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Autofluorescence in the identification of myocardial infarcts
AUTOFLUORESCENCE IN IDENTIFICATION OF MYOCARDIAL INFARCTS I CARLE 19. Little,J. M., and Goodman,A. H.: Cysticadventitialdisease of the popliteal artery. Brit.J. Surg., 57:708, 1970. 20. Milliken,J. C.: Cysticdegenerationof the popliteal artery in a female. Brit. Med.J., 2:769, 1971. 21. Powis, S. J. A., Morrissey, D. M., and Jones, E. L.: Cystic degeneration of the popliteal artery. Surgery, 67:891, 1970.
22. Roth,J. A., Hearney, P., and Wittmann,C.J.: Cysticadventitial degeneration of the common femoral artery. Arch. Surg., 112:210-212, 1977. 23. Savage,P. E. A.: Cysticdisease of the poplitealartery. Brit.J. Surg., 56:77, 1969. 24. Schlesinger,A., and Gottesman,L.: Cysticdegenerationof the popliteal artery. Am. J. Roentgenol.,127:1043, 1976. Box 14424 Omaha, Nebraska 68114 (Dr. Schenken)
A U T O F L U O R E S C E N C E IN T H E I D E N T I F I C A T I O N OF MYOCARDIAL INFARCTS Birdsall N. Carle, M . D . * Abstract A method is described for demonstrating myocardial necrosis by changes in the autofluorescence of routine hematoxylin and eosin or hematoxylin and eosin-phloxine stained sections using a standard microscope with an epifluorescence attachment. Regions of necrosis fluoresce with a brilliant yellow color clearly distinguishable from the dull olive-green to red-brown fluorescence of the neighboring viable cardiac muscle.
Well established myocardial infarcts are not difficult to identify in routine tissue sections stained with hematoxylin and eosin. However, some suspected infarcts, particularly those of recent 6rigin, present a diagnostic problem. The morphologic changes in the myocardium may be so subtle that it is often difficult or impossible to determine whether tile microscopic appearance represents true necrosis, some other lesion, or some vagary of staining. This is a common question in atttopsy examinations. A simple teclmique utilizing autofluorescence of necrotic heart muscle in standard hematoxylin and eosin sections tins proven very usefltl. Many teclmiques lmve been devised to identify cardiac necrosis and particularly earl}, necrosis. These have included teclmiques to demonstrate fat change in the myocardium, fuchsinoplfilia in earl}, infarction, acid hematin staining, a comparison of fuchsinophilia and fuchsinorrhagia, basic fitchsin staining, and hematoxylin-basic fuchsin-picric acid staining) -7 Histochemical methods relating to glycogen have beel~ examined as well as alterations in succinic dehydrogenase, cytochrome oxidase, phosphorylase, ttridine diphosptmte gh|cose-glycogen transferase, /3hydroxybntyrate dehydrogenases, and isocitrate dehydrogenases, sv' Enzyme decay curves (glutamic
oxaloacetic transaminase, glutamic pyruvic transaminase, lactic acid dehydrogenase) have been compared in normal and infarcted hearts. ~'~ Changes in the sodium to potassium ratio within the myocardium have been reported as being perhaps the most reliable measurement for detecting earl}, infarction, la' la Fluorescence of gross specimens of experimentally infarcted rabbit hearts following antemortem injection of tetracycline has been studied as well as macroscopic identification of earl}, myocardial infarcts by alterations in dehydrogenase activity) ~ ~7 Electron microscopic study of ischemic rat myocardium has been reported) s Most of these methods are summarized in tim World Heahh Organization Scientific Group Report on the Pathologic Diagnosis of Acute Ischaemic Heart Disease? 9 Unfortunately these various attempts have as yet failed to produce a generally accepted method for demonstrating tile subtle changes of earl}, myocardial necrosis. This article presents a method that promises to be of.value in making tiffs determination. Many substances, including stained tissue sections, may exhibit characteristic atttofluorescence under ultraviolet light. While examining a variety of tissues with a fluor~xscence microscope it became apparent that bematoxylin and eosin stained sections
Accepted far publicationJuly I, 1980. *Chief, Laboratoryand PathologyScience, Veterans Administration MedicalCenter, Roseburg, Oregon, HUMAN PATIIOLOGY--VOI.UME 12, NUMBER 7 Jul)' 1981
643
HUMAN PATHOLOGY--VOLUME 12, NUMBER 7 July 1981 of necrotic myocardium fluoresced with a brilliant yellow color, which was quite different from the rather dull olive-green to red-brown fluorescence of non-necrotic myocardium. These hearts with obvious recent necrosis all showed the brilliant yellow fluorescence in the necrotic areas. Examination was carried out in hearts in which necrosis was suspected but not definitely ascertained by routine staining. Examination with fluorescence microscopy in 15 o f 22 instances showed areas of bright yellow fluorescence similar to that o f known necrotic muscle. No such fluorescence was seen in noninfarcted heart muscle. T h e altered fluorescence appeared to be specific for myocardial necrosis. Old scars also fluoresce with a somewhat similar yellow response, but such areas are easily recognized on liglat microscopy.
