13.07.2015 Views

BRITISH CHEMICAL AND PHYSIOLOGICAL ABSTRACTS

BRITISH CHEMICAL AND PHYSIOLOGICAL ABSTRACTS

BRITISH CHEMICAL AND PHYSIOLOGICAL ABSTRACTS

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

j293 A ., III.— vr, VASCULAR SYSTEM . 294Dissociation of calcium and magnesium carbonates and bicarbonates.—SeeA., 1942, I, 145.Plasma-uric acid and -urea in eclampsia. M. D. Crawford ■{].Obsld.Gynac., 1941, 48, (¡0— 72).— Plasm a-uric acid and -urea wereexamined., in 42 eclam ptic patients. A rise in plasma-uric acidoccurred in every case im m ediately after the onset of fits and therise was proportional to th e no. of fits. Plasma-urea showed littlechange immediately a fte r fits b u t rose 24 hr. later. . Similar riseswere found in m ental p atients having convulsion therapy and inrabbits in which convulsions were induced b y azoman. Rise inplasma-uric acid a t labour is sim ilar in eclamptic and normalwomen. p . c . W..Changes in blood concentration in normal and toxoemic pregnancy.■'I. D. Crawford (/. Obstet. Gyn&c., 1940, 47, 03—79).—-Hamiatocritreadings show th a t there is lucmoconcn. during the last 7 days ofpregnancy in normal p atients especially in the last 2 days. Thereis rapid blood dilution in th e first 3 days post-partum followed bya gradual return to norm al. T he changes involve the transfer of-0—25% of the plasm a fluid. In pre-eclam ptic toxiem ia there aresimilar changes w ith haemoconcn. for one or more weeks beforedelivery. In cases of chronic toxxm ia w ithout anosmia the changesare similar to those in pre-eclam ptic toxaemia; in those withanimia the h em ato crit changes are norm al except th a t there is nonse during the puerperinm . The post-partum dilution is increasedty ttdema before delivery, haemorrhage a t deliver}', or by infectionduring the puerperiuni. P. C. W.Hyperlipaemia. “ Idiopathic lipsemia.” T. D. Kinney (Amer. J .£is. Child., 1941, 62, 1014— 1024).—The autopsy findings in a caseof hyperlipa:mia w ith hepatosplenom egaly, retinal lipsemia, andxanthomatosis arc described. Histological and chemical exam inationsshowed lack of fa t deposition in the tissues in strikingcontrast to th e high fa t content of th e serum. There was no evidenceof disease of liver, pancreas, bones, or thyroid. C. J. C. B.¡Blood-fat] in old subjects. I. V. Bazilcvitsch and L. I. PravdinaU-Mid. Ukraine, 1940, 10, 1253— 1266).—An increase of lipins andjatty acids was found in th e blood of healthy subjects aged 90— 110,but no sym ptoms of arteriosclerosis were detected. M. K.Grass sickness in horses; biochemical investigation. T- Stew art,"•S. Gordon, and J. W. McCallum (Vet. Rec., 1940, 52, 237—243).I ■--Biochemical stu d y of the blood of 16 horses w ith grass sicknesswowed an anhydra:m ia in th e pcracute and acute types of thedisease. E. G. W.Seasonal ketonesmia in dairy herd, without clinical symptoms. A.Men and H H . Green (Vet. Rec., 1940, 52. 725— 728).—In a herd"no? » cows wide variations in blood-ketone vals. were observed,'®/4 of the cows showing a rise under stall conditions, w ithoutsymptoms. In 1938 th e average w in ter val. was 8-1 m g.-% , thesummer val. 3 m g.-% ; one cow reached 45 m g.-% b u t appearednormal. There was no associated hypoglycem ia and th e plasma-HCOj' was norm al. The ketonnemia was not affected by adding! lb. of b u tter fat or linseed oil to th e ration. E. G. W .Removal of pyruvic acid from human blood in vitro. E. BuedingK. G oodhart (J. Biol. Chem., 1941, 141, 931— 944).—Defibrinated,heparinised, citrated, or oxalated hum an blood removes addedPyruvate. The effect is increased by keeping a t room tem p, for30—60 min. before the ad d itio n ; longer keeping causing a decrease,fne rate of rem oval decreases w ith increasing tim e of incubation" ’th pyruvate and th e am ount removed per ml. of blood is const,irrespective of th e am ount of blood used. P yruvate removal bywhole blood is increased by incubation w ith 0-075m-P04" ' (optimumfa 7-4), b y N aF, and by NaCN (due to form ation of th e cyano-“ydrin), and decreased by 0 -2 % of iodoacetate but is not affectedaneurin, cocarboxylase, glucose, or th e O, tension of the blood,presence of 2% of F ', 83—95% of th e pyruvic acid removedean be recovered as lactic acid and no evidence of decarboxylationor formation of other carboxyl compounds was obtained. The•''-■sponsible enzym e system is heat-labile, located w ithin th e bloodceUs, and activated by a heat-stable, phosphorylated interm ediary°f carbohydrate catabolism , probably triose phosphate. A subsequentincrease in p y ruvate to above th e original val. is observed10 heparinised and defibrinated, b u t not in oxalated, blood.H. G. R.Effects of insulin, metrazol, and electric shock on blood-pyruvate,-lactate, and -glucose. K. A. C. E lliott, T. D. Rivers, F. H . E lliott,« d B. P la tt (J. Lab. clin. Med.. 1941, 26, 1928— 1933).— Insulin,j&etrazol, and electric shock trea tm e n t had no sp. effect on th elevel of blood-pyruvate or -lactate, i.e., none other th an th a t dueto the m uscular contractions produced. The concn. of these substanceswas not related to blood-sugar level or brain functions,clood-pyruvate and -lactate rose and fell to g eth er; th e rises resultedjrom m uscular activity. In m etrazol and electric shock th e rises ofw th substances, and of blood-glucose, were very high; curaredecreased th e efiect of m etrazol convulsions on blood-lactate,'Pyruvate, and -glucose. The changes in blood-pyruvate were lessmarked th an those of -lactate. C. J . C. B.Fate of pyruvic acid content of fresh rat’s blood during glycolysis.H. von Euler, L. Melander, S. Tingstam , and B. Hogberg (Z. physiol.Chem., 1940, 287, 103— 107).