Mikrometrische und histologische Analyse hypertropher menschlicher Herzen

Linzbach, A. J.

doi:10.1007/bf00948300

Cited by 193 publications

(26 citation statements)

References 45 publications

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“…The documentation that conditions of overload, aging, and ischemic heart disease do not alter the relative proportion of the various myocyte populations 130 strongly suggests that the demonstrations of myocyte cellular hyperplasia obtained initially by Linzbach 45,60 and subsequently by other investigators 50,124 -130 are valid. Additionally, mononucleated cells represent 3/4 of the myocytes of the human heart, differing significantly from other mammals, such as mice, 68 rats, 64 and dogs.…”

Section: Heart Failurementioning

confidence: 88%

“…54 -58 Myocyte volume markedly increases postnatally, 52,59 but further hypertrophy is limited in adulthood. 60 As stated in Molecular Biology of the Cell, 61 ". .…”

Section: Postnatal Myocardial Growthmentioning

confidence: 99%

“…45,60 The critical heart weight theory introduced by this author in the late 1940s and early 1950s has suggested that, in the presence of a cardiac weight of Ն500 g, myocyte proliferation begins and that this cellular process constitutes the prevailing mechanism of additional growth of the heart. 116 These findings were restricted to the left ventricle, but subsequent observations have demonstrated that a similar response occurs in the right ventricle.…”

Section: Heart Failurementioning

confidence: 99%

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Ventricular Myocytes Are Not Terminally Differentiated in the Adult Mammalian Heart

Anversa

Kajstura

1998

Circulation Research

335

177

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Section: Heart Failurementioning

confidence: 88%

“…54 -58 Myocyte volume markedly increases postnatally, 52,59 but further hypertrophy is limited in adulthood. 60 As stated in Molecular Biology of the Cell, 61 ". .…”

Section: Postnatal Myocardial Growthmentioning

confidence: 99%

Section: Heart Failurementioning

confidence: 99%

See 1 more Smart Citation

Ventricular Myocytes Are Not Terminally Differentiated in the Adult Mammalian Heart

Anversa

Kajstura

1998

Circulation Research

335

177

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“…7 Since fiber enlargement increases the diffusion distance for essential metabolites, it has been suggested that myocardial hypertrophy is detrimental rather than beneficial. 8 ' ° The conclusion that hypertrophy enables the myocardium to perform more work has been questioned, 10 but other studies 11 ' la have indicated that increased myocardial mass may enhance work capacity.…”

Section: Discussionmentioning

confidence: 99%

Circulatory Response to Release of Chronic Pulmonary Artery Constriction

Tobin

Rastelli

Blundell

et al. 1965

Circulation Research

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• During investigations of the effects of excercise 1 and sympathomimetic amines on right ventricular function in unanesthetized dogs with normal or hypertrophied right ventricles, a circulatory state characterized by a supernormal stroke volume and cardiac output and by a decreased systemic vascular resistance was demonstrated in dogs studied 10 to 14 days after the release of chronic pulmonary artery constriction. The purpose of this report is to record this phenomenon and to discuss its nature and possible significance. MethodsEleven mongrel dogs (12 to 20 kg body weight) were used. After preliminary observations (study I*), the main pulmonary artery of each dog was tightly banded as described previously 2 for a minimal period of three months. Each animal was reinvestigated while its pulmonary artery was constricted (study II). Then, the constricting bands were removed, and observations were made two weeks (study III) and two months (study IV) later.After study IV, each animal was killed and necropsy was performed. The cleaned and fixed ventricular muscle mass was separated by Herrmann's method, 18 and the right ventricular weight was expressed as a ratio of right ventricular weight (RVW) to left ventricular weight (LVVV). In 11 dogs, two months or more after the release of pulmonary artery constriction, the mean ratio of RVW to LVVV of 0.885 exceeded significantly the ratio, 0.715, derived from Herrmann's data for 200 normal dogs.From the Mayo Clinic and Mayo Graduate School of Medicine, Rochester, Minnesota.Supported in part by Research Grants HE-06249 and HE-09374 from the National Institutes of Health, U. S. Public Health Service.Dr. Tobin was a Special Fellow, National Institutes of Health, U. S. Public Health Service.Accepted for publication March 10, 1963. *Study I was not done in the five dogs used for exercise studies. PREPARATION OF DOGSNo general anesthetic or premedication was used. Dogs were familiarized with the laboratory, restrained on an animal board, and trained to run without restraint on a horizontal treadmill on several occasions before the experiments. Only those animals who tolerated the animal board and were able to run freely were selected. With the dog under generous local anesthesia (2% lidocaine (Xylocaine) in saline), one carotid artery and one jugular vein were exposed. Size 6F Lehman catheters were introduced and manipulated under fluoroscopic and manometric control into the pulmonary artery, right ventricle, right atrium, and aortic arch, as required. Size 5F Lehman catheters were introduced into the superior vena cava for the injection of indocyanine green and into the jugular vein for the infusion of drugs. INSTRUMENTATIONSimultaneous pressures were recorded from the same base line by means of Statham strain gauge transducers with equal sensitivities. The zero reference level was fixed at midthorax. 4The catheter-manometer systems had frequency responses uniform to between 15 and 20 cycles/ sec.Cardiac output was measured by the indicator dilution technic. Indocyanine green (...

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“…Those articles are divided into 2 groups: those which are concerned with haemodynamic functions, and the others concerned with biochemical and related structural changes in the myocardium.1)-4),15)- 19) There are, however, many controversial theories on the mechanism of myocardial hypertrophy or contractile deficiency of myocardium. 20) Studying the alterations of some substrates and of functional protein fractions in experimentally induced cardiac hypertrophy and failure through the time course, the author attempted to elucidate the mechanisms of developments of cardiac hypertrophy and cardiac failure.…”

Section: Discusmentioning

confidence: 99%

Studies on Myocardial Protein Metabolism in Cardiac Hypertrophy

Tomita

1966

Jpn Heart J

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Mikrometrische und histologische Analyse hypertropher menschlicher Herzen

Cited by 193 publications

References 45 publications

Ventricular Myocytes Are Not Terminally Differentiated in the Adult Mammalian Heart

Ventricular Myocytes Are Not Terminally Differentiated in the Adult Mammalian Heart

Circulatory Response to Release of Chronic Pulmonary Artery Constriction

Studies on Myocardial Protein Metabolism in Cardiac Hypertrophy

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