Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three levels of iron (5, 29, 307 ppm iron) were fed to rats from conception through the 18th day of lactation. Dams in the 5 ppm iron group and pups in the 5 and 29 ppm iron groups developed anemia characterized by lower hemoglobin and hematocrit values than control animals. Liver and spleen levels of iron in dams and pups in the 5 and 29 ppm iron groups were lower than in the 307 ppm iron groups. Milk iron was lower in the 5 ppm iron group than in the 29 and 307 ppm iron groups. Pups in the 5 ppm iron group had hyperlipidemia characterized by elevated serum triglycerides, cholesterol, and phospholipids. Milk lipids and post-heparin plasma lipoprotein lipase levels in pups did not differ among experimental groups. Triglyceride and CO2 production from [U-14C]glucose were significantly greater in the iron-deficient pups than in control pups. Hyperlipidemia in 18-day-old iron-deficient rat pups appears to be related to increased endogenous production of triglycerides.
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PMID:Iron deficiency hyperlipidemia in 18-day-old rat pups: effects of milk lipids, lipoprotein lipase, and triglyceride synthesis. 61 36

Cardiac norepinephrine (NE) levels exhibit a marked reduction in rats suffering from hemolytic anemia induced with antibodies against rat red blood cells. Administration of antiserum via tail vein resulted in a highly reproducible 70% drop in hemoglobin levels by 72 h. At 96 h cardiac NE levels were decreased by 67%; NE levels in vas deferens and submaxillary gland were not decreased. Within 10 days, both hemoglobin and cardia NE returned to near control levels. Hearts from anemic rats showed a 68% decrease in their ability to accumulate 3H-NE administered in tracer doses at 72 h of anemia. Cardiac NE turnover rates were increased 88% in 72 h anemic animals. These results are consistent with an anemia-induced activation of cardiac sympathetic nerves. Cardiac monoamine oxidase and dopamine-beta-hydroxylase activities in whole heart homogenates were similar in control and anemic animals at 72 h. These results suggest that NE depletion is not the result of decreased synthetic capacity of the nerves or degeneration of existing terminals. The data suggest that cardiac NE depletion during anemic stress is associated with the combined effects of increased NE release and a decrease in the effective NE uptake or binding capacity of sympathetic nerves. Anemia-induced depletion may, therefore, be different from the depletion associated with other forms of cardiovascular stress.
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PMID:Altered state of cardiac sympathetic nerves during immunologically induced anemia. 69 79

Norepinephrine metabolism was investigated in 6-wk-old male Swiss albino copper-deficient and copper-supplemented mice. Beginning 4 d after birth of pups, dams were fed a diet low in copper (Cu) (0.4 mg/kg) and offspring were weaned to this diet at 21 d of age. Half the dams and their respective offspring received Cu (20 micrograms/ml) in the drinking water (+Cu) and served as controls. Unsupplemented offspring (-Cu) had lower liver Cu levels, exhibited anemia, and had increased heart weights but normal body weights compared to +Cu mice. Urinary output of norepinephrine and dopamine was higher, whereas output of creatinine and epinephrine was not different in -Cu mice compared to +Cu mice. Both fractional and calculated turnover of norepinephrine following inhibition of tyrosine 3-monooxygenase by alpha-methyl-p-DL-tyrosine methyl ester (alpha-MT) was higher in hearts from -Cu mice than in those from +Cu mice. Hearts and spleens from -Cu mice appeared to have higher tyrosine 3-monooxygenase activity as judged by increasing rates of L-dihydroxyphenylalanine accumulation following injection of m-hydroxybenzylhydrazine (NSD-1015), an inhibitor of aromatic amino acid decarboxylase. Turnover rates of norepinephrine for cerebellum were not different between +Cu and -Cu mice. Loss of norepinephrine from adrenal glands of mice injected with alpha-MT was not observed in the 8-h period studied. The smaller norepinephrine pool observed in organs of -Cu mice may have resulted from lower synthesis due to limiting dopamine-beta-monooxygenase activity and to higher turnover.
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PMID:Copper-deficient mice have higher cardiac norepinephrine turnover. 230 15

1. The effect of maternal iron deficiency on milk composition and consumption by sucking rats was investigated. 2. Dams (n 42) were fed on semi-purified diets with either 8 (Fe-) or 250 (Fe+) mg Fe as ferrous sulphate/kg throughout gestation and lactation. Total milk intake was determined at days 7, 12 and 17 of lactation from the rate of disappearance of 3H2O from the total body water pool of pups. Measurements of milk constituents and Fe status of animals also were made. 3. Feeding the Fe- diet led to the development of anaemia in dams and pups and to growth retardation of sucking pups. 4. Concentrations of total lipid and Fe in milk from Fe- dams were significantly lower than those from Fe+ dams. Mean milk intakes (ml/d) of Fe-deficient pups were 21 and 28% less than intakes of Fe-sufficient pups on days 12 and 17 respectively. However, when expressed per kg body-weight, mean milk intakes were similar between groups on days 17 and 12 and increased by 47% in the Fe-deficient group on day 17 of lactation. 5. It is concluded that maternal Fe deficiency affects the quality of milk ingested by neonatal rats. However, Fe-deficient pups are at least partially able to compensate for reduced milk energy and nutrient contents by increasing intake in late lactation.
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PMID:Impact of maternal iron deficiency on quality and quantity of milk ingested by neonatal rats. 321 19

