PHYSIOLOGICAL CHE3fISTRT. P h y s i o l o g i c a l C h e m i s t ry. 87 Influence of Wine on Peptic Digestion. By L. HUGOTJNENQ (Bull. 8oc. (?him. [3], 5, 849--855).--Fibrin was digested with dilute hydrochloric acid in the presence of various colouring matters and wines. It was found that peptic digestion is considerably hindered by colouring matters, whether occurring naturally in the wine, or added fraudulently, and in the latter case, whether artificial, such as magenta, azotlavine, and methylene blue, or natural, such as the colouring matters of elder and mallow. Plastered wine was found to exercise a less injurious iufluenoe than wine containing the f u l l aniount of tartrates. JN. W. Coagulation of the Blood. By C. A. PEKELHARING (Virchow’s Festschrift, 1891, Bd.l).-Recently, a number of observations on the importance of calcium salts in the process of blood coagulation have been published. Rriicke first showed that the ash of fibrin always contains calcium. In 1875, Haammarsten found that calcium chloride can take the place of seruiii globulin in tibriu formation. I n 1887, Green (Abstr., 1888, 306) found that in magnesium sulphate plasma, and also in other forms of plasma, coagulation is hastened if small quantities of calcium sulphate is added iu addition to fibrin ferment. Later, Ringer and Sainsbury (Abstr., 1890, 1176) found that t,his result can be brought about by other calcium salts, such as the chloride, and also, but not so vxdily, by means of soluble strontium and barium salts. Freund ( M d . ,Jahrb., 1888, 259) who also noted the hastening of coagulation by calcium salts, considered that the blood corpuscles, as soon as the blood is shed, yield alkaline phosphates t9 the plasma ; meeting with the calcium salts there, tricalciurn phosphate is precipitated, and herein lies the cause of fibrin formation.Latschenberger (Meed. Jnhrb., 1888, 479), and voii St.rauch (Ilissert. Dorpat, 1889) showed certain fallacies in this hypothesis; tlius the addition of alkaline phosphates and calcium salts resulting in the precipitation of tri- oalciuui phosphate does not always lead to the formation of fibrin in filwinogenous liquids ; also the fii+t portions of fibrin formed were found to contain calcium, but no phosphoric acid, and further, in the piaesent research, it is shown t h a t injection of disodium phosphate into the circulation of a liviilg animal is not followed by thrombosis.Arthus and Pages (Arch. de Pliysiol., 1890, No. 4) found that blood coagulation may be entirely prevented i f , immediately on being shed, the blood is mixed with small quantities of subdauces, like oxalates88 ABSTHACTS OF CHEMICAL PAPERS. or flnorides, which precipitate calcium salts as very insoluble com- pounds. On adding to the plasma obtained from this blood a slight excess of calcium chloride, coagulation immediately ensues. Fibrin ferment is, however, essential for the process ; and the action of this agent is considered to be t h e bringing together of fibrinogen and the calcium compound, and thus t h e formation of fibrin. It1 this, they draw a close analogy between fibrin formation and the formation of casein in milk under the influence of t h e rennet ferment.Green attempted to answer t h e question, Does t h e fibrin ferment exist as zymogen in the plasma, arid is such zjmogen converted into the ferment by t.he action of t h e calcium salt ? H e was unable to find a, positive answer ; and thvrefore considered t h a t the calciiim acts in assisting the ferment much as hydrochloric acid in tlit! gastric juice favours the activity of pepsin. This question is again taken lip i n t h e present investigation, and i t was found possible to prepare from plasnia (such as oxalate plasma which contains no ferment) a globulin which has no fibrinoplastic properties, which, however, after contact with calcium chloride, is converted into the ferment,.The zymogen yields an ash contairiiiig little or no calcium, whilst the ferment is rich i n calcium. The material in question arises from t,he formed elements of the blood, and is identical with what is called cell- globulin by Halliburton (Abstr., 1888, 574). Fibrin, moreover, is a calcium compound, and the main a.ction of t h e ferment appears t o be t o transfer