed around the proximal pulmonary artery of cats. This band restricted the lumen to 20% of normal and was left in place for 2 weeks. At that time, hemodynamic variables were measured to insure that right ventricular pressure overload had been produced. The hearts were then perfusion fixed, and papillary muscles from the right ventricle were prepared for light and transmission electron microscopy. Quantitative morphological data were obtained for the volume density both of several tissue components and of several organelles. It was found that there are significant increases in myocyte cross-sectional area and diameter in hypertrophied tissue with a concurrent increase in the volume density of interstitial tissue. There are no alterations in the volume density of organelles in the hypertrophied myocytes. We suggest that the substantial increase in the proportion of connective tissue and the decrease in the surface area to volume ratio that accompany pressure overload cardiac hypertrophy may be early underlying structural changes that relate directly to the abnormal contractile function found in this type of hypertrophy.     

Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.

To determine the effects of chronic anemia on the functional and structural characteristics of the heart, 1-month-old male rats were fed a diet deficient in iron and copper, which led to a hemoglobin concentration of 4.63 g/dl, for 8 weeks. At sacrifice, under fentanyl citrate and droperidol anesthesia, systolic, diastolic, and mean arterial blood pressures were decreased, whereas differential pressure was increased. Left ventricular systolic pressure and the ventricular rate of pressure rise (mmHg/s) were reduced by 9% and 14%, respectively. Moreover, developed peak systolic ventricular pressure and maximal dP/dt diminished 14% and 12%. After perfusion fixation of the coronary vasculature and the myocardium, at a left ventricular intracavitary pressure equal to the in vivo measured end diastolic pressure, a 10% thickening of the left ventricular wall was measured in association with a 13% increase in the equatorial cavitary diameter and a 44% augmentation in ventricular mass. The 52% hypertrophy of the right ventricle was characterized by an 11% thicker wall and a 37% larger ventricular area. The 33% expansion in the aggregate myocyte volume of the left ventricle was found to be due to a 14% myocyte cellular hypertrophy and a 17% myocyte cellular hyperplasia. These cellular parameters were calculated from the estimation of the number of myocyte nuclei per unit volume of myocardium in situ and the evaluation of the distribution of nuclei per cell in enzymatically dissociated myocytes. Myocyte cellular hyperplasia provoked a 9% increase in the absolute number of cells across the left ventricular wall. In contrast, myocyte cellular hypertrophy (42%) was responsible for the increase in myocyte volume of the right ventricle. The proliferative response of left ventricular myocytes was not capable of restoring diastolic cell stress, which was enhanced by the changes in ventricular anatomy with anemia. In conclusion, chronic anemia induced an unbalanced load on the left ventricle, which evoked a hyperplastic reaction of preexisting myocytes, in an attempt to normalize diastolic wall and myocyte stress.     

慢性低氧性肺动脉高压大鼠肾上腺髓质素前体N端20肽的变化

目的：探讨慢性低氧性肺动脉高压和肺血管结构重建时肾上腺髓质素前体N端20肽（PAMP）的变化。方法:将18只雄性Wistar大鼠随机分为对照组和低氧组，每组各9只。常压低氧2周后，以右心导管法测定肺动脉平均压（mPAP），检测右心室与左心室加室间隔比值 ［RV/(LV+S)］，观测肺血管显微和超微结构的变化。并且以放免法测定血浆中PAMP含量，以免疫组化法检测肺组织中PAMP表达，以原位杂交检测肺组织中肾上腺髓质素（ADM） mRNA的表达。结果: 低氧组大鼠mPAP及RV/（LV+S）均明显高于对照组（均P<0.01）。光镜下，肺小血管肌化程度明显增强，肺中、小型肌型动脉相对中膜厚度明显增加。电镜下，肺腺泡内动脉内皮细胞增生、肿胀，内弹力层粗细不均，平滑肌细胞肥厚、向合成表型转化。并且低氧组大鼠血浆PAMP含量明显高于对照组（P<0.01），肺动脉PAMP表达和ADM mRNA表达均明显增强。结论：低氧后肺动脉PAMP表达和血浆PAMP含量的上调可能参与了慢性低氧性肺动脉高压和肺血管结构重建的形成。     