Administration of coenzyme Q10 to humans and animals has a beneficial effect on a number of cardiac diseases. The purpose of the present study was to determine if coenzyme Q10 treatment could ameliorate cardiac abnormalities associated with the carbohydrate x copper interaction in rats. Weanling male rats were provided with a copper-deficient diet (0.6 microgram Cu/g) containing either 62.7% starch (S-Cu) or fructose (F-Cu) for 5 wk. Half of the rats provided with the F-Cu diet were given daily oral supplements of 300 mg coenzyme Q10/kg body weight (F-Cu + Q). Heart hypertrophy, liver enlargement, or pancreatic atrophy were not affected by, nor was body growth or anemia improved by, supplementation with coenzyme Q10 when compared to rats fed only the F-Cu diet. Hearts from rats fed the F-Cu diet had severe inflammation, degeneration, fibrosis, and giant mitochondria with abnormal cristae. Hearts from F-Cu + Q rats had similar mitochondrial changes as the F-Cu rat hearts but without any apparent degenerative changes. None of the F-Cu + Q rats, but 30% of the F-Cu rats, died during the study as a result of heart rupture. These observations show that whereas coenzyme Q10 treatment did not prevent the cardiac hypertrophy of the carbohydrate x copper interaction, it did play a role in maintaining the integrity of the heart.
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PMID:Effect of coenzyme Q10 supplementation on cardiac hypertrophy of male rats consuming a high-fructose, low-copper diet. 768 27

Perinatal death is one of the major causes of calf mortality in Japanese Black beef herds. A series of experiments were carried out to determine causes of perinatal calf mortality in a region of northern Japan. An aetiological survey revealed that the incidence of perinatal mortality in 6475 calves was 4.5% and the majority of neonatal deaths were caused by weak calf syndrome. The weak calves delivered after a normal gestation period had a significantly lower body weight at birth than normal calves (P < 0.01), indicating growth retardation in the uterus during pregnancy. Haematological and histopathological examinations showed that the weak calves had anaemia characterized by a significant decrease of blood cell values and bone marrow hypofunction. The anaemia due to bone marrow hypofunction presumably caused intrauterine growth retardation of the foetus. Dams delivering the weak calves showed significantly lower serum concentrations of estrone sulphate during late pregnancy than those with normal calves (P < 0.01), indicating foeto-placental dysfunction as a possible cause of growth retardation. Effects of sires as well as the maternal family on the incidence of neonatal death and on the rate of weak calves in dead neonates were found in the survey. Intrauterine growth retardation associated with anaemia may be the most important cause of weak calf syndrome in Japanese Black beef calves. The bull and maternal family may also have an influence on the incidence of neonatal death.
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PMID:Intrauterine growth retardation as a cause of perinatal mortality in Japanese black beef calves. 1048 11

Diabetic angiopathy is a serious problem in antidiabetic therapy. We wanted to investigate whether treatment with the endothelin(A) receptor antagonist LU 135252 or with the angiotensin-converting enzyme inhibitor trandolapril might prevent angiopathy in long-term type I diabetes mellitus. Six groups of male Wistar rats were investigated: untreated age-matched control rats, healthy controls treated with trandolapril (0.3 mg/kg), healthy controls treated with LU 135252 (100 mg/kg), untreated diabetic rats, and diabetic rats treated with either trandolapril or LU 135252. Rats were rendered diabetic by injection of streptozotozin. Duration of the disease was 6 months. Thereafter, rats were sacrificed, and hearts, kidneys, and a mesenterial loop were removed. Hearts and kidneys were processed histologically; the mesenterial loop was perfused with saline at constant pressure for investigation of microvessels using microvideoangiometry while treated with either 30 mM KCl, 1 microM acetylcholine, or 1 microM sodium nitroprusside. All diabetic rats developed hyperglycemia without differences among these three groups. Diabetic rats exhibited marked anemia, which was significantly antagonized by both treatments. The heart capillaries/muscle fibers ratio was decreased significantly in diabetic animals, which was prevented fully by both treatments. Renal glomerular diameter was increased in diabetic rats. This was significantly antagonized by LU 135252 but not by trandolapril. Deposition of homogeneous eosinophilic material within the glomeruli was nearly completely prevented by LU 135252. The acetylcholine-induced vasodilation in mesenteric microvessels was significantly attenuated in diabetic rats, which was significantly antagonized by both treatments. We conclude that both angiotensin and endothelin seem to contribute to the development of diabetic angiopathy and that, in addition to angiotensin-converting enzyme inhibition, blockade of endothelin(A) receptors may be an interesting new approach to antiangiopathic therapy.
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PMID:Long-term effects of the endothelin(A) receptor antagonist LU 135252 and the angiotensin-converting enzyme inhibitor trandolapril on diabetic angiopathy and nephropathy in a chronic type I diabetes mellitus rat model. 1077 2

