Arteriosclerosis In Rabbits Research Articles

Pulmonary arteriosclerosis in rabbits receiving a single intravenous infusion of autologous thrombus

Pulmonary arteriosclerosis in rabbits receiving a single intravenous infusion of autologous thrombus

Cellular and humoral immune responses to heat shock protein 65 are both involved in promoting fatty-streak formation in LDL-receptor deficient mice

OBJECTIVESThis study was designed to determine the role of cellular and humoral immune responses to heat shock protein 65 (HSP65) in murine atherosclerosis.BACKGROUNDInflammatory processes appear to influence the progression of atherosclerosis. Immunization with HSP65 was previously shown to induce arteriosclerosis in rabbits and to enhance fatty-streak formation in mice. However, it has not been demonstrated directly whether HSP65-reactive antibodies and lymphocytes are separately capable of influencing lesion formation.METHODSLow density lipoprotein-receptor deficient (LDL-RD) mice were immunized with HSP65 or control bovine serum albumin (BSA). Lymph-node cells, splenocytes and immunoglobulin G (IgG) were obtained from the immunized mice and transferred separately to six groups of syngenic LDL-RD mice.RESULTSAdoptive transfer of HSP65-reactive lymph node cells increased fatty-streak formation in comparison with mice treated with BSA-primed cells. Similarly, transfer of splenocytes reactive with HSP65 led to enhanced fatty-streak generation compared with mice injected with BSA-sensitized splenocytes. Repeated intraperitoneal administration of IgG from serum of HSP65-immunized mice (every 10 days) enhanced fatty-streak formation in mice in comparison with their anti-BSA-IgG injected littermates.CONCLUSIONSAntibodies and lymphocytes reactive to HSP65 promote fatty-streak formation in mice, providing direct evidence for the proatherogenic properties of cellular and humoral immunity to HSP65.

Inhibition of transplant coronary arteriosclerosis in rabbits by chronic estradiol treatment is associated with abolition of MHC class II antigen expression.

Accelerated coronary arteriosclerosis is a major complication in long-term survivors of cardiac transplantation. Estrogen prevents transplant arteriosclerosis in experimental cardiac and aortic allografts and may act by an immune mechanism. New Zealand White rabbits immunosuppressed with cyclosporine were recipients of cardiac allografts from Dutch Belted rabbits. The recipients received either estradiol or placebo daily until they were killed 6 weeks later. Histological cross sections of the cardiac allograft were used for quantification of major histocompatibility complex (MHC) class II antigen expression, T lymphocytes, and macrophages by immunohistochemistry using monoclonal antibodies. MHC class II antigen expression was not detectable in allograft coronary arteries from any of the estradiol-treated recipients, whereas this antigen expression was present in the allograft coronary arteries from all the placebo-treated recipients. Macrophage and lymphocyte infiltration of the allograft coronary artery myointima was significantly less frequent in the estradiol-treated group. Rejection was moderate but slightly less in the estradiol-treated group. These findings were associated with a 60% decrease in allograft coronary artery myointimal thickening (determined by morphometry) in the estradiol-treated compared with the placebo-treated group. Estradiol treatment of cardiac allograft recipients abolishes MHC class II antigen expression in the coronary arteries and decreases macrophage infiltration in all three layers of the vessel wall, whereas T-lymphocyte infiltration is decreased only in the myointima. These findings are associated with estradiol inhibition of myointimal proliferation. Thus, estradiol treatment may have a beneficial effect on graft arteriosclerosis through immune mechanisms.

Injury and repair of smaller muscular and elastic arteries

Indirect immunoperoxidase staining for fibrinogen/fibrin and fibronectin was performed on normal and healing arterial tissue of muscular and smaller elastic arteries. Fibronectin was observed in the wall of the normal arteries, whereas fibrinogen/fibrin could not be demonstrated. Fibronectin was observed in the intima as well as the media deposited in a similar fashion in the femoral and carotid artery during repair. Apart from the early occurrence of fibrin/fibrinogen in the media of both arteries the distribution of fibrinogen/fibrin and degradation products differed. In the femoral artery a progressively weakening positive reaction for fibrinogen/fibrin and degradation products towards the lumen was observed in the intima and the media 7 and 14 days after the lesion. By 28 days the reaction in the media was negative. No thrombus formation was observed. In contrast, all the specimens examined from the common carotid arteries were obliterated by luminal thrombi 28 days after the lesion. The thrombus as well as the damaged intimal thickening and the compressed media were loaded with fibrinogen/fibrin and degradation products. The deposition of fibronectin, fibrinogen, and degradation products in the carotid artery was similar to that previously reported in experimental aortic arteriosclerosis in rabbits as well as in giant cell arteritis.

