Document Mobz7LJGvqV8L0kqqbGEgvp1y

not designed to investigate this speculation, but it is now possible to examine this question experimentally, (151 references) 62. Rilssel, H. (Veterinary College, Hannover, Germany): Uber die Bleiverteilung in Leber bei Vergiftung und die Probeentnahme zur chemiscben Analyse, (DISTRIBUTION OF LEAD IN THE LIVER IN POISON ING AND REMOVAL OF SAMPLES FOR ANALYSIS.) Deutsche TierSrztliche Wochenschrift 74, No. 4:96, 1968. This is a brief summary of the author's dissertation (Abstr. No, 61 ) de signed particularly to guide the veterinarian in the diagnosis of Pb poi soning in livestock. The directions for the removal of samples specify that 4 samples of 100-200 g he removed from different parts of the liver, peripheral and central regions. Diseased tissue should not be used for analysis. The directions for the analyst should identify each section and an average Pb content should be determined for all 4 parts. Schlaepfer, W.W. (Washington Univ., St. Louis, Mo.): EXPERIMENTAL LEAD NEUROPATHY: A DISEASE OF THE SUPPORTING .CELLS IN THE PERIPHERAL NERVOUS SYSTEM. Journal of Neuropathology and Experimental Neurol- r ogy 28:401-18 (July), 1969. / Previous studies of experimental Pb neuropathy have shown a poor correlation between the amounts of axonal and segmental damage. In fact, axonal degen eration has been found in the absence of segmental lesions among individual animals and in certain species such as the rat. Eighteen male Sprague-Dawley rats weighing 200-250 g each were fed 1% Pb acetate solution at a daily dose of *v60 ml/rat, over a period of 3-18 mo. srs No clear-cut neurological deficits were observed during the course of the experiment although 4 rats died from unknown causes. Pairs of the remain ing rats were sacrificed after 3, 4, 5, 6, 9, 12 arid IS mo. Three rats of comparable weight were used as controls. Under ether anesthesia the descend ing aortas were perfused with Ringer's solution containing glutaraldehyde and formalin. The following nerve structures were excised and prepared for examination with 0s-04, and stained with various techniques: sciatic_and tibia! nerves, spinal ganglia, posterior and anterior.rQots of the lumbar anSTsacral regions7~and lumbar spilial'cor'd'. Minced tissues from peripheral nerves, ganglia and anterior horns of the lumbar cord were fixed in O3-O4, and ultrathin sections of Epon-embedded tissue were examined with an elec tron microscope. Sections of unosraicated tissues were examined unstained, others were contrasted with Pb citrate of uranyl acetate. As illustrated in 21 microphotographs, prominent changes were evident in the supporting cellular elements of peripheral nerves, spinal nerve roots and spinal ganglia. Pathological alterations of the Schwann cells were maniJj fested by widespread segmental demyelination and remyelination in the periph-jj eral nerves and spinal nerve roots. A' selective involvement of the capsular cells in the spinal ganglia was characterized by a proliferation of these cells and an accumulation of numerous dense bodies within their cytoplasm. These dense bodies contained a particulate material which had the electron density characteristics of a heavy metallic substance, compatible with Pb, ` in unosmicated and unstained tissue. Similar cytoplasmic dense bodies have been observed in the renal proximal tubular cells, another site of selective Susceptibility to Pb toxicity. These findings suggest the possibility of a direct intervention of Pb in the metabolism of the capsular cells. An 25 N37516 Abstr* 64-66 IV* Ofeservattons on Warm-Blooded Animals "increase of nearofiiaments and a relative paucity of endoplasmic reticulum was seen in some associated sensory ganglion cells. Here striking neuronal alteration occurred in the diafcal peripheral nerves and in the posterior