Blood levels normal values

It is well known that hydrogen cyanide can be liberated during combustion of nitrogen containing polymers such as wool, silk, polyacrylonitrile, or nylons (1, 2). Several investigators have reported cyanide levels in smoke from a variety of fires (3, 4, 5). The levels reported are much below the lethal levels. Thus the role of cyanide in fire deaths would seem to be quite low. However, as early as 1966 the occurence of cyanide in the blood (above normal values) of fire victims was reported (6). Since then many investigators have reported elevated cyanide levels in fire victims (7-13). However, it has been difficult to arrive at a cyanide blood level which can be considered lethal in humans. In this report the results of cyanide analysis in blood of fire victims are reported as well as the possibility that cyanide may, in some cases, be more important than carbon monoxide as the principal toxicant in fire smoke. 

The biosynthesis and release of insulin by the pancreatic B cells (see p. 160) is stimulated by high blood glucose levels (> 5 mM). The insulin released then stimulates increased uptake and utilization of glucose by the cells of the muscle and adipose tissues. As a result, the blood glucose level falls back to its normal value, and further release of insulin stops. 

The concentrations of thorium in both hard and soft tissues of humans have been determined by a few authors. The concentration of thorium-232 in the blood of normal populations (not occupationally or otherwise known to be exposed to levels higher than background level of thorium) in the United Kingdom was 2.42 pg/L. The thorium-232 level in the urine of the same population was below the detection limit of 0.001 pg/L, although the concentration in the urine of exposed workers ranged from less than 0.001-2.24 pg/L. The highest value (2.24 pg/L) was found in a worker in the thorium nitrate gas mantle industry (Bulman 1976 Clifton et al. 1971). 

Such islet grafts permanently returned blood glucose levels in the diabetic animals to normal values. Even more encouraging, this treatment prevented development of diabetic-associated complications of kidney and eye function (which, in human diabetics, can lead to kidney failure and partial blindness). 

Normal blood levels of vitamin B12 are 2 x 1(T10 M or a little more, but in vegetarians the level may drop to less than one-half this value. A deficiency of folic acid can also cause megaloblastic anemia, and a large excess of folic acid can, to some extent, reverse the anemia of pernicious anemia and mask the disease. 

Normal values of aluminum in whole blood have been reported to range from 0.14 to 6.24 mg/L (ppm), and in plasma from 0.13 to 0.16 mg/L (ppm) (Sorenson et al. 1974). Normal values in serum have been reported at 1.46 and 0.24 mg/L (ppm), using neutron activation and atomic absorption analysis, respectively (Berlyne et al. 1970). A normal value of 0.037 mg/L (ppm) for serum using flameless atomic absorption analysis has also been reported (Fuchs et al. 1974). Drablos et al. (1992) analyzed aluminum serum levels in 230 nonexposed workers (controls) and reported a mean aluminum serum level of 0.005 0.002 mg/L (ppm). Research has shown that the levels of aluminum in the serum in the general population do not exceed 0.01 mg/L (ppm) (Cornells 1982). Nieboer et al. (1995) reviewed 34 studies on aluminum levels in serum or plasma, and also reported that aluminum serum levels in the general population were typically <0.01 mg/L (ppm). 

Dog No. 3 was omitted because of insufficient data. It is apparent that a marked uptake of ammonia occurs in tissues in metabolic acidosis. In alkalosis the uptake by tissues is only slightly greater than normal, and the arterial levels of ammonia are comparable with normal values. The elevation of blood ammonia which occurs on vigorous acidification of the animal might not be due to a drop in permeability with pH, but might be due to a phenomenon reported by Krebs and Henseleit (K4). Urea synthesis by liver slices is directly proportional to the pH and C02 content of the medium. Table 2, constructed from data reported in this paper, shows this dependence. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Blood tests were performed and had the following results hematocrit 33% (normal is 38%-45%) reticulocyte count 2.0% (normal is 0.5%-1.5%) mean corpuscular volume 90 (normal). A decreased erythrocyte sedimentation rate and a prothombrin time (PT) of 15 s (normal 11-13 s) were noted. A complete blood cell count values for total protein and albumin, ALT, and AST, fasting glucose, Hb-Alc, as well as amylase and lipase were within normal range. Plasma levels of vitamins A and K were below normal, and there was near absence of vitamin E. Dysmorphic red blood cells (RBC) with multiple thorny projections (acanthocytes) were present on a blood smear. All other laboratory tests and findings were within normal limits. 

No abnormalities were found in Brian s urine and his blood cell count was normal. However, his blood glucose was 8.1 mmol l-1 (normal value 3.5-6.7 mmol l-1) and a glucose tolerance test later indicated impaired glucose tolerance. Tests for plasma insulin and thyroid hormones (T3, T4 and TSH) showed normal levels. Two further tests were then performed. A 24-hour urine sample was collected and Brian s free cortisol excretion was found to be considerably higher than normal. A second test, the dexamethasone suppression test, was also carried out. In this test, the patient is given a dose of dexamethasone at 11 -12 p.m. and plasma cortisol is measured early next morning. 

Iron is rapidly mobilized from tissue stores (ferritin) during early pregnancy. This mobilization is reflected by decreases in serum ferritin levels. Ferritin levels may drop from a normal value of 60 ng/ml to about IS ng/ml during the first 2 months of pregnancy. The iron is being moMlized to expand the blood volume of the mother and to produce placental and fetal tissues. Apparently, the drop in serum ferritin in early pregnancy cannot be diminished by dietary iron supplements. 

Reports concerning metallothionein in plasma and urine of Cd-exposed persons are limited [47-49]. This is at least in part due to the fact that the accurate measurement of Cd and metallothionein levels in plasma appears to be difficult [50]. The concentration of metallothionein in urine and blood has to be measured using the Onosaka saturation method, radio-immunoassay (RIA) or enzyme-linked immunosorbent assay (ELISA). The detection limits in human serum and urine for metallothionein by RIA is 1 pg [50]. For ELISA the detection limits are higher. Normal values range between 0.01-1 ng/ml for serum and between 1-10 ng/ml for urine. Metallothionein concentrations in Cd-exposed workers are reported to vary between 2-11 ng/ml in plasma and 2-155 ng/ml in urine [47]. 

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