PATHOLOGY OF EXPERIMENTAL PULMONARY BONE MARROW EMBOLISM

The author investigated the morphogenesis of pulmonary arteriosclerosis in rabbits at 2 days to 3 months after the infusion of sliced fresh allogeneic bone marrow (500 mg) into the marginal ear vein of 87 rabbits. After 2 to 7 days, granulation tissue was formed in the embolized bone marrow, and new endothelial cells appeared on the surface resulting in recanalization. By 2 weeks, embolized bone marrow developed into fibrous and fibro‐fatty plaques in the arterial wall. Moreover, from 4 weeks on, smooth muscle cells and elastic fibers proliferated in the emboli just beneath the new endothelial lining. The intima of non‐embolized small arteries showed circumferential fibroelastosis, as the result of arteritis and followed by proliferation of medial smooth muscle cells, with narrowing of vascular lumen. The medial smooth muscle cells play an important role in the morphogenesis of pulmonary arteriosclerosis in bone marrow embolism. Pulmonary arterial pressure gradually increased 1 month as well as 3 months after the infusion. It Is considered that narrowing of the vascular lumen resulted from post‐embolic pulmonary arteriosclerosis may produce persistent pulmonary hypertension.

家兎硬化冠動脈の構築障害

We investigated the effect of an anti-arteriosclerotic agent Elastase (Elaszym®) on coronary arteriosclerosis in rabbits by histochemical observation and quantitative analysis of smooth muscle cell (SMC), elastin (EL), collagen (CL), acid mucopolysaccharides (AMPS) and glycoprotein (GP) in coronary media. The subjects were male 38 month-old Japanese White Rabbits. Of the 23 rabbits studied, 8 were healthy (H group), 9 had coronary arteriosclerosis (S group), and 6 had coronary arteriosclerosis and were administered with the Elaszym (A group). Arteriosclerotic rabbits were prepared by the combination of 3 method, the hypoxic method in which N2 gas inhalation was given to the rabbits daily for 2 consecutive weeks, the injury method in which intramuscular administration of norepinephrine was given for 22 weeks, and the preparation method of coronary intimal lesion in which oral administration of cholesterol (0.5g/day) was given for 22 weeks. The rabbits in A group were given Elastase at the dose of 6 cap/day (10.800 EU) once a day for 22 consecutive weeks starting simultaneously with the load of above mentioned preparation. On completion of the treatment, all the rabbits were terminated and histologic specimen was picked up from the left coronary tissue with myocardium for subsequent observation and quantitative analysis of above mentioned 5 components in proximal coronary artery by microspectrophotometry. Comparisons were made of histologic image and quantity of each component among these 3 groups, furthermore, each group was comprehensively evaluated for its characteristics by the principal component analysis of change in 5 components.S group demonstrated decrease in SMC because of hypertrophy, swelling, atrophy, necrosis and extinction. Uniform distribution of EL and CL was observed due to swelling decomposition and local abnormal hyperplasia. More active hyperplasia was recognized in AMPS and GP than in the case of EL or CL as a repair mechanism of damage. There appeared stratified delamination of elastic fibers from internal elastic membrane and it caused hypertrophy of intima as well as diminution on plasmotomy of elastic membrane. In A group, every kind of impairment as observed in S group was suppressed and the basic architecture of coronary artery was well maintained. The values of SMC, EL, CL, AMPS, GP were 65.4, 9.6, 25.7, 14.4, 22.8%E respectively in H group, 46.7, 12.2, 35.6, 20.2, 31.6%E respectively in S group, and 62.6, 11.3, 29.1, 11.8, 26.2%E respectively in A group. In S group, significant decrease was observed in SMC value with significant increase in EL, CL, AMPS and GP compared with those in H group. In A group, these changes were significantly suppressed compared with those in S group. Individual scores in the 1st and 2nd components were plotted in the two-dimensional coodinates for each case. The dots of H group were distributed in the left narrow range while the dots of S group were distributed in the right wide range of the coodinates. Thus these 2 groups showed quite different architectural characteristics of artery. However, the distribution of A group was observed in the left narrow range similarly to that of H group. Therefore, it can be considered that the rabbits in A group have architectural characteristics closely akin to those in H group. These findings suggests an inhibitory effect of Elaszym on development of coronary arteriosclerosis.