the calcium to the fibrinogen. Granting this hypothesis, i t is possible to explain several facts hitherto but little understood in connection with blood coagulation, and to reconcile certain conflicting theo~ies. The action of oxalates in hindering coagulation is explained on the supposition that tlie pre- cipitate of calcium oxalate, on account. of its insolubility, is not avail- able for the conversion of zymogcri into ferment.The action of neutral sa1t.s in restniinitig clotting is explained o n t h e assumption that the ferment is a globulin, and, although the amouut of salt added is not sufficient to precigitate the globulin, yet i t is sufficient. t o lessen those intramolecular r lovements which, i n the end, produce its specific action. The acriop of peptone in hindering coagulation can be explained by t h e affinity betwcen peptone and calciiim couipoulids. It thus pre- vents ttieae from coiivertiiig ',he zyniogeri into ttie fwrnent. This view is suppo~ted b j the fact, thitt other substances, like soaps, which combine with calcium compounds, produce similar symptoms to those set up by yeptoiie (MuII~).Thus, there is loss of coagulability of the blood, low blood pressu :e, suppression of secretions, and wen death. The toxic eflecis app,:ar to tx due to the removal of calcium gaits, which are necessaty, H S Ringer has shown, for all vital processes. A further support to the theory IS obtained from ttie fact t h a t injec- tion into the circulatioir of c:alcicm chloi-ide simultaneonslg with the peptone, or after the peptone, (~L\iates tlle poisolions eflects of the latter ; peptone is then 11o Jonge'r capable of rendering t h e blood un- coagulable. Peptone alsc i*estrairis coagulittion in intrsvascular plasma (or solutions of Ha?nmarsten's filwinogeri), provided t h a t it is added so rapidly that tlie zj-niogeii has not had time to combine withPHYSIOLOGICAL CHEMISTRY.89 the calcium to form the ferment. After the ferment has been once formed in the plasma, or added to the solution of fibrinogen, peptone has no longer any hindering, influence on coagulation. Wooldridge's tissue fibrinogens appear to consist of prote'id, nuclei'n, and lecithin. They contain no fibrin ferment unt,il t,hey have been digested for some time with a litkle calcium chloride ; i t is, therefore, considered that they contain the zymogen of fibrin ferment, and their action in producing intravascular coagulation is explicable on the theory that, in the blood, they come into contact with calcium compounds, so that the zyrnogen is then converted into the ferment. W. U. H. Hematic Glycolysis. Estimation of Glycogen in the Blood. By R. LAPINE and BARRAL ( C o ~ ~ p f .rend., 112, 1414--1416),-The sugar present in the blood of a starving dog was estimated after destroying the glycolytic ferment a t 90'. Four portions of the same blood were maintained a t 39" for 15, SO, 4.5, and 60 minutes respec- t i vel y . Taking the initial sugar at 100, the sugar present at each interval would be represented by 88, 81, 76, and 72, indicating losses foraeach successive 15 minutes of 12, 7, 5, and 4 respectively. Treating the blood of a well-nourished dog in the same manner, the loss of sugar for the first 15 minutes was hardly measurable. There is frequently an augmentation of the quantity of sugar present after the first 15 minutes; this is more frequently the case with serum. The glycolytic ferment is contained in the white corpuscles and not in the serum.Sugar is doubtless produoed a t the expense of the glycogenic matter. To estimate the amount thus formed, blood is raised to 58' to destroy the glycolytic ferment and the sugar titrated as above, yielding for successive periods of 15 minutes, a gain of 18, 2, 0, and 0 respectively. The addition of saliva to the blood did not increase the gain. The glycolytic power of the blood of a starving dog is given by deducting the quantity of su,car obtained after an hour a t 39" from. the initial quantity, the apparelit power only is given for the blood of a well-fed dog; to obtain the real power in the latter case, it is necessarg to add the quantity of sugar produced during the same time to the apparent gljcolytic power. A t 58", the traosformstion of glycogen into sugar is rapid ; after a n hour a t this temperature, the whole of the glycogen of the biood may be estimated as sugar.W. T. Mechanism of the Production of Urea i n the Animal Organism. By POPOFF (Bull. Scc &WL. [ 3 ] , 5, 551-554).