Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 163

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

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Length of anesthesia.

blood before anges-

Percentage of sugar in

blood after anæsthe-

Percentage of increase

in sugar in blood.

Sugar in urine.

Female.

200 gm. of lean meat daily.

Ether (250 cc).

2 hrs.

0.055%

0.077%

0.022%

Female.

200 gm. of lean meat daily.

Ether (250 cc).

2 hrs.

0.064%

0.089%

0.025%

gard to the causes which induce the liver, under the in- of ether, to raise the sugar content of the blood, the re is in much disagreement.

(10) thinks that in an allied condition of asphyxia ria, the cause lies in the presence of an excess of carbon- in the blood and tissues and not a poverty of oxygen. cod (11) states that in asphyxia glycosuria, if the nic fibers to the liver are severed, no glycosuria results. has demonstrated the presence of glycogenetic fibers ver in the splanchnics.

e and Roof (12) suggest that anæesthetics possess the [ combining with tissue protein, and in this way limit- jactivity of the bioplasm, and its power of combining Lies for the purpose of metabolism.

e and Bonlud (13) state that glycosuria in asphyxia

of leucomaines which interfere with glycolysis.

Edie (14) further suggests that the anaesthetic attracts the sugar containing substances in the tissues, setting free sugar.

Seelig (15) claims to be able to remove the effects of ether by intravenous infusions of oxygen.

Thus it is evident that the suggestions as to the cause of ether glycosuria can be largely grouped into three categories :

(1) Due to excess of carbon-dioxide.

(2) Due to poverty of oxygen.

(3) Action through the splanchnic.

In regard to the first suggestion, it was generally noted that the blood taken at the end of anesthesia was quite red and did not suggest a high content of carbon-dioxide.

Further, Seelig did not notice any degree of asphyxia in his animals and does not give much consideration to this explanation.

As regards the administration of oxygen with the ether, we have not been able to prevent the occurrence of a glycosuria by such a procedure.

The control of many functions of glands by nerves is such a well-established process in the body that the possibility of ether acting through the mediation of the splanchnic nerve seemed worthy of study, especially in view of the results of the splendid experiments of Macleod (17), in which he demon- strated the presence of glycogenetic fibers in these nerves.

Accordingly, experiments were undertaken after the follow- ing schema :

(1) Dogs were anæsthetized as above, to determine their initial hyperglycæmia.

(2) Then they were operated upon, and the splanchnic fibers going to the liver cut, together with the hepatic artery. It was found that many of the fibers were so intimately asso- ciated with this artery that they could not be severed without also cutting the artery.

(3) After the animal had recovered, the effect of ether was again tried.

The results are given in the protocols below.

EXPERIMENT No. 19 .- Dog, No. B 63. Female. Diet: 200 gm. lean meat daily. Dog bled from right jugular vein before start- ing anæsthetic.

1. Weight of flask + NaOx + blood = 83.47240 gm.

Weight of flask + NaOx = 31.34960

Weight of blood =52.12280 Percentage of sugar in blood == 0.041 per cent dextrose.

Dog was anæsthetized for 2 hours, using 250 cc. ether, and then bled from same vein.

2. Weight of flask + NaOx + blood = 93.61430

Weight of flask + = 40.85850

Weight of blood =52.75580

Percentage of sugar in blood = 0.159 per cent dextrose.

Increase in sugar of blood, due to anæsthetic = 0.118 per cent dextrose. The urine was positive to Fehling's test.

The dog was operated upon after a few days' rest, and the splanchnics cut, together with the hepatic artery as described

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Female.

200 gm. of lean meat daily.

Ether (250 cc).

2 hrs.

0.066%

0.093%

0.027%

Female. 200 gm. of lean meat daily.

Ether (250 cc).

2 hrs.

0.059%

0.050%

0.009%

Percentage of sugar in

thesia.

sia.

gm.

394

JOHNS HOPKINS HOSPITAL BULLETIN.

[No .:

above. After a week's rest, the dog was then subjected to the ether experiment in same manner as before. Blood was drawn from the left jugular vein, before beginning the anesthesia.

gm.