Aortic proline hydroxylase in hypoxia induced arteriosclerosis in rabbits

Experimental arteriosclerosis was induced in male albino rabbits by daily exposure to acute hypoxia for 14 days. Protocollagen proline hydroxylase was increased 2-fold in thoracic and 4-fold in abdominal segments of aorta when the experiments were conducted during periods of maximum animal sensitivity. No evidence of vascular damage and no increase in aortic proline hydroxylase were observed when the experiments were conducted during the shedding period of the rabbit. The increase in proline hydroxylase activity appears to be specifically related to the vascular injury produced by acute hypoxia since liver and lung enzyme levels are not elevated. These data support the suggestion that elevated aortic proline hydroxylase activity may be an early biochemical lesion in injury-induced plaque formation.

Spontaneous aortic arteriosclerosis in rabbits of the Danish country strain

The occurrence of spontaneous arteriosclerosis of the aorta was studied in male albino rabbits of the Danish Country strain. The frequency of gross arteriosclerosis was compared with the frequency of spontaneous microscopic alterations in aorta. The distribution and frequency of gross aortic arteriosclerosis in 366 rabbits were as follows: the arch of aorta 10%, the descending thoracic aorta 2% and the abdominal aorta no gross changes. These frequencies are rather low in comparison to the frequency of spontaneous gross aortic arteriosclerosis in most other rabbit strains. A detailed investigation of the extent and type of the microscopic changes was done in 30 rabbits. In contrast to the gross changes the microscopic alterations showed the following frequencies: the arch of aorta 90%, the descending thoracic aorta 13% and the abdominal aorta 17%. Thus there is a great discrepancy between the frequencies of spontaneous gross and microscopic changes within the individual parts of aorta. The spontaneous aortic changes were similar to those described in a series of different types of experimental arteriosclerosis. The frequent occurrence of these microscopic alterations in the aortic arch makes this part of aorta unsuited for studies on experimental arteriosclerosis. The studies should be restricted to the descending thoracic aorta and the abdominal aorta which exhibit a low frequency of spontaneous gross and microscopic alterations.

Relative immunity to arteriosclerosis in rabbits during the hair-shedding period

The extent and severity of arteriosclerosis in rabbit aorta induced by exposure to short periods of systemic hypoxia for two weeks were studied during the hair-shedding period (September through December). Two series of experiments were carried out in relation to two different shedding periods with an interval of 1 year. The entire study involved 152 rabbits. Three experiments were performed in shedding and three in nonshedding periods. While shedding, the rabbits exposed to hypoxia developed slight gross arteriosclerosis in contrast to the severe arteriosclerosis that developed while the animals were not shedding. Qualitatively, the gross and microscopic changes did not differ during and outside the shedding periods. Comparison of the biochemical changes in the aortic acid mucopolysaccharides and collagen induced by the systemic hypoxia during the shedding and nonshedding periods showed no statistically significant differences. The resistance to arteriosclerosis during shedding may be due to hormonal factors, which also may be of importance to the development of arteriosclerosis in other species. Furthermore, the phenomenon has to be taken into consideration in experimental studies of rabbit arteriosclerosis.

