Morphometry of right ventricular hypertrophy induced by strenuous exercise in rat

Effects on the myocardium, particularly those structural properties of the capillary network relevant to tissue oxygenation, were studied morphometrically in rats subjected to a severe running program. Physical conditioning produced a 31% increase in right ventricular weight and only a 12% increase in the weight of the left ventricle. Quantitative analysis of right ventricular myocardium demonstrated relative decreases in capillary luminal volume density (-27%) and capillary luminal surface density (-20%) and an increase in the average maximum distance from the capillary wall to the mitochondria of myocytes (14%). In contrast, the contractile mass expanded in proportion to the growth of the ventricle through augmentation of the cross-sectional area (17%) and length (19%) of the average myocyte. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria-to-myofibril volume ratio. In conclusion, the capillary bed controlling oxygen availability, diffusion, and transport suggests that excessive physical activity may be detrimental to the myocardium.     

Morphometry of right and left ventricular myocardium after strenuous exercise in preconditioned rats

Young male rats were exposed to a biphasic training program in which a 7-week preconditioning period of moderate treadmill exercise was followed by 8 weeks of strenuous endurance running. In comparison with sedentary control animals, the trained rats at 20 weeks of age had developed myocardial hypertrophy of the right ventricle (20%) and interventricular septum (23%), but there was no difference in the weight of the left ventricular free wall. Myocyte hypertrophy (26%) in the right ventricle was achieved through an increase in mean cell length (24%) and the addition of new sarcomere units in series. Exercise induced no acceleration of capillary growth in either ventricle, leading to significant decreases in the capillary luminal volume density (-21%) and surface density (-16%) in the right ventricle. Such alterations in the structural properties of the microvasculature implicated in oxygen availability and diffusion suggest that vigorous exercise, even after a preconditioning period, may still be detrimental to the myocardium. The techniques of myocardial morphometry were examined with respect to potential errors associated with oblique tissue sections and the use of light versus electron microscopy for cell counting. It was shown that the practical effects of obliquity are negligible and that electron microscopic resolution is essential.     

Morphometric analysis of the infarcted heart

To determine whether left ventricular hypertrophy following myocardial infarction leads to a complete or incomplete reconstitution of myocardial mass, the left coronary artery in rats was ligated and the animals sacrificed 30 days later. Infarcts affecting an average 43% of the ventricle were characterized by a 90% hypertrophic growth of the remaining myocardium that was inadequate for a full restoration of ventricular tissue. Myocyte hypertrophy, evaluated by changes in mean cell volume per nucleus, was again insufficient for a total recovery of the myocyte compartment of the ventricle. These observations suggest that infarcts comprising nearly 50% of the ventricle produce a sufficiently large stress on the spared myocytes to stimulate their maximal hypertrophic reserve capacity. Cardiac muscle cells, however, appear to be unable to offset by cellular hypertrophy alone the loss of mass induced by infarcts of this size. The inadequate compensatory response of the myocytes could be the underlying structural mechanism responsible for impaired ventricular function in large infarcts.     

Adaptative modifications of right coronary myocytes voltage-gated K+ currents in rat with hypoxic pulmonary hypertension

Chronic hypoxia (CH)-induced pulmonary hypertension (PHT) is well known to alter K+ channels in pulmonary myocytes. PHT induces right ventricle hypertrophy that increases oxygen demand; however, coronary blood flow and K+ channel adaptations of coronary myocytes during PHT remain unknown. We determined whether CH and PHT altered K+ currents and coronary reactivity and what impact they might have on right myocardial perfusion. Right ventricle perfusion, as attested by microspheres, was redistributed toward hypertrophied right ventricle [RV/LV (%)=0.59+/-0.07% in CH rats vs. 0.29+/-0.03 in control rats, P<0.05]. Whole-cell patch clamping showed a reduction of global outward current in hypoxic right coronary artery myocytes (H-RCA), whereas hypoxic left coronary artery myocytes exhibited an increase. K+ channel blockers revealed that a 4-aminopyridine (4AP)-sensitive current (Kv current) was decreased in H-RCA (14.3+/-1.1 vs. 23.4+/-2.5 pA/pF at 60 mV in control RCA, P<0.05) and increased in hypoxic left coronary artery myocytes (H-LCA; 26.4+/-3.8 vs. 11.8+/-1.6 pA/pF at 60 mV in control LCA, P<0.05). Constriction to 4AP was decreased in H-RCA when compared to normoxic control and increased in H-LCA when compared to LCA. Finally, we observed that the expression of Kv1.2 and Kv1.5 were lower in H-RCA than that in H-LCA. This study reveals that CH differentially regulates Kv channels in coronary myocytes. Hypoxia decreases Kv currents and therefore reduces vasoreactivity that contributes to an adaptative response leading to right hypertrophied ventricle perfusion enhancement at rest.     