1. Weight of flask + NaOx + blood = 89.47000

Weight of flask + NaOx = 38.61760

Weight of blood =50.85240

Percentage of sugar in blood = 0.040 per cent dextrose. Dog was then anæsthetized for 2 hours, using 250 cc. ether, and bled at end of anesthesia from left jugular vein.

gm.

2. Weight of flask + NaOx + blood = 92.09410

Weight of flask + NaOx =41.39570

Weight of blood = 50.69840

Percentage of sugar in blood = 0.144 per cent dextrose. Increase in sugar in blood, due to anesthetic = 0.104 per cent dextrose. Urine was positive for Fehling's test.

Remarks .- Cutting the splanchnics had practically no effect on ' the occurrence of ether glycosuria, as shown by the table.

Per cent dextrose.

Increase in sugar in blood before cutting splanchnics == 0.118 Increase in sugar in blood after cutting splanchnics = 0.104

Another experiment was performed under the same con- ditions.

EXPERIMENT No. 20 .- Dog, No. B 65. Female. Dog was on diet of 200 gm. of lean meat daily. Blood taken from right jugular vein before beginning of anæsthesia.

1. Weight of flask + NaOx + blood = 87.82200 gm.

Weight of flask + NaOx = 35.63600

Weight of blood == 52.18600

Percentage of sugar in blood = 0.055 per cent dextrose.

Dog was then anæsthetized for 2 hours, using 250 cc. of ether, and bled from right jugular vein.

2. Weight of flask + NaOx + blood =87.29390 Weight of flask + NaOx = 36.79590

gm.

Weight of blood == 50.49800

Percentage of sugar in blood = 0.111 per cent dextrose.

Increase in sugar in blood due to anæsthetic =0.056 per cent dextrose. Urine showed 1.0745 per cent dextrose.

Animal was allowed to recover for a week and then operated upon and the splanchnics cut, together with the hepatic artery. After a few days' rest the animal was again subjected to the ether experiment as above. Blood was taken from the left jugular vein before ·beginning of anesthesia.

gm.

1. Weight of flask + NaOx + blood = 96.54570 Weight of flask + NaOx

== 45.73080

Weight of blood =50.81490 Percentage of sugar in blood = 0.037 per cent dextrose. Dog was then anæsthetized for 2 hours, with 250 cc. of ether, and at end of anesthesia blood was drawn off from left juglar vein.

2. Weight of flask + NaOx + blood = 104.39320 gm.

Weight of flask + NaOx = 53.28520

Weight of flask = 51.10800

Percentage of sugar in blood = 0.114 per cent dextrose.

Increase in sugar in blood due to anæsthetic = 0.071 ps : dextrose. Urine showed 2.175 gm. dextrose.

Remarks .- The cutting of the splanchnics had no appena influence upon the glycosuria caused by the ether.

Per Y der-

Increase in sugar in blood before cutting splanchnics=0%; Increase in sugar in blood after cutting splanchnics=\ !.

Another experiment was performed under the sacx ditions.

EXPERIMENT No. 21 .- Dog, No. B 66. Female. Dog on be 200 gm. of lean meat daily. Dog bled from right jugokr before beginning anæsthesia.

1. Weight of flask + NaOx + blood =88.22560

Weight of flask + NaOx = 38.36390

Weight of blood = 49.86170

Percentage of sugar in blood = 0.045 per cent dextros: Dog was then etherized for 2 hours, using 250 cc. of etter bled from the right jugular vein at end.

2. Weight of flask + NaOx + blood =86.76400

Weight of flask + NaOx = 36.78050

· Weight of blood = 49.98350

Percentage of sugar in blood = 0.094 per cent dertrex Increase in sugar in blood due to anaesthetic =0.049 ; Urine was positive to Fehling's test.

Dog was then allowed to recover for about & week s !! operated upon as in previous experiments. After a WR !! covery, the ether experiment was again repeated. Bioet : from right jugular vein, before beginning of anæsthesia

1. Weight of flask + NaOx + blood =90.04270 Weight of flask + NaOx = 36.11640

Weight of flask = 53.92630

Percentage of sugar in blood = 0.044 per cent dertr's Dog was then etherized for 2 hours, using 250 cc. of then bled at end, from left jugular vein.

