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K Rakusan

Publications and source records attributed to K Rakusan.

At least 73 records · Page 4Linked to original sources

Myocardial capillary flow pattern as determined by the method of coloured microspheres.

In summary, it can be said that in spite of possible limitations, this technique provides previously unattainable data on capillary flow pattern in the myocardium. Qualitative and quantitative results indicate that the following anatomical and physiological concepts should be incorporated in any further modelling of oxygen transport to myocardium: (1) Concurrent flow pattern (2) Presence of short capillary loops (3) Presence of capillary bundles (4) Staggered arrangements of arteriolar inflow to capillary network.

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Aortic stenosis produces hypertrophy of the rat heart without causing an accumulation of N1-acetylspermidine.

Isoprenaline treatment causes cardiac hypertrophy and an accumulation of N1-acetylspermidine in the rat heart. To determine whether the cardiac hypertrophy is the cause of the increase in N1-acetylspermidine, we produced cardiac hypertrophy by constriction of the aorta and analyzed polyamines in the hearts of these rats 1, 3, and 10 days after the aortic constriction. Our results show that compared to sham-operated animals, this treatment caused a 60% increase in putrescine and a 30% increase in spermidine by day 10, but not the expected increase in N1-acetylspermidine. We conclude that N1-acetylspermidine is not induced by a cardiac overload.

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Improved myocardial capillarisation in spontaneously hypertensive rats treated with nifedipine.

The effect of long term administration of nifedipine on myocardial capillarity was studied in spontaneously hypertensive rats. Nifedipine was given for 20 weeks, mixed into commercial rat chow (0.3 g per 1 kg). Untreated spontaneously hypertensive rats had higher arterial blood pressure and developed cardiomegaly when compared with Wistar-Kyoto rats used as controls. Nifedipine administration in spontaneously hypertensive rats lowered the arterial blood pressure and reduced cardiac weight; however, both values remained far above those for controls. Myocardial capillarity was determined using the recently introduced method of capillary domains. Hearts from untreated spontaneously hypertensive rats were characterised by greater and more variable intercapillary spacing than those from controls. The treatment of spontaneously hypertensive rats with nifedipine resulted in normalisation of morphometric indices characterising capillary spacing, probably as a result of stimulation of capillary growth as indicated by a significant decrease in myocyte to capillary ratio. Thus, despite persistent hypertension and cardiomegaly the treatment of spontaneously hypertensive rats with nifedipine restored mean intercapillary distance and index of heterogeneity of capillary spacing to normal values.

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Effects of chronic exercise on the coronary circulation in conscious rats with renovascular hypertension.

Since various studies suggest that chronic physical conditioning promotes myocardial vascularity, we investigated whether it could prevent the coronary reserve abnormalities of hypertensive cardiac hypertrophy. One week after operation, female Sprague-Dawley rats with two-kidney, one clip Goldblatt hypertension were either subjected to a moderate exercise program by swimming (n = 21) or kept sedentary (n = 16) for 9 weeks. Sedentary (n = 16) and exercised (n = 15) sham-operated rats served as controls. Maximal coronary blood flow and minimal coronary resistance, either per unit mass or for the entire left ventricle, an index of the functional cross-sectional area of the coronary resistance vessels, were determined in conscious, unrestrained rats by left atrial microsphere injection following maximal vasodilation with carbochrome (12 mg/kg). Following exercise, left ventricular mass was moderately (+5-10%) but significantly increased in normotensive rats, whereas left ventricular hypertrophy was significantly accentuated in the hypertensive rats. Minimal coronary resistance for the entire left ventricle was significantly decreased (-24%) in normotensive rats but did not change significantly in hypertensive rats. Minimal coronary resistance per unit mass (the coronary vasodilator reserve) tended to decrease in normotensive rats (-17%), whereas it tended to be further augmented in hypertensive rats (+13%). However, these differences were marginally significant and were not associated with any changes in maximal coronary blood flow per unit mass (the coronary flow reserve). Thus, in normal rats, exercise promoted myocardial arterial vascularity in parallel with the development of cardiac hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Failure of swimming exercise to improve capillarization in cardiac hypertrophy of renal hypertensive rats.

Female Sprague-Dawley rats were made hypertensive by the two kidney/one clip Goldblatt procedure, while control animals were sham-operated. One week later, half of the animals were subjected to a moderate swimming exercise and the other half remained sedentary. Thus, four experimental groups, each consisting of 14 rats, were formed: control animals that were exercised or kept sedentary and corresponding renal hypertensive animals either exercised or sedentary. In hypertensive rats, a significantly increased left ventricular weight and reduced coronary reserve were found. Cardiac hypertrophy in hypertensive rats was characterized by a lower number of capillaries on a tissue cross-section, larger heterogeneity of the capillary net, and a less uniform orientation of capillaries in space. Total length of capillaries in the hypertrophic hearts increased significantly, but less than the increase in cardiac weight, resulting in reduced capillary length density. Chronic swimming for 2 hr/day for a period of 6 weeks, subsequent to a 4-week acclimation period, did not significantly influence any of the investigated indexes of capillaries from hypertrophic hearts. In the normotensive rats, chronic swimming resulted only in a moderate increase in total capillary length associated with a small increase in the left ventricular weight of similar degree. Thus, chronic exercise in normotensive rats induced a moderate increase in total capillary length per left ventricle, while it did not alleviate impaired capillarization of hypertrophic hearts from hypertensive rats.