Carvedilol inhibits right ventricular hypertrophy induced by chronic hypobaric hypoxia

Right ventricular hypertrophy induced by chronic hypoxia is mainly due to a mechanical stress upon the ventricular wall secondary to pulmonary arterial hypertension. However, the hypoxic chronic activation of the sympathetic nervous system can contribute to the development of right ventricular hypertrophy either via myocardial adrenergic receptors and/or a vasoconstriction and remodeling of pulmonary arteries. To highlight the specific role of the sympathetic nervous system on hypoxia-induced right ventricular hypertrophy and particularly the efficiency of carvedilol, our study compared physiological, myocardial, and pulmonary arterial morphometric data in rats treated by α-(prazosin), or β-(propranolol) or αβ-(carvedilol) antagonist and exposed to chronic hypobaric hypoxia (2 weeks at 380 mmHg barometric pressure). In chronic hypoxia, both systolic right ventricular pressure and Fulton’s ratio (right/(left+septum) ventricular weight) were lower in rats treated by prazosin (−16.7 and −13.6%), propranolol (−28.6 and −12.7%) and carvedilol (−15.9 and −14.3%) respectively when compared to glucose (p<0.05). Surprisingly, prazosin was unable to reduce right ventricular hypertrophy induced by chronic hypoxia, whereas, left ventricular weight increased. Wall thickness index of pulmonary arteries increased in chronic hypoxia and was reduced by carvedilol. In conclusion, the hypoxia-induced activation of the adrenergic system participates in the development of right ventricular hypertrophy. Carvedilol is effective in reducing hypoxia-induced right ventricular hypertrophy, pulmonary arterial hypertension, and muscularization of pulmonary arteries.     

Ventricular hypertrophy In sleep apnoea

SUMMARY  Ventricular hypertrophy is associated with an increased risk of cardiovascular death and cardiac events. In response to a haemodynamic load, ventricular hypertrophy may either be eccentric (dilation in response to volume overload) or concentric (increase in wall thickness in response to pressure overload). Ventricular hypertrophy increases with age, weight, blood pressure, and the presence of cardiovascular disease. It is greater in men than in women when adjusting for other variables. Echocardiography is the best method for accurate quantification of left ventricular mass and for detecting right ventricular hypertrophy. In obstructive sleep apnoea there are reports of both eccentric and concentric hypertrophy of the left ventricle. However, many of these reports have failed to control for patient weight or age. More recent reports indicate that much of the hypertrophy of the left ventricle reported in obstructive sleep apnoea can be related to patients' age, blood pressure, or size. However, right ventricular hypertrophy appears to be distinctly associated with the presence and severity of obstructive sleep apnoea. Right ventricular hypertrophy secondary to obstructive sleep apnoea may be the substrate for the eventual development of cor pulmonale and right heart failure. Its pathophysiological significance and potential use as a marker of severe OSA requires further investigation. Further investigation into left ventricular hypertrophy and sleep apnoea must control for the potentially confounding variables listed above and will require population-based and/or carefully matched case control studies.     

Characteristics of isolated cardiomyocytes in concentric and eccentric hypertrophy of the human heart ventricle

Alkaline dissociation of cardiomyocytes was used for investigation of concentric and eccentric myocardial hypertrophy in 8 deceased patients with carions ventricular myocardial mass. For both ventricles and forms of hypertrophy the length, diameter and volume of the cells were found increased, the increase being proportional for the left ventricle (except the volume) and gross for linear enlargement of the right ventricle in eccentric hypertrophy. Absolute number of cardiomyocytes reached maximum in concentric left ventricular hypertrophy showing the same values with normal-mass ventricles in eccentric hypertrophy.     

Ultrastructure of the right ventricle after monocrotaline-induced cor pulmonale in the nonhuman primate (Macaca arctoides).