--To determine whether the transformation of ammonium salts into urea is effected by an unorgamsed ferment, or by the living cell, portions of liver, spleen, and kidney, removed from recently-killed dogs and guinea-pigs, were digested, with antiseptic precautions, f o r mang hours with warm, dilute (0.5-1.0 per cent.), sterilised solutions of various ammonium salts. In no case was any trace of urea formed. The author concludes, therefom, that the formation o€ urea from90 ABSTRACTS OF UHEMIOAL PAPERF.ammonium salts is due to the direct action of the living cells of the various organs, and not to that of soluble ferments secreted by them. JN. W. The Action of Azoimide on Living Organisms. By 0. LOEI\- (Ber., 24, 2!~47-2953).-Expei.iments were made to test the action of xxoimide (N,H) on l i ~ i n g plants and animals. Sodium azoimide WRS found to be a powerful poison in all cases; seedlings died irl about hhree days if attenipts were made t o grow them iu a nutritive Puid containing 0.1 per cent. of the poison. A l p were not affected so readily, but did not grow. Bacteria were killed, aud thus the material in question acts as an antiseptic. Bxxperiments with yeast, penicillium, and other fongi were en tirely confirmatory of the above. To animal life, as tested on infusiorians, various invertebrates, and mammals (mice and rabbits) this substance is equally inimical.There is, first, loss of movement, preceded in mammals by muscular twitch- ings and finally death. ‘l’lie imide is thus not available as a nitrogenous food; and t h e ca,iise of its toxicity is considered to be its sudden decomposition when it comes into relation with the cells and the aldehyde contain- i n g radicles of prote’icl within them. This, occurring within the nerve cells, produces first, stimulation, hence the spasmodic movements, and then kills them. Probably the deccmposition t h a t occurs, may be represented thus, N:,H + H 2 0 = N20 + NH3. It certainly yields aiumonia when acted on by platinizm black. \Y. D. H.PHYSIOLOGICAL CHE3fISTRT.P h y s i o l o g i c a l C h e m i s t ry.87Influence of Wine on Peptic Digestion.By L. HUGOTJNENQ(Bull. 8oc. (?him. [3], 5, 849--855).--Fibrin was digested withdilute hydrochloric acid in the presence of various colouring mattersand wines. It was found that peptic digestion is considerablyhindered by colouring matters, whether occurring naturally in thewine, or added fraudulently, and in the latter case, whether artificial,such as magenta, azotlavine, and methylene blue, or natural, such asthe colouring matters of elder and mallow. Plastered wine was foundto exercise a less injurious iufluenoe than wine containing the f u l laniount of tartrates. JN. W.Coagulation of the Blood. By C. A. PEKELHARING (Virchow’sFestschrift, 1891, Bd.l).-Recently, a number of observations on theimportance of calcium salts in the process of blood coagulation havebeen published.Rriicke first showed that the ash of fibrin always contains calcium.In 1875, Haammarsten found that calcium chloride can take the placeof seruiii globulin in tibriu formation. I n 1887, Green (Abstr., 1888,306) found that in magnesium sulphate plasma, and also in otherforms of plasma, coagulation is hastened if small quantities of calciumsulphate is added iu addition to fibrin ferment. Later, Ringer andSainsbury (Abstr., 1890, 1176) found that t,his result can be broughtabout by other calcium salts, such as the chloride, and also, but not sovxdily, by means of soluble strontium and barium salts. Freund( M d .,Jahrb., 1888, 259) who also noted the hastening of coagulationby calcium salts, considered that the blood corpuscles, as soon as theblood is shed, yield alkaline phosphates t9 the plasma ; meeting withthe calcium salts there, tricalciurn phosphate is precipitated, andherein lies the cause of fibrin formation. Latschenberger (Meed.Jnhrb., 1888, 479), and voii St.rauch (Ilissert. Dorpat, 1889) showedcertain fallacies in this hypothesis; tlius the addition of alkalinephosphates and calcium salts resulting in the precipitation of tri-oalciuui