PROCEDURE A standard Zeiss microscope equipped with a epifluorescence condenser (Model 4FL) illuminated with a 12 volt, 100 watt quartz halogen light source was used with planochromat objectives. Filters used were a primary filter (440 to 490 nanometers), secondary filter (520 nanometers), and dichroic reflector (510 nanometers). With this instrument it is possible to switch light sources from conventional substage tungsten illumination to epifluorescence illumination, readily allowing examination of the same section and field by either manner. Routine autopsy sections of myocardium were stained with hematoxylin and eosin or hematoxylin and eosin-phloxine. Both staining methods gave a similar fluorescence response. Two hundred sixtyfiye hearts were examined. O f this number, 75 had
been identified after gross examination and with ordinary light microscopy as exhibiting areas of recent or fairly recent necrosis. Fifteen other sections of myocardium were from patients who died suddenly. O f this group, four were from cases of coronary occlusion and two of these showed areas of yellow fluorescence denoting recent necrosis but showing no definite change on light microscopy. Eleven of tile 15 showed evidence of severe coronary sclerosis without occlusion. Eight of these showed areas of yellow fluorescence and three did not. Five additional patients with coronary occlusion died less rapidly. Specimens in four of these showed areas of necrosis by tile fluorescence technique and one was negative. One patient who died slowly had severe coronary sclerosis without occlusion and the heart showed areas of yellow fluorescence. In one patient amyloid change was demonstrated in the heart. Tile areas of amyloid showed a somewhat different yellow fluorescence more resembling scar tissue fluorescence than acute necrosis.
DISCUSSION Hearts with obvious areas of infarction ahvays showed a characteristic bright yellow fluorescence in tile areas o f necrosis. Hearts with questionable areas of necrosis when examined by light microscopy showed a bright yellow fluorescence in suspected areas and frequently in areas completely unsuspected on examination by fluorescence microscopy (Figs. l, 2). It is not possible to ascertain with certainty the precise time of coronary occlusion in human patients, and no attempt has been made to determine or speculate about the time interval necessary for the
Figure 1. Earlymyocardialinfarction. (tlematoxylin and eosinphloxine stain. •
644
A U T O F L U O R E S C E N C E IN I D E N T I F I C A T I O N OF MYOCARDIAl, I N F A R C T S - CARLE
Figure 2. Same field and stain as in Figure 1, showing bright yellow -autofluorescence of necrotic myocardium. Olive green autolluorescence of non-necrotic myocardium. (• 200.)
yellow f l u o r e s c e n c e to b e c o m e a p p a r e n t save n o t i n g t h a t it has b e e n seen in patients with v e r y s h o r t clinical histories. Facilities h a v e n o t b e e n available t h u s f a r to s t u d y a n i m a l h e a r t s f o l l o w i n g c o r o n a r y ligation with interval e x a m i n a t i o n s to d e t e r m i n e h o w s o o n t h e yellow f l u o r e s c e n c e b e c o m e s manifest. T h e t e c h n i q u e is o f f e r e d ,as an effective m e t h o d f o r d e m o n s t r a t i n g m y o c a r d i a l necrosis a n d a p p a r e n t ly quite earl), necrosis. It has t h e a d v a n t a g e o f b e i n g simple, r e q u i r i n g o n l y an a d e q u a t e f l u o r e s c e n c e mic r o s c o p e with w h i c h to e x a m i n e r o u t i n e h e m a t o x y l i n a n d eosin stained sections.