2. Weight of flask + NaOx + blood = 93.72710 Weight of flask + NaOx = 43.65580 = 50.07130

Weight of blood

Percentage of sugar in blood = 0.166 per cent destra

Increase in sugar in blood due to anæsthetic=0.]= " dextrose. Urine was positive to Fehling's test. Remarks .- Here, again, cutting the splanchnic nerva. remove the effect of ether causing a hyperglycemia and :**

A fourth experiment is given in which the ani: operated upon and the splanchnics cut without har. determined the extent of the hyperglycemia with the- nies intact. It is given because it adds to the comp. the series.

EXPERIMENT No. 22 .- Dog, No. B 47. Female. No: daily diet of 200 gm. of lean meat. Splanchnics to live as in previous experiment and after a few days' recover: experiment was begun. Animal was bled from the fiz vein before beginning of anæsthesia.

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Weight of blood =52.03840 Percentage of sugar in blood = 0.0302 per cent dextrose.

was then anæsthetized for 2 hours, using 250 cc. of ether, led from the left jugular vein at end.

Weight of flask + NaOx + blood = 86.14350 gm.

Weight of flask + NaOx

= 35.23920

Weight of blood = 50.90430

Percentage of sugar in blood = 0.143 per cent dextrose. 'ease in sugar in blood = 0.0841 per cent dextrose. Larks .- This confirms the preceding experiments. The re- tre put in tabular form for their more ready interpretation.

TABLE No. 4. SPLANCHNIO NERVE EXPERIMENTS.

Dog.

Gender.

Diet.

Anasthetic.

blood before.

blood after.

Increase in sugar in

Appearance of sugar

Amount of sugar in

urine.

B 63 Female. 200 gm. of Ether. 0.041%

0.159%

0.118%

lean meat daily.

B 63 Female. 200 gm. of

Ether. 0.040% 0.144%

0.104%

B 65 Female. 200 gm. of lean meat daily.

Ether. 0.055%

0.111%

0.056%

+ 1.0745 g m. dex- trose.

B 65 Female. 200 gm. of Ether. 0.037%

0.114%

0.077%

2.175 gm. dex- trose.

B 66 |Female. 200 gm. of

Ether. 0.045%

0.094%

0.049%

B 66 Female. 200 gm. of Ether. 0.044%

lean meat daily.

se experiments show clearly that the anaesthetic causes cosuric effect just as well after the splanchnics to the re cut. They further show that with the hepatic artery ed from the circulation the anesthetic works its full ust as well through the portal circulation. This parallels osely the observations of Whipple and Sperry (17), loroform acts just as well and causes the same lesions liver when the hepatic artery is excluded from the cir- 1 by ligation.

e results would lead us to think that the anesthetic ectly upon the liver, and in some unknown way stimu- lat organ to increase the sugar content of the blood. ne glycosuric effect of ether practically disappears when r is excluded from the circulation, we must, it seems ble, conclude that the cause of the increased sugar of the blood lies within this organ, and is not due to ct upon the muscle or other organ glycogen, or upon ulating sugar in the blood.

effect can be brought about by the path of the blood since eliminating the liver from the influence of its

Further investigation is necessary to ascertain whether ether affects the activity of the glycolytic ferments.

Conclusions.

(1) Following the administration of ether to the point of deep anæsthesia, there results, in healthy adult dogs, a well- marked glycosuria.

(2) The reducing body in the urine is dextrose.

(3) The cause of the glycosuria is a definite hypergly- cæmia.

(4) The liver is the organ which furnishes the increase in sugar to the blood, as shown by the absence of the occurrence of a hyperglycemia and glycosuria when the liver is removed from the circulation by an Eck fistula.

(5) Severance of all the splanchnic fibres of the celiac plexus going to the liver did not remove the hyperglycemia and glycosuria. elicited by ether.