phosphate does not always lead to the formation of fibrin infilwinogenous liquids ; also the fii+t portions of fibrin formed werefound to contain calcium, but no phosphoric acid, and further, in thepiaesent research, it is shown t h a t injection of disodium phosphateinto the circulation of a liviilg animal is not followed by thrombosis.Arthus and Pages (Arch.de Pliysiol., 1890, No. 4) found that bloodcoagulation may be entirely prevented i f , immediately on being shed,the blood is mixed with small quantities of subdauces, like oxalate88 ABSTHACTS OF CHEMICAL PAPERS.or flnorides, which precipitate calcium salts as very insoluble com-pounds. On adding to the plasma obtained from this blood a slightexcess of calcium chloride, coagulation immediately ensues. Fibrinferment is, however, essential for the process ; and the action of thisagent is considered to be t h e bringing together of fibrinogen and thecalcium compound, and thus t h e formation of fibrin.It1 this, theydraw a close analogy between fibrin formation and the formation ofcasein in milk under the influence of t h e rennet ferment. Greenattempted to answer t h e question, Does t h e fibrin ferment exist aszymogen in the plasma, arid is such zjmogen converted into theferment by t.he action of t h e calcium salt ? H e was unable to find a,positive answer ; and thvrefore considered t h a t the calciiim acts inassisting the ferment much as hydrochloric acid in tlit! gastric juicefavours the activity of pepsin. This question is again taken lip i nt h e present investigation, and i t was found possible to prepare fromplasnia (such as oxalate plasma which contains no ferment) a globulinwhich has no fibrinoplastic properties, which, however, after contactwith calcium chloride, is converted into the ferment,.The zymogenyields an ash contairiiiig little or no calcium, whilst the ferment isrich i n calcium. The material in question arises from t,he formedelements of the blood, and is identical with what is called cell-globulin by Halliburton (Abstr., 1888, 574).Fibrin, moreover, is a calcium compound, and the main a.ction oft h e ferment appears t o be t o transfer the calcium to the fibrinogen.Granting this hypothesis, i t is possible to explain several factshitherto but little understood in connection with blood coagulation,and to reconcile certain conflicting theo~ies. The action of oxalatesin hindering coagulation is explained on the supposition that tlie pre-cipitate of calcium oxalate, on account.of its insolubility, is not avail-able for the conversion of zymogcri into ferment. The action ofneutral sa1t.s in restniinitig clotting is explained o n t h e assumptionthat the ferment is a globulin, and, although the amouut of saltadded is not sufficient to precigitate the globulin, yet i t is sufficient.t o lessen those intramolecular r lovements which, i n the end, produceits specific action.The acriop of peptone in hindering coagulation can be explained byt h e affinity betwcen peptone and calciiim couipoulids. It thus pre-vents ttieae from coiivertiiig ',he zyniogeri into ttie fwrnent. Thisview is suppo~ted b j the fact, thitt other substances, like soaps, whichcombine with calcium compounds, produce similar symptoms to thoseset up by yeptoiie (MuII~).Thus, there is loss of coagulability ofthe blood, low blood pressu :e, suppression of secretions, and wendeath. The toxic eflecis app,:ar to tx due to the removal of calciumgaits, which are necessaty, H S Ringer has shown, for all vital processes.A further support to the theory IS obtained from ttie fact t h a t injec-tion into the circulatioir of c:alcicm chloi-ide simultaneonslg with thepeptone, or after the peptone, (~L\iates tlle poisolions eflects of thelatter ; peptone is then 11o Jonge'r capable of rendering t h e blood un-coagulable. Peptone alsc i*estrairis coagulittion in intrsvascularplasma (or solutions of Ha?nmarsten's filwinogeri), provided t h a t it isadded so rapidly that tlie zj-niogeii has not had time to combine witPHYSIOLOGICAL CHEMISTRY.89the calcium to form the ferment. After the ferment has been onceformed in the plasma, or added to the solution of fibrinogen, peptonehas no longer any hindering, influence on coagulation.Wooldridge's tissue fibrinogens appear to consist of