ADDENDUM S u b s e q u e n t to writing the f o r e g o i n g t h e r e has b e e n o p p o r t u n i t y to e x a m i n e a u t o p s y tissues in a case o f systemic n e c r o t i z i n g arteritis u s i n g t h e a u t o f l u o r e scence t e c h n i q u e with r o u t i n e h e m a t o x y l i n a n d eosin s t a i n e d sections. F i b r i n o i d necrosis o f t h e i n v o l v e d vessel walls s h o w e d b r i g h t ),ellow a u t o f l u o r e s c e n c e m u c h like t h a t o f n e c r o t i c m y o c a r d i u m . R e c o g n i t i o n o f vascular nectosis does n o t p o s e the p r o b l e m t h a t is f r e q u e n t in r e c o g n i z i n g earl)' m y o c a r d i a l necrosis. E v e n so, t h e a t t t o f l u o r e s c e n c e t e c h n i q u e m i g h t be h e l p f u l at times in cases o f arteritis. I n this o n e case it brilliantly o u t l i n e d n e c r o t i c s m o o t h m u s c l e in the walls o f i n v o l v e d vessels.
ACKNOSVLEDGMENTS T h e author wishes to express Iris thanks to Doctors Charles E. Dunlap and William H: Sternberg of the Tulane University School of Medicine and to Doctor A. Gerson Hollander of the Veterans Administration Medical Center,
Roseburg, Oregon, for their encouragement and helpfid suggestions, to Mrs. Delila Randall for teclmical assistance, and to Mrs. Vernetta Calderwood for typing the manuscript.
REFERENCES 1. Wartman, W. B., Jennings, R. B., Yokoyama, H. O., and Clabaugh, G. F.: Fatty change of the myocardium in earl)' experimental infarction. A.M.A. Arch. Path., 62:318-323, 1956. 2. Pole)', R. W., Fobes, C. D., and Hall, M.j.: Fuchsinophilia in early myocardial infarction. Arch. Path., 77:325-329, 1964. 3. Niles, N. R., and Barnhouse, D. L.: The acid hematin stain and myocardial damage. Arch. Path., 83:407--410, 1967. 4. Lie, J. T.: Detection of earl)' myocardial infarction by the acid filchsin staining technic. Am. J. CIin. Path., 50.317-319, 1967. 5. Zugibe, F. T., jr., and Zugibe, F. T.: Fuchsinophilia and fuchsinorrhagia staining techniques. Arch. Path., 96:243245, 1973. 6. Nayar, A., and Olsen, E. G. J.: The use of the basic fi~chsin stain in the recognition of earl)" myncardial ischaemia. Cardiovasc. Res., 391:394, 1974. 7. Lie, J. T., Holley, K. E., Kampa, W. R., and Titus, J. L.: New histochemical method for morphologic diagnosis of earl)' stages of myocardial ischemia. Mayo Clin. Proc., 46:319327, 1971. 8. Yokoyama, H. O., Jennings, R. B., Clabaugh, G. F., and Wartman, W. B.: Histochemical studies of earl)' expcrimental myocardial infarction. A.M.A. Arch. Path., 59:347-354, 1955. 9. Shnitka, T. K., and Nachlas, M. M.: Histochemical alterations in ischemic heart muscle and early m)ocardial infarction. Am. J. Padl., 42:507-527, 1963. 10. Fine, G., Morales, A. R., and Scerpella, J. R.: Experimental myocardial infarction. Arch. Path., 82:4-8, 1966. I 1. Morales, A. R., and Fine, G.: Earl)" human myocardial infarctlon. Arcli. Path., 82:9-14, 1966. 12. Braunstein, tt.: Effect of postmortem interval on histochemi-
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12, N U M B E R 7 July 1981
cal reactions of the myocardium. Am.J. Clin. Path., 49:224231, 1966. 13. Zugibe, F. T., Conley, T. L., Bell, P.,Jr., and Standish, M. L.: Enzyme decay curves in normals. Arch. Path., 93:308-311, 1972. 14. Zngibe, F. T., Bell, P., Jr., Conley, T., and Standish, M. L.: Determination of myocardial alterations at autopsy in the absence of gross and microscopic changes. Arch. Path., 81:409--411, 1966. 15. McVie, J. G.: Postmortem detection of inapparent myocardial infarction. Arch. Path., 23:203-209, 1970.