nerve roots in the form of Wailerian degeneration. The accumulation of ^ncid^pfLOSph activity in the nodal axoplasm of some peripheral nerve fibers appeared as an early form of axonal injury and attested to a special reactivity of the nodal region. The author concludes by stating that the coexistence of segmental demye- lination and Wailerian degeneration in the peripheral nerves of pb neuropathy has been postulated to result from a common metabolic lesion of the support ing Schwann and capsular cells- This same pattern of pathological changes has been noted in some human polyneuropathies and may reflect a similar pathogenesis. (58 references) 64* Shiraishi^ Yf (Nihon 0niv., Japan): (EXPERB^NTAL STUDIES ON THE / DUP050044011 Abstr. 187^189 IV > Observations on Warm-Blooded Animals basis of measurements over the thorax during a 150~day retention intervals Values for the half-life of clearance were 235 and 290 days, respectively, for the long-term component. The relative concentrations of 228xh, 224^a, and 212pB in tissues at ''steady state11 were expressed in terms of the initial LRT burden extrapolated from the long-term clearance phase/ These concen trations gf the daughters were discussed in terms of their application to the estimation of industrial exposure to Th02 and the calculation of radia tion dose subsequent to Th02 incorporation. (From Nuclear Science Abstracts 23:Abstr. No. 50280, 1969) /. 187. Bolanowska, W. > and Piotrowski, j, (Inst, pldd. Praey, Lodz, Poland): Kinetyka rozmieszczania i wydalania oZowiu (Pb-210) u szczurow. 11. Wydalanie Jednorazowej dawki dozylnej oZowiu. (KINETICS OF DlSTRIBIjTlpN AND EXCRETION OF LEAD- (2ljb) IN RATS, II. EXCRETION OF A SINGLE INTRAVENOUS LEAD DOSE.) Medycyna Praey 19, No. 2:133. 42, 1968, ` Adult albino male rats weighing 200-250 g^were injected into the tail vein a Pb nitrate solution labeled with 21-0p^/in a single dose of 1,0 and 0,1 mg/ kgK, The Pb excretion in urine and fecfl was observed during 98 days. The coursre of excretion is presented. Thf# excretion of Pb in feces is a factor that: especially decides the amount gi total excretion. In the 3 mo period 2/3 of the'^b dose was totally excreted. No essential differences iri Pb excretion were, seen after administration of 2 different doses of 1.0 and 0.1 mg/kg; nevertheless the exertion of Pb in urine was somewhat higher for the lower dosex For the kihetic description of Pb excretion, the power and exponential models were used. The extrapolation of excretion equations to infinity seems to cbnfirnj/the hypothesis of the existence of an unex changeable pool the size of which is evaluated as being about 20% of Pb dose* (From authors1 summary) 188. Gabbiani, 0, (Upiv, Montreal, Canada): EFFECT OF PHOSPHATES UPON EXPERIMENTAL SXIN CALCINOSIS. Canadian journal of Physiology and / Pharmacology 44:203-7 (Mari), 1966. Three experiments using 17 groups, each group including 10 female SpragueDawley rats (Holtzpihn strain) , mean bddy weight 99 g, were conducted to test effects of phosphates upon calcification produced by treatment with Pb acetate and polyriiyxin (PMX). In the 1st experiment all rats received a 4 mg dose of Plyacetate in 1 ml of disti1led\water intravenously (iv) and 30 pg PMX in Q .5 mi water subcutaneously (sc)Ssand then iv injections of 8 mg adenosipe triphosphate (ATP), 7 mg Na pyrophosphate, 7 mg Na metaphosphate, 25 mg Na orthophosphate dibasic, and 13\jg Na citrate. In the 2nd experiment each rat'received 4 mg Pb acetate iv, apd sc 30 pg PMX alone or rmixed with 1 of the following: 5 mg ATP, 2 mg"N^ pyrophosphate, 2 mg Na orthophosphate monobasic, 2 mg Na orthophosphate dibasic, or 10 mg Na citrate* In the 3rd experiment each animal received 2 mg Pb acetate iv; and sc 30 pg PMX, 12 mg Na orthophosphate monobasic, and 12 mg PMX plus 12 mg Na orthophosphate dibasic. After 3 days the rats were sacrificed. Results showed that calcinosis was inhibited by ATP and pyro- and metaphosphate, but aggravated by mono- and di-basic orthophosphate, (24 refer ences) 189* Go^dzik-Zolnierkiewicz, T., and Moszynski, B, (Otolaryngological 80 DUP050044012 IV. Observations on Warm-Blooded Animals Abstr. 