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.     

Myocardial response to infarction in the rat. Morphometric measurement of infarct size and myocyte cellular hypertrophy.

For determination of the effects of myocardial infarction on the recovery potential of muscle mass in the surviving tissue, ligation of the left coronary artery was performed in 3-month-old rats, and the infarcted ventricles were analyzed morphometrically a month after surgery. Comparisons were made with 4-month-old control rats that underwent sham operations and with 3-month-old control rats that were not operated upon for evaluation of the magnitude of infarct size and discrimination of the relative contribution of tissue growth that occurred in the surviving myocardium solely as a result of the change in age, from 3 to 4 months (postoperative tissue growth, or POTG), from the additional growth induced by infarction (hypertrophic growth, or HG). Coronary occlusion induced a 276-cu mm loss of ventricular tissue volume that corresponded to 43% of the total left ventricular mass, 648 cu mm. Over a 30-day period the remaining 372 cu mm of viable tissue expanded by 90% with an overall volume gain of 334 cu mm. This tissue augmentation consisted of 20% POTG, 67 cu mm, and 80% HG, 267 cu mm. Total myocyte volume increased 89%, from 302 cu mm to 571 cu mm, and average myocyte cell volume per nucleus increased 92%, from 16,500 cu mu to 31,600 cu mu. The expansion of the myocyte mass was the result of a 21% POTG and a 79% HG. Corresponding values for the myocyte population were 19% and 81%.     

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.     

Anatomy and vasculature of a minke whale heart

The heart from a 4-m-long minke whale (Balaenoptera acutorostrata) was studied to determine the details of its anatomy and to consider cardiac adaptations to diving. The volume fraction (Vvc) of capillaries in the wall of the left ventricle was determined at different levels from base to apex and at different depths from epi- to endocardium using a light microscopic stereologic technique. Typical of cetaceans, this minke whale heart was distinctly flattened dorsoventrally. A moderator band, characteristic of ungulate hearts, spanned the right ventricle. The right and left atrioventricular valves were tricuspid and bicuspid, respectively. The right coronary artery supplied the dorsal and right lateral myocardium. The left coronary artery supplied the ventral and left lateral myocardium. An anastomosis between the dorsal and ventral interventricular arteries occurred in the dorsal interventricular groove. Stereologically, a decreasing transmural gradient in Vvc was identified between the epicardium and the subepicardium at 15 cm from the apex. Our results, however, did not reveal any significant deviations in the pattern of capillary distribution in the wall of the left ventricle between this baleen whale and terrestrial mammals. Measurements of the heart, great vessels, coronary vasculature, and ventricular walls are also given, and they suggest a physiologic and adaptive right ventricular hypertrophy. Based on these and other observations, we propose that the relatively great thickness of the right ventricle and the distinctive shape of the cetacean heart are adaptations to the hemodynamic changes and collapse of the thorax associated with apneic diving.     

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. PS_cr-EDTA, PS_B12 and the ratio PS_cr-EDTA/PS_B12 (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.     

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. I. Determination of myocyte size.

A method for determining the mean absolute volume of a specific population of cells within a tissue is described and applied to the measurement of endocardial and epicardial myocytes in the left ventricle of normal and hypertensive rats. The technique, based on nuclear counts per unit area in tissue slices of different known thicknesses, measures the mean cell volume per nucleus independent of previously unknown nuclear dimensions and systematic counting errors. Duplicate determinations, demonstrating reproducibility, were made in mutually perpendicular longitudinal and transverse sections of the myocardium. Combining these light microscopic measurements with electron microscopic data enabled the evaluation of the mean diameter and length of the cylindrical myocyte nuclei showing those in the epicardial cells to be significantly longer than the nuclei in endocardial cells. It was estimated that 2 to 4 per cent of ventricular myocytes are binucleate. After 1 to 4 weeks of hypertension, induced by constriction of the left renal artery, endocardial myocytes were enlarged 21 per cent, from 10,370 +/- 410 to 12,520 +/- 490 cu. micrometer., while epicardial myocytes showed a 37 per cent hypertrophy, from 12,600 +/- 1,600 to 17,300 +/- 1,100 cu. micrometer. The availability of a reliable determination of cell volume will make possible the interpretation of much biochemical, functional, and morphometric data at the whole cell level.     

Myocardial capillary density and muscle fibre size in rats born and raised at simulated high altitude.

Rats were born in a hypobaric chamber at a pressure of 500 mmHg and kept there at 460 mmHg for 5, 9 or 13 weeks. The myocardial capillary bed was labelled by perfusion with India ink. The density of myocardial capillaries and the area of cross-section of myofibres was estimated from histological sections. In the left ventricle there was a steady reduction in capillary density with increasing age which was similar in test and control rats. There was also an increase in myofibre size which was similar in test and controls. Hypoxia therefore failed to induce capillary proliferation or a reduction in myofibre diameter in the left ventricle and this is reflected in a constant capillary:fibre ratio. In the right ventricle, ventricular hypertrophy in the hypoxic rats induced a striking reduction in capillary density due to a two-fold increase in myofibre size. There was nevertheless some degree of capillary proliferation, probably a consequence of hypertrophy rather than the direct influence of hypoxia.     