16. Sybers, H. D., Ashraf, M., Braitwaite, J. R., and Lock, M.-P.: Earl). myocardial infarction. Arch. Path., 93:49-54, 1972. 17. Nachlas, M. M., and Shnitka, T. K,: Macroscopic identification of earl)' myocardial infarcts by alterations in dehydrogenase activity. Am. J. Path., 42:379-404, 1963. 18. Bryant, R. E., Thomas, W. A., and O'Neal, R. M.: An electron microscopic study of myocardial ischemia in the rat. Circ. Res., 6:699-709, 1958. 19. WHO Scientific Group: The pathological diagnosis of acute ischaemic heart disease. WHO Technical Report Series No. 441, 1:27, 1970. Laboratory and Pathology Service Veterans Administration Medical Center Roseburg, Oregon 97470
U L T R A S T R U C T U R E OF MALIGNANT RHABDOID OF T H E K I D N E Y
TUMOR
A Distinctive Renal T u m o r of Children Joel E. Haas, M.D.,* Nigel F. Palme~, M.D.,"f Arthur G. Weinberg, M.D.,$ and J. Bruce Beckwith, M.D. w
Abstract An unusual and highly malignant childhood renal tumor has been noted among the specimens of the National Wihns' Tumor Study. Prominent nncleoli, PAS positive cytoplasmic inclusions, and light microscopic features suggestive of rhabdomyoblastic differentiation are l m l l m a r k s o f this t u m o r . U l t r a s t r u c t u r a l e x a m i n a t i o n o f 1 1 s p e c i m e n s r e v e a l e d t h e f i l a m e n t o u s
Accepted for publication May 6, 1980. This study was supl)orted ill part by grant CA-11~'22 from tile National Institutes of Heahh (National Wilms' Tmnor Study). *Assistant Professor of Pathology and Pediatrics, University of Washington School of Medicine.H cad, l'athology Division, Department of Laboratories, Children's Orthopedic Hospital and Medical Center, Seattle, Washil!gton. "~Assistant Professor of Pathology, Ohio State University College of Medicine, Cohm~ms, Ohio. TProfessor of Patholo~" and Pediatrics, University of Texas Heahh Science Center at Dallas. Director of Laboratories, Children's Medical Center, Dallas, Texas. w of Pathology and Pediatrics, Uriiversity of Washington School of Medicine. Director'of Laboratories, Children's Orthopedic Hospital and Medical Center, Seattle, Washington.
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HUMAN PATItOLOGY--VOLUME 12, NUMBER 7 July 1981
22. Roth,J. A., Hearney, P., and Wittmann,C.J.: Cysticadventitial degeneration of the common femoral artery. Arch. Surg., 112:210-212, 1977. 23. Savage,P. E. A.: Cysticdisease of the poplitealartery. Brit.J. Surg., 56:77, 1969. 24. Schlesinger,A., and Gottesman,L.: Cysticdegenerationof the popliteal artery. Am. J. Roentgenol.,127:1043, 1976. Box 14424 Omaha, Nebraska 68114 (Dr. Schenken)
A U T O F L U O R E S C E N C E IN T H E I D E N T I F I C A T I O N OF MYOCARDIAL INFARCTS Birdsall N. Carle, M . D . * Abstract A method is described for demonstrating myocardial necrosis by changes in the autofluorescence of routine hematoxylin and eosin or hematoxylin and eosin-phloxine stained sections using a standard microscope with an epifluorescence attachment. Regions of necrosis fluoresce with a brilliant yellow color clearly distinguishable from the dull olive-green to red-brown fluorescence of the neighboring viable cardiac muscle.