The present study is concerned with the ultrastructural changes that occur in the right ventricle of Macaca arctoides monkeys following subcutaneous injection of the pyrrolizidine alkaloid monocrotaline. The monkeys showed right ventricular hypertrophy and congestive heart failure within 7 months following the initial injection of monocrotaline. At sacrifice, all of the monkeys had developed marked dilatation and hypertrophy of the right ventricle. Focal cytolysis involving myocytes, intracellular edema, and fibrosis were observed light microscopically. Ultrastructural changes of the right ventricle included hypertrophy and hyperplasia of the mitochondria, increase in intracellular matrical material, streaming and clumping of the Z-band material, disorganization and degeneration of myofibrils, dilatation of the sacroplasmic reticulum and transverse tubular system, increased number of free and attached ribosomes, and proliferation of intercellular collagen fibers.     

缺氧性肺动脉高压大鼠右心室重构

摘要目的：研究缺氧性肺动脉高压大鼠右心室重构情况。方法：常压间断缺氧法复制缺氧性肺动脉高压大鼠模型，采用右心导管法测定平均肺动脉压力，通过测量右心室流入及流出道长度、左心室壁和右心室壁厚度、右心室和左心室 室间隔重量对其右心室重构情况进行定性研究。结果：缺氧14d后大鼠平均肺动脉压力显著升高，右心室流出道长度及右心室肥大指数显著增加，缺氧21d后右心室游离壁重量显著增加；右心室流人道长度及左、右心室壁厚度与对照组无统计学差异。结论：缺氧性肺动脉高压大鼠右心室早期表现为离心性肥大。     

Hyperplasia of the carotid body

The histopathology of hyperplasia of the carotid bodies was studied in 6 cases of hypoxaemia and right ventricular hypertrophy secondary to pan-acinar emphysema, and in five cases of systemic hypertension with left ventricular hypertrophy. The features of the hyperplasia were the same in the two groups. There was proliferation of sustentacular (type II) cells and compression of central cores of chief (type I) cells. It is speculated that the hyperplasia of sustentacular cells is associated in some way with the prevention of retention of sodium ions and water which characterises hypoxic cor pulmonale in "blue bloaters", systemic hypertension, and ascent to high altitude with the complications of acute mountain sickness, and pulmonary and cerebral oedema.     

Gax在肺动脉高压大鼠肺动脉中的表达变化

目的:使用低氧及野百合碱(monocrotaline,MCT)诱导的两种肺动脉高压(pulmonary arterialhypertension,PAH)大鼠模型,观察生长终止特异性同源盒(growth arrest-specific homeobox,Gax)在肺动脉的表达变化。方法:Sprague Dawley大鼠随机分为四组:低氧模型组(n=16)、低氧对照组(n=16)、MCT模型组(n=16)及MCT对照组(n=16)。采用插管法测定大鼠的右心室压力及肺动脉压力。右心室质量除以左心室和室间隔质量,计算右心肥厚指数。采用定量RT-PCR法测定肺动脉主干及肺组织Gax mRNA表达;采用Western免疫印迹法测定肺动脉主干Gax蛋白表达;免疫组织化学染色观测Gax在肺内的分布及表达变化。结果:低氧模型组及MCT模型组大鼠的右心压力、肺动脉压力及右心肥厚指数均显著高于相应对照组(P<0.01),两种模型大鼠的肺动脉血管均出现明显重构。与对照组比较,Gax mRNA在两种模型组大鼠的肺组织表达降低(P<0.05),而在肺动脉主干表达升高(P<0.05)。Gax蛋白在肺内主要表达在微小动脉。与对照组比较,两种模型组大鼠的肺动脉主干和肺微小动脉Gax蛋白表达均升高(P<0.05),而肺组织Gax蛋白表达下降(P<0.05)。结论:Gax主要表达在肺微小动脉,在PAH发生时表达上调。     

Reversibility of the structural effects of pressure overload hypertrophy of cat right ventricular myocardium

The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophing in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.     