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. II. Ultrastructure of myocytes and interstitium.

The left ventricular myocardium of normal and hypertensive rats has been characterized morphometrically in the endocardial and epicardial zones. Compared to the epicardial regions, the normal endocardial regions contain 30 per cent more myocytes, 27 per cent less interstitial space, 48 per cent less capillary volume, 17 per cent less capillary surface, and the same capillary length per unit tissue volume. In terms of both the relative and absolute volumes and surface areas of their organelles, the cytoplasmic composition of normal endocardial and epicardial myocytes is nearly identical. After 14 weeks of hypertension, induced by constriction of the left renal artery, left ventricular weight is increased by 30 per cent, wall thickness by 42 per cent. The number of myocytes and the total length of capillaries remain constant. The epicardial region enlarged 37 per cent with proportional increases of myocyte and interstitial volumes. In contrast, the endocardial enlargement was only 26 per cent, comprised of 21 per cent hypertrophy of myocytes and a 55 per cent increase in interstitial components. Expansion of capillary lumina accounted for much of the interstitial enlargement throughout the myocardium. Hypertrophy of myocytes is 76 per cent greater in the epicardial region and is accompanied by a reduced mitochondria to myofibril ratio and disproportionately large increases (2- to 3-fold) in both smooth endoplasmic reticulum and T-system volume and surface area. On a cellular basis the absolute morphometric characteristics of myocytes from hypertensive rats are significantly different from normal, and significant differences occur between the inner and outer layers of the myocardium for practically every cytoplasmic component.     

Structural adaptation of the rat left ventricle in response to changes in pressure and volume loads

Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were used to explore the structural changes of cardiac dimensions in connection with a sustained hyperkinetic circulation, as induced by pregnancy or thyroxine administration. Cardiac design was assessed by recordings of the diastolic left ventricular pressure-volume relationships in isolated arrested hearts. Left ventricular weight: body weight and end-diastolic volume (EDV) for given end-diastolic pressures (EDP), were both increased about 50% in control SHR, with a marginal reduction of the wall:lumen ratio (w:ri) compared with control WKY. During the hyperkinetic circulatory states of pregnancy and hyperthyroidism, EDV was in WKY increased about 30% and 50%, respectively, with concomitant w:ri reductions. In SHR pregnancy did not significantly alter left ventricular dimensions, whereas EDV was increased by about 20% in hyperthyroid SHR. Thus, the rat left ventricle can, within 3 weeks, markedly alter not only the wall mass but also, and independently, the luminal design in response to different haemodynamic interventions. Early established SHR hypertension is characterized mainly by eccentric left ventricular hypertrophy, despite the elevated arterial pressure. Volume overloads in WKY due to pregnancy or hyperthyroidism can induce marked structural widening of the left ventricle. In SHR these structural luminal changes were only minor, perhaps because considerable eccentric hypertrophy is already present. Such a structural cardiac enlargement may allow delivery of an increased stroke volume for a given myocardial fibre shortening.     

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.     

Methodische Untersuchungen zur polarographischen Messung der Atmung und des „kritischen Sauerstoffdrucks” bei Mitochondrien und isolierten Zellen mit der membranbedeckten Platinelektrode

Summary In growing rats adapted to a simulated altitude of 3500 m for about 4 weeks and in their controls the evolution of cardiac ventricular weight was followed. The increase of total ventricular weight found in the adapted animals can be attributed exclusively to the increase of right ventricular weight. In other adapted and control animals cardiac capillary densities, muscle fiber diameter and external capillary radius were estimated and fiber—capillary ratio and diffusion distance were calculated. There was an increase of capillary density together with a decrease of muscle fiber density, fiber-capillary ratio and diffusion distance in the right but not in the left ventricle of the adapted rats. The muscle fiber diameters, however, were larger in both heart ventricles of the rats exposed to a simulated high altitude, especially in the right ventricle. This indicates that true hypertrophy of the muscle fibers is mainly responsible for the increase of right ventricular weight. In the left ventricle, however, a hypertrophy of the muscle fibers together with a decrease of stroma components is demonstrated. The physiological importance of the shorter diffusion distance in the right ventricle of the high altitude adapted rats is discussed and it is suggested that the shorter diffusion distance may help to keep the tissue O₂ partial pressure above the critical value, mainly also in extreme situations with high myocardial O₂ consumption.     

Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts

Data are reported which show significant regional capillary differences in left ventricular endocardium and epicardium of normal rats and of rats with hyperthyroid-induced cardiac hypertrophy. The epicardial region of control rats has 38% more capillaries than the endocardial region. Control endocardial myocytes are 62% larger in cross-sectional area than epicardial myocytes. Hypertrophic hearts exhibit regional differences in capillary density similar to those in the normal hearts, but there is an overall reduction of 12 and 17.5% in capillary density in both regions. The average cross-sectional area of myocytes increases 34.5% in the epicardium and 22.5% in the endocardium.     

Proliferation of myocytes of the left atrium and ventricle after various types of myocardial injury in adult rats

An infarct of the myocardium of the left ventricle was produced in adult rats weighing 120–160 g by ligating the left coronary artery at different levels: in the atrial region, at the level of the first third of the left ventricle, and in its middle. In other series of experiments the left atrium was damaged by applying a ligature to its anterior wall or to the auricle. Animals undergoing a mock operation during which the pericardium was removed acted as the control. The left half of the heart was investigated on the 5th day after the operation. Mitotically dividing myocytes were found in the atrium or auricle of the animals in those series of experiments in which these parts of the heart had been directly injured and had a thickened epicardium (in 35 of 49 cases); the mitotic index varied from 0.9 to 10%. After litigation of the coronary artery in the middle of the ventricle mitoses were not found in the myocytes of the atrium and auricle. In all series of experiments mitoses were rare in the myocytes of the ventricle (in seven of 49 cases) and were located at a distance from the infarct, in subepicardial zone; the mitotic index there varied from 1 to 2%.Laboratory of Growth and Development, Institute of Human Morphology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. P. Avtsyn.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 8, pp. 998–1002, August, 1976.     

Anatomical study of a left single coronary artery with special reference to the various distribution patterns of bilateral coronary arteries

A left single coronary artery of heart was observed during anatomy practice at Kumamoto University School of Medicine in a 73-year-old female cadaver who died from a thalamic hemorrhage. The left single coronary artery, having a single orifice in the left aortic sinus, bifurcated into the anterior interventricular (IVa) and circumflex (CIR) arteries. No orifice of the right coronary artery was found on the aortic wall. Giving off a branch which traversed the upper part of the infundibulum to supply the anterior upper region of the right ventricle, the IVa descended in the anterior interventricular sulcus to supply the apex of the heart. The CIR curved leftwards in the atrioventricular sulcus to reach the posterior surface, after which it continued to emerge again into the anterior surface. The atrial arteries showed no anomalous distribution pattern and histological observation revealed no pathological abnormality other than a slightly thickened tunica intima. Furthermore, we observed the distribution patterns of bilateral coronary arteries in 377 hearts dissected during anatomical practice over 13 years at Kanazawa University (1980–1986) and Kumamoto University (1993–1998). Although the reason why only the right coronary artery was absent is left unexplained, it was concluded that the left single coronary artery in this study, having the developed left conal and circumflex branches, was an extreme case of the left dominant series of coronary arteries. The formation of single coronary arteries can be explained embryologically by the change of flow in the capillary plexus established on the ventricle wall.     

Regional changes in myocyte size and number in propranolol-treated hyperthyroid rats

The effects of beta-adrenergic blockade and hyperthyroidism on cardiac myocyte structure was examined. Isolated myocytes were prepared from controls and rats treated for 10 weeks with desiccated thyroid hormone (T), propranolol, and desiccated thyroid hormone plus propranolol (TP). Cells were collected from the right and left ventricle. Cell volume was measured with a Coulter Channelyzer system. Cell length was measured directly using a phase microscope. Myocyte cross-sectional area was calculated from cell volume/length. In addition, hearts from animals in each group were perfusion-fixed and myocyte volume percent was determined morphometrically from tissue sections. The number of right and left ventricular myocytes was calculated using data from isolated cells and whole-sectioned tissue. Propranolol normalized heart rate in hyperthyroid rats. Heart weight to body weight ratios were elevated to a similar extent in both T and TP groups. Compared with controls, myocyte volume was increased (p less than 0.01) in each region of T and TP. Right ventricles had a greater degree of myocyte hypertrophy than left ventricles in both rat groups treated with thyroid hormones. Cell length was increased (p less than 0.01) in T and TP. Most of the myocyte hypertrophy, however, was due to an increase in cross-sectional area. Although volume was unchanged with propranolol treatment alone, myocytes from each region had an increase in length (p less than 0.01) and a reduction in cross-sectional area (N.S.). Myocyte number was slightly reduced in each treatment group, but changes were not statistically significant. In conclusion, thyroid hormones stimulate myocyte hypertrophy by increasing both length and cross-sectional area. Propranolol modifies myocyte dimensions in both euthyroid and hyperthyroid rats, but does not prevent thyroid hormone induced cardiac hypertrophy.     

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。