Well established myocardial infarcts are not difficult to identify in routine tissue sections stained with hematoxylin and eosin. However, some suspected infarcts, particularly those of recent 6rigin, present a diagnostic problem. The morphologic changes in the myocardium may be so subtle that it is often difficult or impossible to determine whether tile microscopic appearance represents true necrosis, some other lesion, or some vagary of staining. This is a common question in atttopsy examinations. A simple teclmique utilizing autofluorescence of necrotic heart muscle in standard hematoxylin and eosin sections tins proven very usefltl. Many teclmiques lmve been devised to identify cardiac necrosis and particularly earl}, necrosis. These have included teclmiques to demonstrate fat change in the myocardium, fuchsinoplfilia in earl}, infarction, acid hematin staining, a comparison of fuchsinophilia and fuchsinorrhagia, basic fitchsin staining, and hematoxylin-basic fuchsin-picric acid staining) -7 Histochemical methods relating to glycogen have beel~ examined as well as alterations in succinic dehydrogenase, cytochrome oxidase, phosphorylase, ttridine diphosptmte gh|cose-glycogen transferase, /3hydroxybntyrate dehydrogenases, and isocitrate dehydrogenases, sv' Enzyme decay curves (glutamic
oxaloacetic transaminase, glutamic pyruvic transaminase, lactic acid dehydrogenase) have been compared in normal and infarcted hearts. ~'~ Changes in the sodium to potassium ratio within the myocardium have been reported as being perhaps the most reliable measurement for detecting earl}, infarction, la' la Fluorescence of gross specimens of experimentally infarcted rabbit hearts following antemortem injection of tetracycline has been studied as well as macroscopic identification of earl}, myocardial infarcts by alterations in dehydrogenase activity) ~ ~7 Electron microscopic study of ischemic rat myocardium has been reported) s Most of these methods are summarized in tim World Heahh Organization Scientific Group Report on the Pathologic Diagnosis of Acute Ischaemic Heart Disease? 9 Unfortunately these various attempts have as yet failed to produce a generally accepted method for demonstrating tile subtle changes of earl}, myocardial necrosis. This article presents a method that promises to be of.value in making tiffs determination. Many substances, including stained tissue sections, may exhibit characteristic atttofluorescence under ultraviolet light. While examining a variety of tissues with a fluor~xscence microscope it became apparent that bematoxylin and eosin stained sections
Accepted far publicationJuly I, 1980. *Chief, Laboratoryand PathologyScience, Veterans Administration MedicalCenter, Roseburg, Oregon, HUMAN PATIIOLOGY--VOI.UME 12, NUMBER 7 Jul)' 1981
643
HUMAN PATHOLOGY--VOLUME 12, NUMBER 7 July 1981 of necrotic myocardium fluoresced with a brilliant yellow color, which was quite different from the rather dull olive-green to red-brown fluorescence of non-necrotic myocardium. These hearts with obvious recent necrosis all showed the brilliant yellow fluorescence in the necrotic areas. Examination was carried out in hearts in which necrosis was suspected but not definitely ascertained by routine staining. Examination with fluorescence microscopy in 15 o f 22 instances showed areas of bright yellow fluorescence similar to that o f known necrotic muscle. No such fluorescence was seen in noninfarcted heart muscle. T h e altered fluorescence appeared to be specific for myocardial necrosis. Old scars also fluoresce with a somewhat similar yellow response, but such areas are easily recognized on liglat microscopy.
PROCEDURE A standard Zeiss microscope equipped with a epifluorescence condenser (Model 4FL) illuminated with a 12 volt, 100 watt quartz halogen light source was used with planochromat objectives. Filters used were a primary filter (440 to 490 nanometers), secondary filter (520 nanometers), and dichroic reflector (510 nanometers). With this instrument it is possible to switch light sources from conventional substage tungsten illumination to epifluorescence illumination, readily allowing examination of the same section and field by either manner. Routine autopsy sections of myocardium were stained with hematoxylin and eosin or hematoxylin and eosin-phloxine. Both staining methods gave a similar fluorescence response. Two hundred sixtyfiye hearts were examined. O f this number, 75 had
been identified after gross examination and with ordinary light microscopy as exhibiting areas of recent or fairly recent necrosis. Fifteen other sections of myocardium were from patients who died suddenly. O f this group, four were from cases of coronary occlusion and two of these showed areas of yellow fluorescence denoting recent necrosis but showing no definite change on light microscopy. Eleven of tile 15 showed evidence of severe coronary sclerosis without occlusion. Eight of these showed areas of yellow fluorescence and three did not. Five additional patients with coronary occlusion died less rapidly. Specimens in four of these showed areas of necrosis by tile fluorescence technique and one was negative. One patient who died slowly had severe coronary sclerosis without occlusion and the heart showed areas of yellow fluorescence. In one patient amyloid change was demonstrated in the heart. Tile areas of amyloid showed a somewhat different yellow fluorescence more resembling scar tissue fluorescence than acute necrosis.