NOTE .- During the time of preparation of this article, Hawk has published two communications, dealing with the subject of post-anesthetic glycosuria. In one (18) he concludes that this type of glycosuria is due primarily to the effect of ether in stimu- lating the transformation of glycogen into dextrose. The second (19) paper deals more largely with the rate of urine formation under ether anesthesia. There occurs an inhibition of the urine- forming function during the time anesthesia is induced, but such inhibition is quickly followed by a stimulated urine flow which is initialed as soon as the period of anesthesia terminates. The inhibition of the urine formation was probably due to the effect of ether in constricting the arterioles of the kidney's blood supply.

LITERATURE.

1. Ruschhaupt: Archiv für Experimentelle Pathologie und Phar- makologie, 1900, XLIV, 127-141.

2. Seelig: Archiv für Experimentelle Pathologie und Pharma- kologie, 1905, LII, 481-494.

3. Hawk: American Journal of Physiology, 1903-1904, X, 37.

4. Macleod: American Journal of Physiology, 1907, XIX, 388-407.

5. Underhill: Journal of Biological Chemistry, 1905-1906, I, 113-130.

6. Seelig: Archiv für Experimentelle Pathologie und Pharma- kologie, 1905, LII, 481-494.

7. Oppler-Bertrand: Zeitschrift für physiologische Chemie, 1910, LXIV, 393.

8. Seelig: Archiv für Experimentelle Pathologie und Pharma- kologie, 1906, LIV, 206-216.

9. Seelig: Archiv für Experimentelle Pathologie und Pharma- kologie, 1905, LII, 481-494.

10. Edie: Biochemical Journal, 1906, I, 455-473.

11. Macleod: Journal of the American Medical Association, 1910, LV, 2133.

12. Mone and Roff: Proceedings of the Royal Society, 1904, LXXIII, 382.

13. Lepine and Bonlud: Comptes rendus de l'Académie des Sciences, 1902, CXXXIV. 582.

14. Edie: Biochemical Journal, 1906, I, 455-473.

15. Seelig: Archiv für Experimentelle Pathologie und Pharma- kologie, 1905, LII, 481-494.

16. Macleod: American Journal of Physiology, 1903-1904, X, 37.

17. Whipple and Sperry: Johns Hopkins Hospital Bulletin, 1909, XX, 278.

18. Hawk: Archives of Internal Medicine, 1911, VIII, 39.

19. Do: Idem, 1911, VIII, 174.

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lean meat daily.

0.166%

0.122%

...

lean meat daily.

Percentage of sugar in

blood.

in urine.

396

JOHNS HOPKINS HOSPITAL BULLETIN.

THE EFFECT OF OCCLUSION OF THE VARIOUS HEPATIC VESSEL UPON THE LIVER.

By M. C. WINTERNITZ, M. D., Associate in Pathology, The Johns Hopkins University.

Although the intrahepatic branches of the hepatic vessels are terminal, their capillary communications are so abundant that, as a rule, embolism or thrombosis of either of them causes no interference with the circulation of the liver. De- spite this fact, various pathological changes, varying from simple congestion to true red and white infarcts, characterized by coagulative necrosis in the area supplied by the occluded vessel or vessels, are recognized and have been reproduced ex- perimentally. These will be briefly discussed and a few original cases added.

OCCLUSION OF THE PORTAL VEIN.

Occlusion of the portal vein, either thrombotic or embolic, is not rare. This is very evident from Lissauer's report.1 Among 26,687 cases which came to autopsy at the University of Breslau from 1878-1907, Lissauer found 68 instances of complete or partial thrombotic occlusion of the portal vein or its branches. Most of these occurred as a secondary mani- festation in a number of conditions. Portal thrombosis, how- ever, may be primary and is then characterized by a symptom complex of circulatory ileus, as in the case of Lewis and Rosenau.' These authors collected 20 other cases from the literature.

As a rule such occlusion has no effect upon the liver paren- chyma, since the hepatic artery supplies the blood by the anas- tomosis between the two systems. That is, while the branches of the portal vein alone supply the acini of the liver with blood and the hepatic artery supplies the interlobular tissue, still the capillaries arising from the hepatic artery empty into the interlobular branches of the portal vein. In this way the hepatic artery, through its anastomosis with the in- terlobular vein, is capable of compensating when the larger branches of the portal vein are occluded. As long as the small branches of the portal vein are not involved, so long will the hepatic artery be able to nourish the liver parenchyma.