prote'id,nuclei'n, and lecithin. They contain no fibrin ferment unt,il t,heyhave been digested for some time with a litkle calcium chloride ; i t is,therefore, considered that they contain the zymogen of fibrin ferment,and their action in producing intravascular coagulation is explicableon the theory that, in the blood, they come into contact with calciumcompounds, so that the zyrnogen is then converted into the ferment.W.U. H.Hematic Glycolysis. Estimation of Glycogen in the Blood.By R. LAPINE and BARRAL ( C o ~ ~ p f . rend., 112, 1414--1416),-Thesugar present in the blood of a starving dog was estimated afterdestroying the glycolytic ferment a t 90'. Four portions of the sameblood were maintained a t 39" for 15, SO, 4.5, and 60 minutes respec-t i vel y .Taking the initial sugar at 100, the sugar present at each intervalwould be represented by 88, 81, 76, and 72, indicating losses foraeachsuccessive 15 minutes of 12, 7, 5, and 4 respectively. Treating theblood of a well-nourished dog in the same manner, the loss of sugarfor the first 15 minutes was hardly measurable. There is frequentlyan augmentation of the quantity of sugar present after the first15 minutes; this is more frequently the case with serum.Theglycolytic ferment is contained in the white corpuscles and not in theserum. Sugar is doubtless produoed a t the expense of the glycogenicmatter. To estimate the amount thus formed, blood is raised to 58'to destroy the glycolytic ferment and the sugar titrated as above,yielding for successive periods of 15 minutes, a gain of 18, 2, 0, and0 respectively. The addition of saliva to the blood did not increasethe gain.The glycolytic power of the blood of a starving dog is given bydeducting the quantity of su,car obtained after an hour a t 39" from.the initial quantity, the apparelit power only is given for the blood ofa well-fed dog; to obtain the real power in the latter case, it isnecessarg to add the quantity of sugar produced during the sametime to the apparent gljcolytic power.A t 58", the traosformstionof glycogen into sugar is rapid ; after a n hour a t this temperature, thewhole of the glycogen of the biood may be estimated as sugar.W. T.Mechanism of the Production of Urea i n the AnimalOrganism. By POPOFF (Bull. Scc &WL. [ 3 ] , 5, 551-554).--Todetermine whether the transformation of ammonium salts into ureais effected by an unorgamsed ferment, or by the living cell, portionsof liver, spleen, and kidney, removed from recently-killed dogs andguinea-pigs, were digested, with antiseptic precautions, f o r manghours with warm, dilute (0.5-1.0 per cent.), sterilised solutions ofvarious ammonium salts. In no case was any trace of urea formed.The author concludes, therefom, that the formation o€ urea fro90 ABSTRACTS OF UHEMIOAL PAPERF.ammonium salts is due to the direct action of the living cells of thevarious organs, and not to that of soluble ferments secreted by them.JN.W.The Action of Azoimide on Living Organisms. By 0. LOEI\-(Ber., 24, 2!~47-2953).-Expei.iments were made to test the actionof xxoimide (N,H) on l i ~ i n g plants and animals. Sodium azoimideWRS found to be a powerful poison in all cases; seedlings died irlabout hhree days if attenipts were made t o grow them iu a nutritivePuid containing 0.1 per cent. of the poison. A l p were not affectedso readily, but did not grow. Bacteria were killed, aud thus thematerial in question acts as an antiseptic. Bxxperiments with yeast,penicillium, and other fongi were en tirely confirmatory of the above.To animal life, as tested on infusiorians, various invertebrates, andmammals (mice and rabbits) this substance is equally inimical. Thereis, first, loss of movement, preceded in mammals by muscular twitch-ings and finally death.‘l’lie imide is thus not available as a nitrogenous food; and t h eca,iise of its toxicity is considered to be its sudden decompositionwhen it comes into relation with the cells and the aldehyde contain-i n g radicles of prote’icl within them. This, occurring within the nervecells, produces first, stimulation, hence the spasmodic movements, andthen kills them. Probably the deccmposition t h a t occurs, may berepresented thus, N:,H + H 2 0 = N20 + NH3. It certainly yieldsaiumonia when acted on by platinizm black. \Y. D. H