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Distribution of mitochondria in normal and hypertrophic myocytes from the rat heart.

The spatial distribution of mitochondria in myocytes from two regions of normal hearts and hearts hypertrophied due to renal hypertension was analyzed. First, the cross-sectional area of myocytes on electron micrographs was divided into two approximately equal portions with respect to the closest capillary wall. Volume density of mitochondria was then determined in both portions by the point counting method. Similarly, the cross-section of myocytes was divided into approximately equal parts with respect to the cell surface and evaluated as above. Analysis of variance revealed that the volume density of mitochondria was significantly higher in tissue portions close to the capillary wall and cell surface than in the remaining tissue (31.6% and 31.1% v. 26.2% and 26.1%, P less than 0.01) and P less than 0.05). No significant differences between subepicardial and middle regions were found. We conclude that there is a preferential distribution of mitochondria with respect to cell surface and capillary wall; the gradient, however, is much smaller than some 'typical' illustrations may imply.

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Merits and pitfalls in morphological assessment of cardiac growth.

The basic principles of quantitative morphological analysis of myocardial tissue are presented. Particular attention is paid to the effects of stimulated cardiac growth on the relationship between cell size and various indices of myocardial capillary supply in pressure-overloaded rat hearts. The importance of adequate sampling and of the number of measurements is stressed with respect to reliable estimation of the mean values but even more for assessment of variability of the measured data. When estimating myocardial capillary supply by average values of capillary density and/or of areas supplied by a single capillary, this crucial information is missing. Therefore the merits of more advanced techniques allowing for the estimation of variability of capillary spacing are critically examined and the significance of their application to myocardial tissue is outlined (method of concentric circles and method of triangular nets). Finally, the importance of variability of capillary spacing on oxygen supply is demonstrated. The variability of capillary spacing alone may affect oxygen supply independently of the average values of intercapillary distance.

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The effect of heterogeneity of capillary spacing and O2 consumption--blood flow mismatching on myocardial oxygenation.

The effect of heterogeneity of capillary spacing on myocardial oxygenation was estimated for various sizes of tissue cylinder radii ranging from 8 to 18 microns, which are the values expected from the histological measurements. Similarly, the effect of mismatching between myocardial oxygen consumption and capillary blood few was analyzed. The results are summarized in charts which demonstrate that both heterogeneities are important independent tissue oxygen determinants irrespective of the mean values of these parameters. Therefore they should be included in any future evaluation of the oxygen supply to tissue.

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Protamine inhibits capillary formation in growing rat hearts.

Various indices of capillary supply to the rat heart were studied in neonatal rats injected for 2 or 4 weeks with protamine sulfate in saline (subcutaneously, 60 mg/kg body weight, 2 times/day). Cardiac capillarization was evaluated not only by traditional indices for the capillary supply, such as mean capillary density and myocyte-to-capillary ratio, but also by a more advanced morphometric method of capillary domains. This method allows the estimation of both the average radius of the Krogh tissue cylinder and its variability, which reflects the heterogeneity of capillary spacing found to be an independent morphological determinant of oxygen diffusion in the tissue. The results were evaluated with respect to regional differences (subendocardial vs. middle section), age differences, and the effect of protamine. No regional differences in capillary supply were found in this experimental situation. Hearts from older rats had significantly decreased capillary supply, expressed as lower capillary density, larger capillary domains, and greater radius of the tissue cylinder. On the other hand, the heterogeneity of capillary spacing decreased significantly with age. Protamine-injected animals, when compared to their control littermates, had a significantly higher cell-to-capillary ratio, lower capillary density, larger capillary domains, greater radius of the tissue cylinder, and larger variability in capillary spacing. Thus, protamine was effective in impeding rapid capillary growth in the hearts from rats in the early postnatal period. Close to half of all the existing capillaries in the adult rat hearts are formed during the first 3-4 postnatal weeks.

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Coronary blood flow in genetic cardiac hypertrophy.

