Myocardial Ultrastructure in Acute and Chronic Hypoxia

Ferrans, Víctor J.; Roberts, William C.

doi:10.1159/000169357

Cited by 37 publications

(7 citation statements)

References 40 publications

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“…Also given in these tables are corresponding data on the eight patients previously reported to have similar morphologic abnormalities. The average age of our six patients, 16 months (range 6 to 24), was similar to the 15 months (range 8.5 to 24 months) found in the other eight patients; the average age for the entire group was 15.5 months. Four of our six patients and all eight previously reported patients were girls.…”

Section: Clinical Observationssupporting

confidence: 81%

Infantile cardiomyopathy with histiocytoid change in cardiac muscle cells. Report of six patients.

Ferrans¹,

McAllister²,

Haese³

1976

Circulation

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Clinical and pathologic findings are presented in 14 patients (six newly reported, eight described previously), all children ranging in age from 6 to 24 months, with a clinicopathologic syndrome termed "infantile cardiomyopathy with histiocytoid change in cardiac muscle cells." This syndrome is manifested clinically by severe, eventually fatal cardiac arrhythmias, and is characterized pathologically by cardiac hypertrophy and by a distinctive type of focal degeneration of the muscle cells, which lose their myofibrils, undergo marked mitochondrial hyperplasia, become rounded in shape and enlarged, and resemble histiocytes. Evidence is presented to support the conclusions that these manifestations are those of a cardiomyopathy, that cardiac hypertrophy precedes the onset of the clinical features, that the focal degeneration is likely to be a cause rather than a consequence of the arrhythmias, and that the latter develop only in the late stages of the disorder. The etiology of this cardiomyopathy remains unclear.

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Section: Clinical Observationssupporting

confidence: 81%

Infantile cardiomyopathy with histiocytoid change in cardiac muscle cells. Report of six patients.

Ferrans¹,

McAllister²,

Haese³

1976

Circulation

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“…After the initial 15-to 20-minute period in hypoxic solution, the first changes in ultrastructure which appeared were the loss of intramitochondrial particles, a somewhat swollen appearance of mitochondria and their relatively electron-lucent matrix, and a decrease in the content of glycogen granules. These are compatible with findings for ischemic or anoxic myocardium of human hearts and experimental animal hearts observed by others (Kottmeir and Wheat, 1966;Ferraris and Roberts, 1971;Goldstein et al, 1977).…”

Section: Relationship Between Ultrastructural Changes and Electrical supporting

confidence: 93%

“…As soon as the oxygen tension within the cell becomes limiting, mitochondria cease to function, and a series of functional and ultrastructural alterations of mitochondria occur (Trump et al, 1971). In fact, observations on the mammalian ventricular myocardium exposed to acute or chronic hypoxia have revealed that ultrastructural characteristics include mitochondrial change, swelling of the sarcoplasmic reticulum, glycogen loss, and myofibrillar damage (Ferraris and Roberts, 1971;Schwartz et al, 1973;Goldstein et al, 1977;Schaper et al, 1977). However, little information is available concerning ultrastructural alterations of sinoatrial nodal cells exposed to hypoxia.…”

mentioning

confidence: 99%

Changes in electrical activity and ultrastructure of sinoatrial nodal cells of the rabbit's heart exposed to hypoxic solution.