Etiology .- Lissauer concluded, from his analysis of the literature, that slowing of the blood stream is not in itself sufficient to bring about portal thrombosis, that " marantic " thrombi must be exceptionally rare, and that one of the fol- lowing conditions is essential :

Primary authoctonus atheroma.

Inflammation of the vein wall by extension. Compression of the vein.

Purulent pylephlebitis.

Lewis and Rosenau, however, conclude from their clinical and experimental studies that bacterial infection plays a very important rôle in portal thrombosis. This is in agreement

' Lissauer: Virchow's Arch., 1908, CXCII, 278.

2 Lewis and Rosenau: Arch. Int. Med., 1909, III, 233.

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with the findings of other authors-Welch,' etc., in t bosis elsewhere.

OBLITERATION OF THE PORTAL VEIN WITHOUT HET. CHANGES.

. This subject has been reviewed very recently by M. i. He cites, as a typical example of fresh thrombosis portal vein, a case reported by Saxer in 1902, where occluded all of the portal radicals. Despite this, the li- only somewhat small and anemic. The circulation !: dently been carried on by the hepatic artery. Ver- quotes a number of cases of old thromboses of the per.

1. A case of Umber's where the vein was ochal- thrombus judged to be from 20 to 30 years old. The :. bus was 1 cm. long and just at the hilus of the line: liver was relatively small, but otherwise normal. Nad collateral circulation to the liver was determined. The . vein also contained a thrombus and the spleen was en enlarged.

2. A case described by Heller where the thrombis ". ing the portal vein had been extensively canalized. T. ent had suffered for many years from a very much r. spleen which gradually decreased in size. He died at : tured verrucose vein of the stomach. The liver shit marked changes.

3. A case reported by Risel showed the formatin? merous new veins besides canalization of the thromb .: extended into the hepatic branches. The spleen se: enlarged. Death was caused by a fresh clot in the . mesenteric vein.

4. A case of Pick's where death followed rup": varix of the œesophagus. The portal vein was occlu. Pick considered that the thrombosis had been str :" a true hemangioma arising in the wall of the portal we" extensive collateral circulation had been established al-

Versé then includes a case of his own where an .. thrombus occupied the splenic and the larger brands portal vein. A tremendous collateral circulation as i lished itself to carry off the portal blood. This we- through the colic, gastric, œesophageal, omental and I. by its communication with the adrenal, veins. Thx ceived a large amount of portal blood through a cavernous vessels of which the original canalized "

3 Welch: Tr. Ass. Am. Phys., 1900. XV, 441.

+ Versé: Beiträge z. path. Anat. u. z. allg. Path., 19! 520.

" Verse discusses the nature of this hemangioma. He agree with Pick that this is a true blastoma, but coEx .: formation secondary to the thrombosis-as in his case.

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mentally the portal vein has been ligated repeatedly production of Eck fistula. In several of these cases re- by Whipple " the liver, 10 to 11 weeks after ligation portal, showed the following picture: "In one dog tula between the portal vein and vena cava was quite (4 x 6 mm.) and the ligature about the portal vein che fistula was not effective, the opening admitting only ints of the scissors. In the other animal the fistula was arge and the ligature of the portal vein was efficient. le livers were practically the same in both cases. The was small, flabby, and rather tough. The lobules were presenting a brown, translucent edge and minute cen- ellow dot. Microscopically there was considerable y and fatty degeneration of the central half of the liver "

ur autopsy reports the following cases of thrombosis of ortal vein without marked hepatic changes have oc- . 7

. W., white, age 49 years. Autopsy No. 175.

omical Diagnosis .- Carcinoma of the stomach; metastases gastro-hepatic glands; carcinomatous thrombus of the portal multiple carcinomata of the liver; ascites; hydrothorax ; emphysema; bronchiectasis; bronchitis; bronchopneu- with fresh pleurisy.

" is very large, covered by tumor masses. The hepatic is slightly thickened. The portal vein is of normal size. very entrance into the liver there projects into it a large, carcinoma nodule (4 x 21/2 cm.). The veins arising in the of the thrombus are likewise filled with the tumor tissue, large mass in the left lobe of the liver is directly continu- :h the vein thrombus.

re is in this case no note which would indicate any in the hepatic tissue resulting from the portal oc-

. B., white female, age 59 years. Autopsy No. 214.