Iron deficiency anemia is the most common nutritional disorder in the world. Anemia is especially serious during pregnancy, with deleterious consequences for both the mother and her developing fetus. We have developed a model to investigate the mechanisms whereby fetal growth and development are affected by maternal anemia. Weanling rats were fed a control or iron-deficient diet before and throughout pregnancy and were killed at Day 21. Dams on the deficient diet had lower hematocrits, serum iron concentrations, and liver iron levels. Similar results were recorded in the fetus, except that the degree of deficiency was markedly less, indicating compensation by the placenta. No effect was observed on maternal weight or the number and viability of fetuses. The fetuses from iron-deficient dams, however, were smaller than controls, with higher placental:fetal ratios and relatively smaller livers. Iron deficiency increased levels of tumor necrosis factor alpha (TNFalpha) only in the trophoblast giant cells of the placenta. In contrast, levels of type 1 TNFalpha receptor increased significantly in giant cells, labyrinth, cytotrophoblast, and fetal vessels. Leptin levels increased significantly in labyrinth and marginally (P = 0.054) in trophoblast giant cells. No change was observed in leptin receptor levels in any region of the placentas from iron-deficient dams. The data show that iron deficiency not only has direct effects on iron levels and metabolism but also on other regulators of growth and development, such as placental cytokines, and that these changes may, in part at least, explain the deleterious consequences of maternal iron deficiency during pregnancy.
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PMID:Effect of iron deficiency on placental cytokine expression and fetal growth in the pregnant rat. 1180 70

Interstitial fluid fluxes are much greater in the fetus than in the adult, and filtration rates are increased over control in most tissues of the anaemic fetus. Increased capillary filtration may lead to cardiac oedema which, in turn, severely impacts cardiac function. Mechanisms that underlie these differences in flux are incompletely understood. One possible mechanism is an increase in capillary water permeability. Therefore, the goal of our study was to determine the level of expression of the water channel aquaporin 1 (AQP1) during cardiac development and in the anaemic fetal sheep heart. Hearts from chronically instrumented anaemic sheep fetuses and hearts from normal early fetal, late fetal, neonatal and adult sheep were used for Northern and Western analyses and immunohistochemistry. We found that AQP1 mRNA levels were lower in the young fetal left ventricle than in the adult left ventricle (P < 0.05). We also found that cardiac AQP1 expression was increased in anaemic fetuses compared to age-matched controls (P < 0.05). Expression of AQP1 in all groups was greatest in the microvascular endothelium. These data suggest that AQP1 plays an important role in the physiological accommodation to fetal anaemia.
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PMID:Anaemia stimulates aquaporin 1 expression in the fetal sheep heart. 1460 67

Dietary copper (Cu) deficiency was produced in Swiss albino mice to determine the temporal relationship between depletion of Cu and changes in the cardiovascular and nervous system. Dams were placed on a Cu-deficient diet 4 days after parturition. Half the dams were provided with deionized water and their offspring are referred to as Cu-deficient (-Cu). Half the dams were given cupric sulfate in their drinking water (20 microg Cu/mL) and their offspring are referred to as Cu-adequate (+Cu). At 6 weeks of age a sample of the -Cu mice were repleted with CuSO(4). Mice were sampled 1 day after birth and at weekly intervals for 7 weeks. Both +Cu and -Cu mice grew at the same rate: birth weight increased 16-fold at 6 weeks of age. Liver Cu more than doubled between 1 and 7 days of age. At 2 weeks of age -Cu mice were anemic (lower hematocrit and hemoglobin) and had lower liver Cu and plasma ceruloplasmin activity compared to +Cu mice. Liver Fe was not elevated in -Cu mice until 2 weeks after anemia developed. At weaning first signs of altered catecholamine metabolism included elevation of dopamine in both heart and spleen. Norepinephrine concentrations and content, in contrast, were not both lowered in -Cu mice until 5 weeks of age. Heart weight was first elevated in -Cu mice at 6 weeks of age and relative weight (mg/g body wt) at 4 weeks of age. Liver Cu concentration was lower in 1-week repleted mice than in +Cu mice. Anemia preceded the development of cardiac hypertrophy and altered catecholamine levels in -Cu mice.
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PMID:Development of copper deficiency in neonatal mice. 1553 31


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