Nishi¹,

Yoshikawa²,

Sugahara³

et al. 1980

Circulation Research

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We studied the effects of hypoxia on the electrical activity and ultrastructure of pacemaker cells of sinoatrial nodal tissue excised from rabbit heart. The slope of slow diastolic depolarization was markedly reduced within 15-20 minutes after gassing Tyrode's solution with nitrogen, whereas other action potential parameters were not much affected. At 60-90 minutes in the hypoxic solution, the maximum diastolic potential decreased by 13 mV, and the peak potential decreased to -5 mV, but abbreviated action potentials continued to occur for another 30-60 minutes. After 60-90 minutes of hypoxia, reoxygenation did not produce complete recovery of the action potential. In glucose-free solution, action potentials ceased within 40 minutes of hypoxia, but reoxygenation restored electrical activity. A good correlation was found between the duration of hypoxia and the extent of ultrastructural change in sinoatrial nodal cells. After 15-20 minutes of hypoxia, mitochondria showed decreased electron density of their matrix and loss of intramitochondrial particles. The glycogen content was reduced. After 60-90 minutes of hypoxia, further changes in the mitochondria occurred: clearing of the matrix, fragmentation of cristae, rupture of the outer membrane, and formation of myelin figures. Glycogen had almost completely depleted after reoxygenation. These changes were partly reversible except for the glycogen content. Our results provide electrophysiological evidence that cells in the sinoatrial nodal tissue can withstand long exposure to hypoxia, using energy produced by the anaerobic glycolytic pathway. MethodsAlbino rabbits of either sex, weighing about 2 kg, were anesthetized with ether, and the heart was by guest on March 22, 2015 http://circres.ahajournals.org/ Downloaded from by guest on March 22, 2015 http://circres.ahajournals.org/ Downloaded from K Nishi, Y Yoshikawa, K Sugahara and T Morioka exposed to hypoxic solution. Changes in electrical activity and ultrastructure of sinoatrial nodal cells of the rabbit's heart

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“…In contrast to the predominant pattern of muscle cell necrosis in the outer peripheral regions of the infarcts, central regions of the infarcts with severely reduced blood flow contained necrotic muscle cells without contraction bands or calcium deposits. This pattern of myocardial necrosis previously has been shown to be typical of areas rendered maximally ischemic by permanent coronary occlusion (32)(33)(34)(38)(39)(40). Such regions have also been shown to develop a severe impairment to myocardial perfusion within 90-120 min after onset of coronary occlusion (22,28).…”

Section: Tsupporting

confidence: 52%

“…The occurrence of significant levels of perfusion in the outer peripheral zones of the transmural infarcts is explicable on the basis of collateral blood flow to these regions (25)(26)(27) fusion occurs throughout or at some time during the evolution of injury (28)(29)(30)(31)(32)(33)(34). Ultrastructural studies from our own and other laboratories have shown that calcium deposits in the irreversibly injured muscle cells are localized to the mitochondria and occur in the form of apatite-like spicules or deposits of subcrystalline, finely granular material (35)(36)(37)(38).…”

Section: Tmentioning

confidence: 99%

Pathophysiology of technetium-99m stannous pyrophosphate and thallium-201 scintigraphy of acute anterior myocardial infarcts in dogs.

et al. 1976

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A B S T R A C T In 17 dogs with acute myocardial infarcts produced by ligation of the proximal left anterior descending coronary artery, a comparative study was made of myocardial scintigrams obtained with technetium-99m stannous pyrophosphate ("mTc-PYP) and thallium-201 ('Tl), tissue levels of 'Tc-PYP and 'Tl uptake, histopathologic alterations, and regional myocardial perfusion measured with radioactive microspheres. 9 of the 10 hearts examined histologically had transmural infarcts with outer peripheral, inner peripheral, and central zones characterized by distinctive histopathologic features. A progressive reduction in myocardial blood flow was demonstrated between normal myocardium and the centers of the infarcts, and correlated well with progressive reduction in 'Tl uptake in the same regions. Marked mTc-PYP concentration occurred in areas with partial to homogeneous myocardial necrosis and residual perfusion located in the outer peripheral regions of the infarcts. The latter areas also were characterized by the presence of muscle cell calcification. The patterns of distribution of "'Tc-PYP and m'°Tl explained the filling defects on 'Tl myocardial scintigrams and the doughnut patterns on 99mTc-PYP myocardial scintigrams in dogs with transmural infarcts. One dog with a subendocardial infarct had a small homogeneous area of activity on the "Tc-PYP myocardial scintigram, and showed marked uptake of 'mTc-PYP in subendocardial areas of extensive necrosis and calcification still receiving some coronary perfusion.Dr.

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Myocardial Ultrastructure in Acute and Chronic Hypoxia

Cited by 37 publications

References 40 publications

Infantile cardiomyopathy with histiocytoid change in cardiac muscle cells. Report of six patients.

Infantile cardiomyopathy with histiocytoid change in cardiac muscle cells. Report of six patients.

Changes in electrical activity and ultrastructure of sinoatrial nodal cells of the rabbit's heart exposed to hypoxic solution.

Pathophysiology of technetium-99m stannous pyrophosphate and thallium-201 scintigraphy of acute anterior myocardial infarcts in dogs.

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