DISCUSSION Hearts with obvious areas of infarction ahvays showed a characteristic bright yellow fluorescence in tile areas o f necrosis. Hearts with questionable areas of necrosis when examined by light microscopy showed a bright yellow fluorescence in suspected areas and frequently in areas completely unsuspected on examination by fluorescence microscopy (Figs. l, 2). It is not possible to ascertain with certainty the precise time of coronary occlusion in human patients, and no attempt has been made to determine or speculate about the time interval necessary for the
Figure 1. Earlymyocardialinfarction. (tlematoxylin and eosinphloxine stain. •
644
A U T O F L U O R E S C E N C E IN I D E N T I F I C A T I O N OF MYOCARDIAl, I N F A R C T S - CARLE
Figure 2. Same field and stain as in Figure 1, showing bright yellow -autofluorescence of necrotic myocardium. Olive green autolluorescence of non-necrotic myocardium. (• 200.)
yellow f l u o r e s c e n c e to b e c o m e a p p a r e n t save n o t i n g t h a t it has b e e n seen in patients with v e r y s h o r t clinical histories. Facilities h a v e n o t b e e n available t h u s f a r to s t u d y a n i m a l h e a r t s f o l l o w i n g c o r o n a r y ligation with interval e x a m i n a t i o n s to d e t e r m i n e h o w s o o n t h e yellow f l u o r e s c e n c e b e c o m e s manifest. T h e t e c h n i q u e is o f f e r e d ,as an effective m e t h o d f o r d e m o n s t r a t i n g m y o c a r d i a l necrosis a n d a p p a r e n t ly quite earl), necrosis. It has t h e a d v a n t a g e o f b e i n g simple, r e q u i r i n g o n l y an a d e q u a t e f l u o r e s c e n c e mic r o s c o p e with w h i c h to e x a m i n e r o u t i n e h e m a t o x y l i n a n d eosin stained sections.
ADDENDUM S u b s e q u e n t to writing the f o r e g o i n g t h e r e has b e e n o p p o r t u n i t y to e x a m i n e a u t o p s y tissues in a case o f systemic n e c r o t i z i n g arteritis u s i n g t h e a u t o f l u o r e scence t e c h n i q u e with r o u t i n e h e m a t o x y l i n a n d eosin s t a i n e d sections. F i b r i n o i d necrosis o f t h e i n v o l v e d vessel walls s h o w e d b r i g h t ),ellow a u t o f l u o r e s c e n c e m u c h like t h a t o f n e c r o t i c m y o c a r d i u m . R e c o g n i t i o n o f vascular nectosis does n o t p o s e the p r o b l e m t h a t is f r e q u e n t in r e c o g n i z i n g earl)' m y o c a r d i a l necrosis. E v e n so, t h e a t t t o f l u o r e s c e n c e t e c h n i q u e m i g h t be h e l p f u l at times in cases o f arteritis. I n this o n e case it brilliantly o u t l i n e d n e c r o t i c s m o o t h m u s c l e in the walls o f i n v o l v e d vessels.
ACKNOSVLEDGMENTS T h e author wishes to express Iris thanks to Doctors Charles E. Dunlap and William H: Sternberg of the Tulane University School of Medicine and to Doctor A. Gerson Hollander of the Veterans Administration Medical Center,
Roseburg, Oregon, for their encouragement and helpfid suggestions, to Mrs. Delila Randall for teclmical assistance, and to Mrs. Vernetta Calderwood for typing the manuscript.