The effects of vagotomy on compensatory ovarian hypertrophy and follicular activation after unilateral ovariectomy

Following unilateral ovariectomy in the rat, the remaining ovary undergoes rapid compensatory changes including an increase in the number of antral follicles (follicular activation) and an increase in ovarian weight (compensatory ovarian hypertrophy). The ovary is innervated by the vagus nerve (Burden et al., 1983). In the present study, the effects of right and left cervical vagotomy and abdominal vagotomy on follicular activation and compensatory ovarian hypertrophy in the remaining right or left ovary were compared 15 days after unilateral ovariectomy. Neither right nor left cervical vagotomy affected compensatory ovarian hypertrophy of the right or left ovaries but abdominal vagotomy depressed compensatory ovarian hypertrophy in both the right and left ovaries. Left cervical vagotomy did not inhibit follicular activation, but right cervical vagotomy prevented follicular activation in the right but not left ovary. Also, abdominal vagotomy inhibited follicular activation in the right but not the left ovary. In animals with both ovaries which were subjected to the left or right cervical vagotomy or abdominal vagotomy follicular counts in both right and left ovaries were similar. Collectively, these data indicate that the vagus nerve participates in follicular activation after unilateral ovariectomy. The data also indicate that the right ovary is more dependent on vagal influences for follicular activation than the left ovary.     

致心律失常性右室心肌病心力衰竭期的病理特点分析

目的 通过分析致心律失常性右室心肌病(ARVC)心力衰竭期的病理改变,以进一步了解其临床分期与病理表型的关系.方法 从2004-2007 年在阜外心血管病医院接受心脏移植的心力衰竭病例中,收集病理诊断为ARVC的受体心脏8例,测量心脏重量,评价左右心室心腔扩张、心肌细胞肥大、脂肪浸润、纤维化、附壁血栓和伴发心肌炎等指标,注意左心室受累情况,并进行病理分型.结果 8例中的7例为经典型(即右心室改变为主),1例为左优势型(左心室改变为主),未见双室型病例.组织学均为纤维脂肪型,未见单纯脂肪型病例.经典型病例的右心室中、重度扩张,少数有室壁瘤形成,其中6例伴左心室受累,受累左心室轻、中度扩张,心肌广泛间质纤维化,部分病例伴替代性疤痕,而脂肪浸润量小,多局限于心外膜下.左心室心肌细胞肥大普遍.而左优势型的左心室重度扩张,弥漫间质纤维化和局部透壁性脂肪浸润.8例中3例左心室明显肥厚,3例查见双室附壁血栓,1例伴局灶性心肌炎.结论 ARVC心力衰竭期的左心室受累多见而严重,左心室间质纤维化突出,心肌细胞肥大明显,但脂肪替代少见和局限.左、右心室多扩张,可见附壁血栓,应注意与扩张型心肌病等鉴别.     

Weights of the body and cardiac ventricles in pulmonary emphysema

Summary We analysed statistically the association of emphysema, determined on inflation fixed specimens, with the weights of the body and heart, and of the cardiac ventricles, weighed separately, in 170 male and 86 female adult autopsies. The cases were grouped according to the cause of death into cardiovascular, cancer and other deaths. In men the body weight was inversely proportional to the severity of emphysema, but no association existed between the body weight and the cause of death. In male cardiovascular deaths the total heart weight, total ventricular weight and the weight of the left ventricle with the septum were also inversely proportional to the severity of emphysema while this was not true in the other deaths. In male cardiovascular deaths a decrease, and in the other deaths an increase, of the weight of the free wall of the right ventricle was associated with an increasing severity of emphysema. In all male deaths, however, the left to right ratio decreased with an increasing severity of emphysema. Thus, pulmonary emphysema is associated both with a general atrophy, including the myocardium, and a mainly relative right ventricular hypertrophy. An absolute right ventricular hypertrophy, however, seems to accompany emphysema only in the absence of other major cardiovascular diseases.     

Functional and stereologic estimations of myocardial capillary exchange capacity in treated and untreated spontaneously hypertensive rats.