Prevention of Arteriosclerosis in Rabbits on a Hypercholesterolemic Diet by Ileal Bypass.

s1 October 1964Prevention of Arteriosclerosis in Rabbits on a Hypercholesterolemic Diet by Ileal Bypass.Henry Buchwald, M.D.Henry Buchwald, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-798_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA group of 12 New Zealand white rabbits with an average whole blood cholesterol of 86 mg/100 ml and a group of 6 New Zealand white rabbits, which had previously undergone ileal bypass and had an average whole blood cholesterol of 69 mg/100 ml, were simultaneously placed on a 2% cholesterol diet for 4 months. The ileal by-pass was performed from the bowel midpoint to the cecum and therefore excluded the distal five-sixths of the ileum, as well as the ileocecal valve. At the end of the 4-month test period, the nonoperated group had a whole blood cholesterol average of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Minneapolis, Minn. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 798-799KeywordsBloodCecumCholesterolDietHematologic testsIleumRabbits Issue Published: 1 October 1964 PDF DownloadLoading ...

The Effect of the Active Form of Vitamine B<SUB>6</SUB> on the Experimental Arteriosclerosis in Rabbits

Purpose Since Rinehart has succeeded to cause arteriosclerosis in monkeys by administration of B6 deficient diet, many studies on the relationship between B6 and arteriosclerosis have been reported. Recently in our clinic, it was succeeded to cause arteriosclerosis in B6 deficient monkeys. Many factors to cause arteriosclerosis have been considered but they have not been clarified yet. However, it is supposed that metabolic disturbances of the high energy phosphate due to B6 deficiency may accelerate the occurrence of arteriosclerosis. Since Hahn has reported the relationship between Lipemia Clearing Factor (LCF) and arteriosclerosis, many similar studies have been reported. In one of them, it was reported that LCF was decreased by B6 deficiency and could be restored by the administration of pyridoxal phosphate (PAL-P). It may suggest there is a close relationship between B6 (active form) and LCF. Considering of these observations, the author has studied the effect of B6 on the experimental arteriosclerosis in rabbits. Method s Both preventive and therapeutical experiments were performed. Preventive experiment : Pyridoxine (PIN), PAL-P or pyridoxamine phosphate (PAM:-P) (respectively 10mg/day) was injected, while administering lanolin in rabbits. The data were compared with those of the noninjected control group. Therapeutic experiment : 1) In rabbits, which were made arteriosclerotic by lanolin administration for 1 6 weeks, PIN, PAL-P or PAM-P was injected and usual diet was given for 1 2 weeks. And the data were compared with those of the noninjected group. 2) In rabbits, which were made arteriosclerotic by the same procedure, the effects of the combined treatment with PIN or PAL-P injection and lanolin feeding for 12 weeks were studied. In the above experiments, serum total cholesterol and phospholipids were determined and then, the animals were killed after 12 weeks and investigated histologically.

The hypocholesterolemic effect of nicotinic acid and its relationship to the autonomic nervous system.

Nicotinic acid, well known physiologically and chemically as a vitamin if administered in small quantities, has many interesting additional properties when given in relatively large amounts. Altschul (2, 3) found that it markedly decreased the levels of cholesterol in rabbits made hypercholesterolemic by diet, and Altschul, Hoffer and Stephen (4) found that in divided dosages of three grams per day this vitamin produced appreciable decreases in the cholesterol levels of healthy young subjects and in patients from a general hospital. The decrease was related linearly to the initial cholesterol levels while the percentage decrease increased as the initial cholesterol levels were elevated. The incorporation of nicotinic acid into atherogenic diets inhibited the development of arteriosclerosis in rabbits (Altschul (2)). Of seventeen animals tested, two showed intense arteriosclerosis, six showed mild change, and nine showed no arteriosclerosis. Without nicotinic acid, at least thirteen of the rabbits would have had severe arteriosclerosis on the basis of many previous studies by Altschul (2) and by many other investigators.

Aortic arteriosclerosis in rabbits: Maegraith, B. G., and Carleton, H. M.: J. Path. and Bact. 48: 33, 1939

A method is described, by means of which the glycosides digitoxin, digitoxigenin-bis-digitoxoside, digitoxigenin-mono-digitoxoside, digoxin, digoxigenin-bis-digitoxoside, digoxigenin-mono-digitoxoside as well as the genins digoxigenin and digitoxigenin are isolated from animal tissue (the blood and heart of rats) after extraction by chloroform and cleaning through Sephadex G 200 on the basis of thin-film chromatography ; these compounds can be prepared separately.Compared with conventional methods, this procedure is about one decimal power more sensitive and permits the isolation as well as the test reaction of each 25 ng of the mentioned compounds in the heart or the blood of an animal.