REFERENCES 1. Wartman, W. B., Jennings, R. B., Yokoyama, H. O., and Clabaugh, G. F.: Fatty change of the myocardium in earl)' experimental infarction. A.M.A. Arch. Path., 62:318-323, 1956. 2. Pole)', R. W., Fobes, C. D., and Hall, M.j.: Fuchsinophilia in early myocardial infarction. Arch. Path., 77:325-329, 1964. 3. Niles, N. R., and Barnhouse, D. L.: The acid hematin stain and myocardial damage. Arch. Path., 83:407--410, 1967. 4. Lie, J. T.: Detection of earl)' myocardial infarction by the acid filchsin staining technic. Am. J. CIin. Path., 50.317-319, 1967. 5. Zugibe, F. T., jr., and Zugibe, F. T.: Fuchsinophilia and fuchsinorrhagia staining techniques. Arch. Path., 96:243245, 1973. 6. Nayar, A., and Olsen, E. G. J.: The use of the basic fi~chsin stain in the recognition of earl)" myncardial ischaemia. Cardiovasc. Res., 391:394, 1974. 7. Lie, J. T., Holley, K. E., Kampa, W. R., and Titus, J. L.: New histochemical method for morphologic diagnosis of earl)' stages of myocardial ischemia. Mayo Clin. Proc., 46:319327, 1971. 8. Yokoyama, H. O., Jennings, R. B., Clabaugh, G. F., and Wartman, W. B.: Histochemical studies of earl)' expcrimental myocardial infarction. A.M.A. Arch. Path., 59:347-354, 1955. 9. Shnitka, T. K., and Nachlas, M. M.: Histochemical alterations in ischemic heart muscle and early m)ocardial infarction. Am. J. Padl., 42:507-527, 1963. 10. Fine, G., Morales, A. R., and Scerpella, J. R.: Experimental myocardial infarction. Arch. Path., 82:4-8, 1966. I 1. Morales, A. R., and Fine, G.: Earl)" human myocardial infarctlon. Arcli. Path., 82:9-14, 1966. 12. Braunstein, tt.: Effect of postmortem interval on histochemi-
645
HUMAN PATHOLOGY-VOLUME
12, N U M B E R 7 July 1981
cal reactions of the myocardium. Am.J. Clin. Path., 49:224231, 1966. 13. Zugibe, F. T., Conley, T. L., Bell, P.,Jr., and Standish, M. L.: Enzyme decay curves in normals. Arch. Path., 93:308-311, 1972. 14. Zngibe, F. T., Bell, P., Jr., Conley, T., and Standish, M. L.: Determination of myocardial alterations at autopsy in the absence of gross and microscopic changes. Arch. Path., 81:409--411, 1966. 15. McVie, J. G.: Postmortem detection of inapparent myocardial infarction. Arch. Path., 23:203-209, 1970.
16. Sybers, H. D., Ashraf, M., Braitwaite, J. R., and Lock, M.-P.: Earl). myocardial infarction. Arch. Path., 93:49-54, 1972. 17. Nachlas, M. M., and Shnitka, T. K,: Macroscopic identification of earl)' myocardial infarcts by alterations in dehydrogenase activity. Am. J. Path., 42:379-404, 1963. 18. Bryant, R. E., Thomas, W. A., and O'Neal, R. M.: An electron microscopic study of myocardial ischemia in the rat. Circ. Res., 6:699-709, 1958. 19. WHO Scientific Group: The pathological diagnosis of acute ischaemic heart disease. WHO Technical Report Series No. 441, 1:27, 1970. Laboratory and Pathology Service Veterans Administration Medical Center Roseburg, Oregon 97470
U L T R A S T R U C T U R E OF MALIGNANT RHABDOID OF T H E K I D N E Y
TUMOR
A Distinctive Renal T u m o r of Children Joel E. Haas, M.D.,* Nigel F. Palme~, M.D.,"f Arthur G. Weinberg, M.D.,$ and J. Bruce Beckwith, M.D. w
Abstract An unusual and highly malignant childhood renal tumor has been noted among the specimens of the National Wihns' Tumor Study. Prominent nncleoli, PAS positive cytoplasmic inclusions, and light microscopic features suggestive of rhabdomyoblastic differentiation are l m l l m a r k s o f this t u m o r . U l t r a s t r u c t u r a l e x a m i n a t i o n o f 1 1 s p e c i m e n s r e v e a l e d t h e f i l a m e n t o u s
Accepted for publication May 6, 1980. This study was supl)orted ill part by grant CA-11~'22 from tile National Institutes of Heahh (National Wilms' Tmnor Study). *Assistant Professor of Pathology and Pediatrics, University of Washington School of Medicine.H cad, l'athology Division, Department of Laboratories, Children's Orthopedic Hospital and Medical Center, Seattle, Washil!gton. "~Assistant Professor of Pathology, Ohio State University College of Medicine, Cohm~ms, Ohio. TProfessor of Patholo~" and Pediatrics, University of Texas Heahh Science Center at Dallas. Director of Laboratories, Children's Medical Center, Dallas, Texas. w of Pathology and Pediatrics, Uriiversity of Washington School of Medicine. Director'of Laboratories, Children's Orthopedic Hospital and Medical Center, Seattle, Washington.
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HUMAN PATItOLOGY--VOLUME 12, NUMBER 7 July 1981