6he effects of cardiac hypertrophy on coronary circulation was evaluated in 4 related strains of rats: the M520/N strain (n = 7), which has genetic cardiac hypertrophy but a normal blood pressure; the LA/N strain (n = 8), which has a somewhat small heart with normal blood pressure; the SHRSP/N strain (n = 8), which is hypertensive with marked left ventricular (LV) hypertrophy; and the WKY/N strain (n = 7), from which the SHR-Sp was developed. At 11 to 12 weeks of age, systemic and coronary hemodynamics were studied by 15-mu radioactive microspheres injected through the left atrium in conscious, unrestrained rats. Coronary blood flow was determined both at rest and after maximal vasodilation by carbochrome (6 mg/kg). LV weight was significantly higher in both the SHRSP/N (3.19 +/- 0.10 mg/g [+/- standard error], p less than 0.01) and the M520/N (2.82 +/- 0.08 mg/g, p less than 0.01) strains than in the WKY/N strain (2.30 +/- 0.08 mg/g); it was significantly smaller in the LA/N strain (1.96 +/- 0.04 mg/g, p less than 0.01). Coronary flow at rest was similar among the 4 groups; however, carbochrome-induced "maximal" flow differed among the groups. It was almost equal among the SHRSP/N (1,176 +/- 151 ml/m/100 g), the LA/N (1,356 +/- 149 ml/m/100 g) and the WKY/N strains (1,263 +/- 143 ml/m/100 g), but it was markedly decreased in the M520/N strain compared with the 3 other groups (632 +/- 83 ml/m/100 g, p less than 0.05 vs WKY/N and p less than 0.01 vs SHRSP/N and LA/N).(ABSTRACT TRUNCATED AT 250 WORDS)

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The effect of blood O2 affinity on the efficiency of O2 transport in blood at hypoxic hypoxia.

An index of the efficiency of O2 transport in blood and delivery to tissues, the capacitance coefficient beta, was theoretically analyzed as a function of the position of the blood O2 dissociation curve (ODC). The P50 at which beta reaches its maximum is high at normoxia and decreases with lowering the ambient PO2. At very deep hypoxia this value becomes lower than the normal P50 of human blood. An increase of blood O2 capacity enlarges beta, particularly at deep hypoxia, and also increases the P50 at which maximal beta is reached. Changes of (a-v)O2 have ambivalent effects, depending on both P50 and PaO2. The capacitance coefficient beta was further calculated as a function of PaO2 at three values of P50, simulating the effect of a shift of the ODC. The capacitance coefficient is several times higher at deep hypoxia than at normoxia at all values of P50 used. A shift of the ODC to the left results in a moderate decrease of beta at mild hypoxia but in a large increase at severe hypoxia; a shift to the right has a reverse effect.

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The effect of cell size and capillary spacing on myocardial oxygen supply.

Recently, we collected basic morphometric data from normal and hypertrophic rat hearts: median and mean values of the cell diameter and of the intercapillary distance as well as their variabilities. In the present communication we used these data, first for analysis of the effect of the heterogeneity of capillary spacing on the myocardial tissue PO2. Comparison of tissue PO2 histograms calculated for a situation in which the capillaries are evenly distributed as in the Krogh model, with a situation based on the same capillary but variable intercapillary distances clearly demonstrates the importance of heterogeneity of the capillary spacing as a separate oxygen determinant. This is even more important in the hypertrophic hearts which are characterized by longer and more variable intercapillary distances. In the second part, we compared the classical Krogh model with a model of concentric diffusion in which the oxygen consumption was either uniform or divided into two zones of distinctive rates. Oxygen profiles calculated for the Krogh model with excentric diffusion were similar to those derived for the two models of concentric diffusion.

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Functional capillary density in normal and transplanted rat hearts.

The subepicardial capillaries were visualised under normoxemia and hypoxemia by cinemicrophotography of the beating heart in open-chest rats. The functional intercapillary distances (ICD) were directly measured from focused frames. Under normoxemia, the average ICD was 19.2 micrometers and under hypoxemia, 17.9 micrometers (p less than 0.01). This decrease of 1.3 micrometers under hypoxemia corresponds to an average recruitment of an additional 416 capillaries/mm2 (from 2762 to 3178). During postnatal development, both the normoxemic and hypoxemic ICD's increased with left ventricular weight. The regression analysis of this relationship indicates that the hypoxemic ICD's remain significantly shorter within the observed range. In heterotopically isotransplanted, empty, beating rat hearts, there was no difference in functional ICD between normoxemia and hypoxemia either in 1-day-old (18.5 versus 18.6 micrometers) or in 7-day-old (17.1 versus 17.1 micrometers) transplants. Unlike the hearts in situ which could be observed only through a long working distance, low power objective (11 X), the heterotopic transplants could also be observed through a higher power (22 X) lens with an optical penetration of less than 5 micrometers. On the same hearts almost identical ICD's were obtained by both lenses during normoxemia and hypoxemia. Therefore, recruitment of capillaries observed on the normal hearts could not be due to different optical characteristics of the hypoxemic myocardium.

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