190 Clinic, Warsaw, Poland): VIII NERVE IN EXPERIMENTAL LEAD POISONING. Acta Oto-Laryngologies 68:85-9 (July-Aug.), 1969. 9^ Forty young guinea pigs (weight, 300-350 g) were given ip injections of 1% solution Ph acetate at a total dose of 300 fag/kg given once a week for 7 wk; 10 guinea pigs served as controls. Eight of the Pb group died before the end of the experiment; the remaining were weak, lost weight, and growth was inhibited. The 5 that were able to run slowly appeared to have mild paraly sis of their hind limbs. The animals were killed at the end of the 7-wk period, the temporal bones were removed for histologic examination and Pb in blood was determined by a polarographic method (Teisinger et at, 1956). Sections of the temporal bones of 16 animals were stained with hematoxylin- eosin, etc, according to Gomori, and those of 16 remaining animals, by a modified Heidenhain and Roger-Foot method for the demonstration of myelin sheaths and axons. Pb in blood of the control group ranged from 0.025-0.33 mg%; in the ex perimental group, 0,31-0.42 mg%. Histologic examination showed no patho logical changes in the sensory cells of the inner ear or in spiral and vestibular ganglion cells. The VIII nerve in the majority of poisoned animals showed Segmental deraye 1 inatiotTan3~*axona1 degeneration (as"Tilus- tratea in 4 figures). The authors discuss theories on the etiology and pathogenesis of the tieuropathologic changes in chronic Pb poisoning and point to the resemblance of such early symptoms in man to those seen in other demyelinating syndromes. While the sensory cells of the inner ear were found to be most resistant to the effect of Pb, their work showed that Pb poisoning in guinea pigs might produce chronic demyelinating neuropathy of the VIII nerve with axon de generation. The degree of changes differed as to animals, suggesting in dividual sensitivity* (14 references) 190. Hine, C.H., Oavaiii, R.D., and Beltran, S.M. (Univ. Calif .; Stand ard Oil Co., Calif.; Golden Gate Hosp., San Francisco): PERCUTANEOUS ABSORPTION OF LEAD FROM INDUSTRIAL LUBRICANTS. Journal of Occupa tional Medicine 11:568-75 (Nov.), 1969. This study was undertaken to determine whether unusual cphtact with Pb naphthenate, contained as a component of greases and ,iiidustrial oils, would increase the Pb burden'the body. Test materials comprised 4 oils and greases, 3 of them commercial,products containing Pb naphthenate and 1 experimental with its Pb in the form of an^organic compound other than Pb naphthenate. The test animals were"2p New Zealand albino rabbits divid ed into 4 groups of 5, each group receiving 1 of the test oils. The 4 * compounds were: (1) gear oil (1.35% Pb/w), x(3) lubricating grease (0.80% Pb/w), (3) asphaltic gear lubricant (1.15% Pb/w), (4) experimental gear 011 (d.55% Pb/w). In addition,,,4 study was mad\of the effects of gear oil No. I on the skin of 10 huiman subjects and on\their total body burden of Pb and Pb excretion. / Applications of 1.0 mlAcg were made on the backs of the rabbits (clipped areas 5 x 10 cm) and afer 8 hr the remaining materialwas removed with gauze sponges and acefcbne, Twenty applications were made at the rate of 5 applications/wk for 4 wk. Prior to the 1st applfcatioA\cardiac blood samples were drawn^and a 2nd blood specimen was drawn 24 htN after the last application, bot>K for analysis of Pb content. At the end oh the experiment the rabbits were sacrificed* The human subjects were examined before and 81 DUP050044013