Myocardial capillary exchange capacity was investigated by stereologic and functional techniques in parallel during pressure-overload cardiac hypertrophy and after long-term antihypertensive therapy with the vasodilator felodipine. In 26-week-old female spontaneously hypertensive rats (SHR) blood pressure increased by 25% and left ventricular weight (LVW/BW) increased by 18% compared to Wistar-Kyoto rats (WKY). Myocardial capillary surface and volume densities normalized for organ weight were similar in both ventricles for both strains. Moreover, capillary surface density was higher sub-epicardially (EPI) than in the subendocardium (ENDO) in the left ventricle of SHR. Thirteen weeks of felodipine-therapy (SHR-Felo) normalized blood pressure without affecting LVW/BW although a transition from concentric to eccentric hypertrophy is known to occur. Myocardial capillary surface and volume densities and the left ventricular ENDO-EPI-gradient in surface density were similar to untreated SHR. However, felodipine-treatment increased right ventricular weight and capillary volume density. Functional capillary exchange was estimated in terms of permeability surface area products (PS) for Cr-EDTA and vitamin B12 and normalized for organ weight. PSCr-EDTA, PSB12 and the ratio PSCr-EDTA/PSB12 (an index of capillary permeability) were similar in SHR and WKY. Furthermore, the relation between functional and stereological indices of exchange capacity was investigated in a multiple linear regression analysis. However, no significant correlation between PS and neither capillary surface nor volume density was found. In conclusion, myocardial capillary exchange capacity was well adapted to the pressure overload cardiac hypertrophy present in female SHR. Despite induction of right ventricular hypertrophy, felodipine-treatment did not affect capillary exchange capacity. Furthermore, when functional and stereologic estimates were performed in parallel, the importance of dynamic factors for myocardial capillary exchange capacity (e.g. heterogeneity) was illustrated.     

Muscle Fiber Orientation in the Development and Regression of Right Ventricular Hypertrophy in Pigs

The development and regression of right ventricular hypertrophy was investigated in 12 pigs with special reference to changes in ventricular function and myocardial fiber orientation. Nine ventricles were pressure -loaded by banding the pulmonary artery for 28–81 days, and four of them were then released from the load by removing the band. Right ventricular systolic pressure (RVSP), end-diastolic pressure (RVEDP) and end systolic volume index (ESVI) increased significantly during banding and decreased after debanding. End diastolic volume index (EDVI) and stroke volume index (SVI) showed no significant change during banding and after debanding. The weight of the right ventricle relative to both ventricles (RV/TV) and the thickness of muscle fibers were increased significantly in the loaded ventricles, and reduced again to the control level in ventricles released from the load. The intramyocardial distribution of angles ( θ ) of inclination of muscle fibers from the transverse plane of the outflow tract was estimated histometrically. There was a significantly larger proportion of circularly oriented fibers (|θ|≦30) in the pressure loaded ventricles than in the control, whereas these fibers decreased again to the control level after removal of the pressure load. The present findings indicates that 1) the right ventricular hypertrophy induced by pressure loading is characterized not only by an increase in ventricular weight and muscle fiber thickness, but also by a change in intramyocardial fiber orientation, and 2) the hypertrophic right ventricle can regress both functionally and morphologically to a normal state after removal of the pressure load.     

Muscle fiber orientation in the development and regression of right ventricular hypertrophy in pigs

The development and regression of right ventricular hypertrophy was investigated in 12 pigs with special reference to changes in ventricular function and myocardial fiber orientation. Nine ventricles were pressure-loaded by banding the pulmonary artery for 28-81 days, and four of them were then released from the load by removing the band. Right ventricular systolic pressure (RVSP), end-diastolic pressure (RVEDP) and end-systolic volume index (ESVI) increased significantly during banding and decreased after debanding. End-diastolic volume index (EDVI) and stroke volume index (SVI) showed no significant change during banding and after debanding. The weight of the right ventricle relative to both ventricles (RV/TV) and the thickness of muscle fibers were increased significantly in the loaded ventricles, and reduced again to the control level in ventricles released from the load. The intramyocardial distribution of angles (theta) of inclination of muscle fibers from the transverse plane of the outflow tract was estimated histometrically. There was a significantly larger proporation of circularly oriented fibers (magnitue of theta less than or equal to 30 degrees) in the pressure-loaded ventricles than in the control, whereas these fibers decreased again to the control level after removal of the pressure load. The present findings indicates that 1) the right ventricular hypertrophy induced by pressure loading is characterized not only by an increase in ventricular weight and muscle fiber thickness, but also by a change in intramyocardial fiber orientation, and 2) the hypertrophic right ventricle can regress both functionally and morphologically to a normal state after removal of the pressure load.