Aortic arteriosclerosis in rabbits

The Journal of Pathology and BacteriologyVolume 48, Issue 1 p. 33-40 Article Aortic arteriosclerosis in rabbits B. G. Maegraith, B. G. Maegraith Sir William Dunn School of Pathology and the Department of Physiology, OxfordSearch for more papers by this authorH. M. Carleton, H. M. Carleton Sir William Dunn School of Pathology and the Department of Physiology, OxfordSearch for more papers by this author B. G. Maegraith, B. G. Maegraith Sir William Dunn School of Pathology and the Department of Physiology, OxfordSearch for more papers by this authorH. M. Carleton, H. M. Carleton Sir William Dunn School of Pathology and the Department of Physiology, OxfordSearch for more papers by this author First published: January 1939 https://doi.org/10.1002/path.1700480105Citations: 6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume48, Issue1January 1939Pages 33-40 RelatedInformation

Cholesterol-induced arteriosclerosis in rabbits, with variations due to altered status of thyroid: Menne, Frank R., Beeman, Joseph A. P., and Lobby, Daniel H.: Arch. Path. 24: 612, 1937

Cholesterol-induced arteriosclerosis in rabbits, with variations due to altered status of thyroid: Menne, Frank R., Beeman, Joseph A. P., and Lobby, Daniel H.: Arch. Path. 24: 612, 1937

The Pituitary Factor in Arteriosclerosis Its Experimental Production in Rabbits

Article1 December 1930The Pituitary Factor in Arteriosclerosis Its Experimental Production in RabbitsROBERT C. MOEHLIG, M.D., EUGENE A. OSIUS, M.D.ROBERT C. MOEHLIG, M.D.Search for more papers by this author, EUGENE A. OSIUS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-6-578 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptExperimental production of arteriosclerosis in rabbits has been accomplished by several workers. Anitschkow and Chalatow1, Bailey2 and others, have used various sorts of diets high in fats or fat-like substances to produce these changes.Certain facts led us to approach the problem from a new angle. The relationship between the pituitary gland and fat and carbohydrate metabolism suggested that the pituitary secretion might be concerned in arteriosclerosis.While the exact pathogenesis of arteriosclerosis is somewhat in doubt, nevertheless the cholesterol infiltration of the blood vessels is definitely established.The importance of the suprarenal cortex in cholesterol metabolism is well recognized....References ANITSCHKOWCHALATOW NS: Uber experimentelle Cholesterinsteatose und ihre Bedeutung für die Entstehung einiger. pathologischer Prozesse. Centralbl. f. allg. Path. u. Anat. 24:1, 1913. Google Scholar BAILEY CH: Atheroma and Oother Lesions Produced in Rabbits by Cholesterol Feeding. J. Exper. Med. 23:69, 1916. CrossrefMedlineGoogle Scholar GOLDZIEHER M: The Adrenals. The Macmillan Co., New York, 1929, p. 250-251. Google Scholar MOEHLIG RC: A Study of the Ductless Glands: Detroit Med. J. 14:268, 1914; Ductless Gland Cell Control, Monograph, 1918, p. 87; Selective Tissue Action of Posterior Pituitary Gland: Med. Jour. and Rec. 120, (August 20) 55, 1924. Selective Action of the Suprarenal Cortex on Mesothelial Tissues: Am. J. M. Sc. 168, 553, 1924. Embryohormonic Relations of the Pituitary Gland to Mesenchymal Tissues; Ann. Int. Med. 1:563, 1928. Embryohormonic Relations of the Suprarenal Cortex to Mesothelial Tissues: Ann. Int. Med. 1:828, 1928; Pituitary Gland and Suprarenal Cortex, Arch. Int. Med. 44:339, 1929. Google Scholar MOEHLIGAINSLEE RCH: Posterior Pituitary Extract and Cholesterol Metabolism, Am. J. Physiol. 80:649, 1927. Pituitary Gland and Cholesterol Metabolism: Ann. Clin. Med. 5:772, 1927. CrossrefGoogle Scholar KROGH A: The Capillaries. Yale Press, 1922. Google Scholar SHAPIRO S: The Relation of Certain Glands of Internal Secretion to the Development of Atherosclerosis. Endocrinology, 11:279, 1927. CrossrefGoogle Scholar SACKETT GE: Modification of Bloor's Method for Determination of Cholesterol in Whole Blood or Blood serum. Jour. Biol. Chem. 64:203, 1925. CrossrefGoogle Scholar ISCOVESCO H: Sur les propriétés d'un lipoïde Extrait de la partie corticale des capsules surrénales, Compt. rend. Soc. Biol. 75:510, 1913. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Detroit, Michigan*This work was carried out with the assistance of the technical staff of Harper Hospital laboratory. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byArteriosklerose und Innere SekretionDie Krankheiten des HypophysenzwischenhirnsystemsDie Bedeutung der Hypophyse für die Pathologie der BlutgefäßeCongenital medial sclerosis of the coronary artery 1 December 1930Volume 4, Issue 6Page: 578-592KeywordsBlood vesselsCarbohydrate metabolismCholesterolDietFatsPathogenesisPituitary glandRabbitsResearch laboratories ePublished: 1 December 2008 Issue Published: 1 December 1930 PDF downloadLoading ...