›mical Diagnosis .- Syphilitic deformity of the liver of ex- degree; chronic passive congestion of spleen with peri- s and perihepatitis; chronic thickening of peritoneum, ly around the liver; recent portal thrombosis; fat necrosis ; acute diffuse peritonitis; chronic diffuse nephritis; nsufficiency; hypertrophy of left ventricle; calcification in [ of splenic vein with parietal thrombus.

portal vein is very wide, circumference 61/2 cm. Just as it the liver its lumen is filled with a fresh grayish-red is adherent in places to the intima, but in general easily I. It extends a short distance into the main branches of . and looks very recent in its formation. The vessels in ato-duodenal ligament are enveloped in a mass of dense tissue.

: from a marked syphilitic cirrhosis, no lesion was 1 the liver. Here again the portal occlusion was with- et. The etiological factor probably was syphilis.

ple and Sperry: Johns Hopkins Hosp. Bull., 1909, XX,

protocols will be abstracted as briefly as possible. Only rts of particular interest to the subject at hand will be

per lobes; amyloid infiltration, spleen and kidneys; tuberculous ulceration of large and small intestine; thrombosis of intrahepatic branches of portal vein.

Liver .- 1250 grams. Surface smooth. Margin round. Lobules visible. Consistency rather increased. Portal vein large, 2 cm. in diameter. Hardened sections.of liver show slight increase in connective tissue. Thrombi in portal veins with extensive liver- cell emboli in same vessels. Slight dilatation of the capillaries.

4. L. G. Autopsy No. 462. Dr. Flexner.

Anatomical Diagnosis .- Diffuse suppurative cellulitis of left leg. (streptococcus) ; ascites; chronic adhesive peritonitis; chronic perisplenitis; perihepatitis; thrombosis of the portal vein; chronic diffuse nephritis with acute exacerbation; chronic pleuritis, etc.

Liver .- 1700 grams, 21 x 15 x 9 cm. It is everywhere adherent. The capsule is thickened, white fibrous-looking and in places reaches 4 mm. in thickness. On section it presents a mottled aspect. The surface is in general cloudy, deep reddish brown in color, with many lighter yellowish areas. Heavy bands of con- nective tissue proceed in from the porta and the capsule. By this means circumscribed areas of liver tissue are completely marked off. In general the lobules are more distinctly isolated than normally, and the central veins are quite prominent. The consistency of the liver is much increased. In the portal vein are thrombi. The main branch, beginning at the junction of the principal abdominal veins, is almost completely filled by a mixed thrombus which is only slightly adherent. At the entrance into the liver the vein is filled with a more firmly adherent, laminated, somewhat softened thrombus which does not fill the lumen. Some of the principal branches of the portal vein in the liver contain thrombus masses, some of which are recent, scarcely adherent and continuous with the laminated thrombus.

Microscopically there is an increase in connective tissue plus fatty degeneration of the liver cells.

It is quite probable that the mottled appearance of the liver in this case is related to the portal occlusion. The coarse bands of fibrous tissue also suggest a syphilitic cirrhosis.

5. B. S., white female, age 51 years. Autopsy No. 483.

Anatomical Diagnosis .- Carcinoma of the head of the pancreas with extension into the duodenum and stomach; multiple metas- tases to lymph glands, both adrenals, liver and lung; thrombosis of portal vein.

The portal vein is thrombosed just before it enters the liver by a partially decolorized thrombus mass. Aside from the tumor metastases, section of the liver is brownish red in color and homogeneous.

6. L. F., white male, age 45 years. Autopsy No. 567.

Anatomical Diagnosis .- Perforating ulcer of stomach; old ad- hesive peritonitis around perforation; ulceration into splenic artery and into small pyloric artery; thrombosis of splenic artery; extension of clot into celiac axis and abdominal aorta; infarction of spleen; complete thrombosis of splenic vein, with extension of thrombus into portal vein; thrombosis of many in- terlobular veins in liver, etc.

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 163

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189