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At least 19 recordsLinked to original sources

Hypertrophy and reversal of hypertrophy in rat pelvic ganglion neurons.

An experimental procedure which chronically reduces the lumen of the urethra in adult female rats produced distension of the bladder and conspicuous thickening of its wall, resulting within 6-8 weeks in a ten-fold increase in muscle weight (muscle hypertrophy). During this process, the neurons in the pelvic ganglion that innervate the bladder undergo a large increase in size (neuronal hypertrophy). The average neuronal volume increased by 83%; small neurons became less numerous and large neurons became more numerous than in controls, but there was no increase in the maximum neuronal size. Six weeks after re-operation and removal of the urethral obstruction, the weight of the bladder was reduced (although not quite to the control levels), while the average neuronal size reversed to values very close to controls. In separate experiments, the pelvic ganglion of one side was removed. The nerve fibres in the hemidenervated bladder sprouted, grew and spread to innervate the whole bladder. The neurons in the surviving pelvic ganglion hypertrophied, the average cell volume increasing by 50% in seven weeks. The experiments showed that: (i) the pelvic neurons of adult rats are capable of very extensive growth when the tissue they innervate (bladder muscle) undergoes hypertrophy; (ii) the neuronal hypertrophy is reversible. This was taken to imply that there are factors within the bladder, including trophic substances, that regulate nerve cell volume not only by inducing growth but also by inducing the opposite effect, a cell size reduction; (iii) unilateral ganglionectomy, which did not induce muscle hypertrophy but doubled the amount of muscle innervated by the contralateral ganglion, was followed by marked neuronal hypertrophy.

Animals

Quantitative analysis of muscle cell changes in compensatory hypertrophy and work-induced hypertrophy.

The cytological characteristics of two modes of muscle hypertrophy were studied in the extensor digitorum longus muscle of the rat. Comprensatory hypertrophy (CH) was produced by tenotomy of the tibialis anterior muscle and work-induced hypertrophy (WIH) was produced by forced swimming of the animal. While both methods produced an increase in muscle weight and cell size, these two parameters did not correlate. Morphometric analyses of the hypertrophied muscle cells demonstrated that in CH-muscle there was an increase in mitochondrial volume density, a decrease in myofibrillar volume density and no change in sarcotubular or nuclear volume density. WIH-muscle demonstrated an increase in sarcotubular volume density but no change in mitochondrial, myofibrillar or nuclear volume density. It is concluded that in CH-muscle, the cell volume increase is attributable to mitochondrial volume increase and that there is no increase in the contratile myofibrillar component of the cell. WIH-muscle, on the other hand, has a cell volume increase which is attributable to a proportional increase in these organelles.

Animals

Effect of captopril on the prevention and regression of myocardial cell hypertrophy and interstitial fibrosis in pressure overload cardiac hypertrophy.

This article reports on the effects of captopril on both the prevention and the regression of myocardial cell hypertrophy and interstitial fibrosis in experimental animals (rats) with pressure overloaded hearts. Constriction of the abdominal aorta just below the diaphragm during periods of 20 days (prevention experiment) and 40 days (regression experiment) resulted in hypertension and cardiac hypertrophy. In the prevention experiment, captopril was able to inhibit the development of high blood pressure levels and cardiac hypertrophy in aortic-constricted rats. Similarly, the treatment of sham-operated rats with captopril led to a reduction in the weight of the heart and in the myocyte diameter compared with controls. The myocyte volume fraction of the left ventricles of both aortic-constricted and sham-operated animals that were treated with captopril was significantly diminished compared with that of the control group. The interstitial collagen volume fraction of all experimental groups was elevated as compared with the control group. As a consequence, the ratios of myocytes to interstitial collagen in groups of aortic-constricted rats, aortic-constricted rats that were treated with captopril, and sham-operated rats that were treated with captopril were reduced compared with the control group; that is, although captopril was able to prevent myocardial cell hypertrophy after aortic constriction, it could not prevent the maintenance of a normal ratio of myocytes to interstitial collagen, which was due to increased collagen volume fraction. In the regression experiment, captopril lowered high blood pressure levels and augmented heart weights to control values. The mean myocyte transverse diameter in aortic-constricted rats that were treated with captopril was significantly smaller than that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

The diffuse hypertrophy of the lower esophagus and the focal hypertrophy of the pyloric musculature in adults.

The diffuse hypertrophy of the lower esophagus is a hypertrophy and hyperplasia of the smooth muscle fibres of the M. propria, together with a distortion of the muscular architecture. The esophagogram reveals an impaired peristalsis and expansile ability of the esophagus lumen. The focal hypertrophy of the pyloric musculature in adults is a locally circumscribed hypertrophy and hyperplasia of the M. propria. The concentric pattern of the M. propria is no longer maintained. Radiologically one recognizes a benign pylorus stenosis with a complete systole and an impaired diastolic dilatation. On the basis of these macroscopical, microscopical and radiological findings both lesions differ from the circular pyloric or esophageal stenosis which occurs at the same anatomical sites. We therefore feel, that both lesions are different entities.