— During the first 28 hr., th e pyrruvicacid content of the whole blood increases (to four-fold) and thendecreases to approx. zero vals.; th e lactic acid content follows asim ilar course; the sugar level steadily falls from 90 m g.-% to nil.W ith the serum for the first 24 hr., the three levels rem ain approx.const., a p art from relatively slight up-and-dow n variations.F. O. H .Changes in blood-phosphorus of rats subjected to blood regenerationby repeated bleedings. G. E. Youngburg and M. V. Youngburg(J. Lab. clin. Med., 1930, 21, 798— 808).—After repeated w ithdrawalsof i } of the to tal blood of rats m aintained on norm aldiets there was little change in the inorg., org. acid-sol., and lipin-Pof th e plasma and corpuscles; for rats on a low-P diet, plasm a-and corpuscle-P were thereby rcduced and some P was transferredfrom the tissues to the blood. P became norm al on resum ption ofnormal diet. Endogenous P is lim ited, so th a t plasm a and corpusclesbecome depleted when the food source is lacking. Oneclass of I’ compounds is not readily converted into another.Ch. A b s . (el)Insulin hypoglycsemia. R. D. Lawrence (Lancet, 11)41, 241, 602).—W hen diabetics are first given insulin hypoglycremic reactions th eyshow m arked autonom ic disturbances, e.g., faintness, sw eatingtrem ors, and hunger pains, before signs of affection of th e centralnervous system appear, e.g., m ental confusion, sym ptom s like alcoholicintoxication, convulsions, and coma. A fter a few years ofinsulin usage the prem onitory autonom ic sym ptom s fail to appearand central nervous sym ptons ap p ear w ithout warning.C. A. K.Hyperglycsemia due to ingesting fatty acids and liver-glycogens.S. Markees (Schweiz, med. Wschr., 1941, 71, 486—490).—Oral a d ­m inistration of N a b u ty rate and hexoate in rabbits increases theblood-sugar; excision of liver tissue showed a dim inution in liverglvcogenwhich was observed in th e fasting and glucose-treatedanim al. The source of fatty* acid hyperglyca:mia is the liverglycogen.A. S.Modification of alimentary hyperglycsemia by ingestion of fat. F.Sciclounoff and E . M artin (Schweiz, med. Wschr., 1941, 71, 490—492).— Hyperglycaimia due to ingestion of glucose is prevented,delayed, or m arkedly dim inished by sim ultaneous ingestion of fator oil. T he phenom enon is interpreted in term s of delayed phosphorylationof glucose in th e presence of fat. A. S.Causation and diagnostic difficulties of spontaneous hypoglycsemia.L. Michaud (Schweiz, med. Wschr., 1941, 71, 347— 349).— Severalcases of spontaneous hypoglycem ia, clue to hyperplasia of th eLangerhans islets or p itu itary disturbance, are discussed. Onewoman of 47 suffered from internal frontal hyperostosis (M orgagni-Stew art-M orel syndrome). A. S.Yl.— VASCULAR SYSTEM.Sequence of fractionate contraction at different surface regions onright auricle and ventricles of dog’s heart. J,. A. E. E yster andW. J. Meek (Amer. J . Physiol., 1941, 134, 513— 516).—The occurrenceof fractionate contraction a t different regions of th e surfaceof th e dog's heart is coincident w ith th e m ain peak of th e differentialp o tential-tim e curve recorded from th e sam e region. Differencesin tim e of onset of fractionate contraction in different regions ofth e h eart were ap p arent. The interval betw een the first and lastregions involved w as 0-03 sec. for th e right auricle and 0-02 sec.for th e ventricles. The first regions entering into fractionate contractionon th e surface of th e right auricle are those contiguousto th e upper p a rt of th e sulcus term inalis and from here contractionproceeds in regular fashion to th e appendage and downward to theauriculo-ventricular junction. In th e vcntricles, th e first surfacecontractions ap p ear on th e rig h t ventricle contiguous to th e in terventriculargroove. O ther regions en ter in to contraction in a waywhich fails to show progressive involvem ent such as exists in th eright auricle. In general, th e surface of th e right ventricle becomesinvolved before the left, w ith the exception of the conus of thepulm onary artery which always enters into contraction late.M. W . G.Effect of temperature on critical oxygen pressure for heart beatfrequency in embryos of Atlantic salmon and speckled trout. K. C.Fisher (Canad. J . Res., 1942, 20, D, 1— 12).— W hen in ta c t em bryosof speckled tro u t and A tlantic salmon are exposed to aq. solutionsof N , and O,, there is an 0 2 partial pressure below which th e frequencyof the h eart b eat is n o t m aintained a t th e norm al levelcharacteristic of higher O, p artial pressures, and it is concludedth a t a “ critical " O , partial pressure exists for h e art b eat frequency.D ata for th e determ ination of this val. a t 5 tem p, are given. Thecrit. 0 3 pressures for th e tw o types of em bryos are sim ilar, and increasefrom 3— 5 mm. H g a t 1-5® to 40— 50 mm. a t 20°. T his crit. pressureand its tem p, coeflf. are characteristic of th e intracellular respiratorysystem s. There is a linear relationship betw een log crit. partialpressure and 1/tem p . J . N. A.

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!