THE ROLE OF THE POSTERIOR PITUITARY GLAND IN THE EXPERIMENTAL PRODUCTION OF ARTERIOSCLEROSIS*

Periodically sufficient data accumulate to permit us to view certain unsolved problems from a new angle. Such a condition, I believe, now exists in the problem of arteriosclerosis. In this paper will be shown that the posterior pituitary gland secretion is an important factor in the experimental production of arteriosclerosis. Experimental production of arteriosclerosis in rabbits has been accomplished by several workers using various sorts of diets high in fats or fat-like substances to produce these changes. The relationship between the pituitary gland and carbohydrate and fat metabolism suggested that the pituitary secretion might be concerned in arteriosclerosis. Likewise the pressor effect of posterior lobe extract on the blood vessel wall was another consideration that suggested the use of this substance. At present it is recognized that fat metabolism is linked with the production of arteriosclerosis. That an intimate relation exists between cholesterol and atheromatous changes in the blood vessels...

Note on Arteriosclerosis in Rabbits Caused by Some Samples of Uranium Nitrate

Note on Arteriosclerosis in Rabbits Caused by Some Samples of Uranium Nitrate

Note on Arteriosclerosis in Rabbits Caused by Some Samples of Uranium Nitrate

Note on Arteriosclerosis in Rabbits Caused by Some Samples of Uranium Nitrate

Kidney hypertrophy produced by diets unusually rich in protein

In preliminary reports Osborne and Mendel demonstrated that rats can grow to considerable size on diets consisting of nine-tenths or more of protein, provided that they receive a suitable supply of vitamins A and B as well as of inorganic salts. Both casein and washed meat were used as the sources of the protein. Similar tests have since been made with rations containing about 75 per cent. of protein in the diet. It seemed unlikely that rations on which young rats grew from 60 to 260 grams could be extremely harmful to the organism. However Squier and Newburgh have concluded, in harmony with a widespread popular belief, that “a high protein diet in man is a renal irritant” and Newburgh and Clarkson have described the production of arteriosclerosis in rabbits on “diets containing 27 and 36 per cent. of protein derived chiefly from beef.” For this reason it seems worth while to give a preliminary account of our observations on some of the organs of rats growing on our diets very high in protein. The only striking change was found in the kidneys, which in the animals on the high protein diets were greatly hypertrophied. The average weight of the kidneys was almost twice that of the kidneys of control animals and their size about one-third greater. Microscopic examination showed no changes of an inflammatory or degenerative nature. The exact histological condition of the kidneys and of the other organs will be reported in full in asubsequent paper. Hypertrophy of the kidneys existed without hypertrophy of the heart. The ratio of the weight of the heart as well as of the liver to the body weight was about the same in the animals fed the high protein diets as in the control animals. The ratio of the weight of the kidneys to the body weight in the animals on the high protein diets was, on the average, almost double that of the control animals.