Adult

[Ulcer location in the stomach and pylorantral hypertrophy: problem of correlation of the ulcer location and wall hypertrophy in ulcus ventriculi].

Relationship between gastric ulcer (n = 100) site and antropyloric wall hypertrophy was examined in a prospective study. Irrespective of ulcer multiplicity most ulcers were found to be located at the lesser curvature and at the posterior wall (p less than 0,001); men had significantly more ulcers at the posterior wall than females (p less than 0, 001). Single ulcers and those connected with pyloric stenosis were more distant to the pylorus than multiple ulcers (p less than 0,001). Ulcer location did not relate to hypertrophy of the pyloric channel wall. Observed differences between single and multiple ulcers were limited to wall parts only: the musculature of high located single ulcers was significantly less hypertrophied 2,5 cm orally of the pylorus (p less than 0,02) and that of high multiple ulcers was more hypertrophied at the pylorus (p less than 0,02) than in the other parts. These findings suggest that ulcer variations do not influence the diffuse antropyloric disease in gastric ulcer patients and suggest that the generalized antral changes are prior to gastric ulcer occurance.

Female

Different fractions in the normal and hypertrophied rat ventricular myocardium: an analysis of two models of hypertrophy.

Long-term hemodynamic overload of the heart leads to an increase in myocardial mass. In most cases it is not known to what degree the single components in the myocardium (water, protein, nonprotein substance) increase. As an answer to the overloading of the myocardium, many authors have established an intensification in the synthesis of myocardial proteins. It is, however, little known which proteins are then more intensively created and accumulated. This study examines the dynamics of the protein and nonprotein content as well as of single protein fractions (sarcoplasmic, myofibrillar, and stromal) in both hypertrophied and normal tissue from rat myocardia. The results revealed that in Goldblatt rats, 4-24 weeks after stenosis of one renal artery, no noteworthy differences in the relationships of protein and nonprotein content were caused by hypertrophy (34-54%) due to left ventricular pressure overload. The same is true of the tissue from moderately hypertrophied myocardia (12-17%) of rats exercised for several weeks by swimming training. Determination of hydroxyproline concentration showed that significant differences in the content of the collagen tissue in relation to control animals of the same age occurred only in Goldblatt rats 24 weels after operation. However, greater alterations in the concentrations of various protein fractions could be registered. The increase in the concentration of myofibrillar proteins in hypertrophied myocardial tissue is of particular significance and is to be considered as an adaption of the muscle to the increased mechanical demands. Certain changes regarding the relation of the single components within the myofibrillar fraction (relation of actomyosin concentration to T-fraction; relation of both components to total fraction), whose cause and significance is as yet unclear, could be observed.

Animals

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.

Anemia

[Hypertrophy or hyperplasia of myocytes in heart hypertrophy?].

One of the most controversial problem in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia there occurs proliferation of the myocyte. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention it has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p < 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. From these parameters only coronary artery diameters significantly influenced on LV weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly

Renal hypertrophy in experimental diabetes: a comparison to compensatory hypertrophy.

The kidney growth seen after the induction of experimental diabetes in rats has been compared to the compensatory renal growth after one-sided nephrectomy. After five days the kidney weight had increased from 650 +/- 15 mg in a group of controls to 778 +/- 21 mg in diabetic rats, and 764 +/- 17 mg in unilaterally nephrectomised rats. The increased weight was in both groups reflected in an increased DNA content and increased RNA/DNA and protein/DNA ratios. In a group of rats made diabetic and nephrectomised at the same time, kidney weight increased to 953 +/- 22 mg after five days. When rats were unilaterally nephrectomised after 20 days of untreated diabetes, compensatory growth was much more pronounced than in non-diabetic rats, kidney weight rising from 780 +/- 21 to 1144 +/- 39 mg in five days. Similarly, in rats with established compensatory renal hypertrophy, diabetes induced a very rapid growth of the remaining kidney (1226 +/- 46 mg after five days).

Animals

Cardiac hypertrophy due to physical exercise--an example of hypertrophy without decrease of contractility: unreliability of conventional estimation of contractility by simple parameters.

In 100 young, male Sprague-Dawley rats, a long term swimming training (2 hr/day for 8-12 weeks) produced an increase in heart weight of 10 percent, and an increase of about 15 percent in the relation of heart weight to body weight compared with control rats of the same age and initial weight. In examinations of the mechanical properties of the whole ventricle as well as of trabecular preparations, there was no evidence of impaired myocardial contractile ability because of the swimming training. Some parameters for the estimation of "contractility" increased, whereas others decreased. At a muscle length near lmax, the developed force and the maximal rate of force development were slightly augmented. The results reveal the limited value of some indices of contractility. Alterations in the shape of the contraction curve must to be considered adequately in order to avoid misinterpretations.

Animals