effects of gestation and lactation on rat gastric fundus

6
Effects of gestation and lactation on rat gastric fundus' Received June 1 3, 1980 JOH.HCOEB!K, L., J. ASSELIN, and J. ORIS IS SET. 1981. Effects of gestation and lactation on rat gastric fundus. Can. J. Physiol. Pharmacol. 59: 96- 101. This study evaluated the effects of gestation and lactation on stomach growth in rats. Constant increases were observed in gastric fundus weight during pregnancy and lactation, with a naaximtam obtained after 3 weeks of lactation. 'This increase in tissus weight was not associated with hyperplasia of the gastric fundbas as in no instance did total DNA contents frorn mated females differ significantly from those of the binmated controls. Mild hypertrophy, as evidenced by significant increases in cellular Inass and WNA and protein concentrations, was observed during late lactation. Gastrin rnight be responsible for these modest changes in the gastric fundus. JOI.IC'OE~JR, L., J. ASSEI.IN et 9. ORIS IS SET. 8981. Effects of gestation and lactation on rat gastaic fundus. Can. J. Physiol. Pharmacol. 59: 96- 10%. Cettc recherche fut entreprise afin d'kvaIuer Ies effets de la gestation et de la lactation sur la croissance de l'estc~mac de rat. Ilks 1e dkbut de la gestation et ce ji~squ'ala fin de la lactation, on a not6 des augmentations progressives du poids d~a fundus gastriqaae atteignant un naaximum aprks 3 semaines de lactation. Gette crcsissance rkgulikre ne peut pas s'expliqucr par une hyperplasie des tissus car les q~aantitks totales d'ADN des feanelles accouplCes n'ont jamais ete significativernent diffkrentes tie celles des fcmelles vierges. A en juger par les augmentations significatives des naasses cellulaires et des concentrations de protkincs et d' AWN, on peut cependant diaglaostiquer une lkgkre hypertrophic dia fundus gastrique qui apparait tardiveanent au cours de la lactation. Nobas croyons que la gastrine pourrait Ctrc responsable de ces Ikgeres modifications au niveau du fundus gastrique. Introduction Materials and methods Growth of the alimentary tract is accelerated during lactation in several species such as the rat and the sheep and it coincides with the increased food consump- tion occurring during this period (Fell et ill. 1963; Campbell and Fell 1964; Fell et al. 1964; Long 1969; Lichtenberger and Trier 1979b. Growth of the stomach during the reproductive cycle has been evaluated mainly by ~norphologicaland his- tological techniques. Fell et al. (1963) found that Iacta- tion was associated with hypertrophy, as they observed increases in organ weight and hypertrophy of parietal cells examined histologicaIly. Crean and Rurnsey 4 B 97 1 ) found hyperplasia of the gastric mucosa as evid- enced by increases in fundus weight and total parietal and peptic cell populations. This staldy was designed to reevaluate the phenome- non of gastric fundus growth by means of biochemical criteria not only during lactation bait also during pregnancy and after weaning. An evaluation of fundus DNA contents, concentrations and contents of pepsin, protcin, and RNA was perfomcd to distinguish between hyperpIasia and (or) hypertrophy of the gland. his work was siapported lay the Natural Sciences and Engi- neering Research Council of Canada, grant No. A-6369. A reirnt11.s A population of baby female Sprague-Dawley rats from our own colds~~y was selected at birth and grown until they were 3 months old. At this age sotrae females were selected at random for itrapregnation and the others were ciesignatcd as their iannaated controls. Each female and hcr control were then allocated according to a predetermined random order to one of' nine sample groups which were killed at weekly intervals corresponding to different stages of the pregnancy and Iracta- tion of the impregnated rat. The anaimals in cach group were caged by pair in the same cage throughoa~t the experiment except for the period extending Srorn 1 week before parturition until the end of the period of lactation when the darn was housed in a separate large plastic cage with her pups. After parturition the nunaber of rats per titter was reduced or corn- plctecf to 10 as previously described by L,arose and Mc~risset (1977). Between 10 and 13 pairs of rats were selected in each sample group. For the purpose of mating. six females were hoiased in a single Iarge cage with one fertile male. Vaginal smears were examined each tnorning and i~npregnatiasn was considered to have occupretl on the day that spermatozoa werc first c~bserved. In this experiment lactatidsr~ was pem-nitted fur 2 8 days following delivery. All anlrr~als were fasted overnight before sacrifice. 'I'heir final body weight was rccorated just before death; in the case of the pregnant animrals (i.e., those in groups 2 and 3) final body weight was estimated as the difference between their body weight before death aaad the wet 0008-42 1218 1 /020096-06$0 1 .00/0 "'1981 National Research Cobancil c~f Ciae~ada/Gonseil tlational de recherches du Canada Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by UNIV WINDSOR on 11/14/14 For personal use only.

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Page 1: Effects of gestation and lactation on rat gastric fundus

Effects of gestation and lactation on rat gastric fundus'

Received June 1 3, 1980

JOH.HCOEB!K, L . , J. ASSELIN, and J. ORIS IS SET. 1981. Effects of gestation and lactation on rat gastric fundus. Can. J. Physiol. Pharmacol. 59: 96- 101.

This study evaluated the effects of gestation and lactation on stomach growth in rats. Constant increases were observed in gastric fundus weight during pregnancy and lactation, with a naaximtam obtained after 3 weeks of lactation. 'This increase in tissus weight was not associated with hyperplasia of the gastric fundbas as in no instance did total DNA contents frorn mated females differ significantly from those of the binmated controls. Mild hypertrophy, as evidenced by significant increases in cellular Inass and WNA and protein concentrations, was observed during late lactation. Gastrin rnight be responsible for these modest changes i n the gastric fundus.

JOI.IC'OE~JR, L., J. ASSEI.IN et 9. ORIS IS SET. 8981. Effects of gestation and lactation on rat gastaic fundus. Can. J . Physiol. Pharmacol. 59: 96- 10%.

Cettc recherche fut entreprise afin d'kvaIuer Ies effets de la gestation et de la lactation sur la croissance de l'estc~mac de rat. Ilks 1e dkbut de la gestation et ce ji~squ'a la fin de la lactation, on a not6 des augmentations progressives du poids d~a fundus gastriqaae atteignant un naaximum aprks 3 semaines de lactation. Gette crcsissance rkgulikre ne peut pas s'expliqucr par une hyperplasie des tissus car les q~aantitks totales d'ADN des feanelles accouplCes n'ont jamais ete significativernent diffkrentes tie celles des fcmelles vierges. A en juger par les augmentations significatives des naasses cellulaires et des concentrations de protkincs et d' AWN, on peut cependant diaglaostiquer une lkgkre hypertrophic dia fundus gastrique qui apparait tardiveanent au cours de la lactation. Nobas croyons que la gastrine pourrait Ctrc responsable de ces Ikgeres modifications au niveau du fundus gastrique.

Introduction Materials and methods Growth of the alimentary tract is accelerated during

lactation in several species such as the rat and the sheep and it coincides with the increased food consump- tion occurring during this period (Fell et ill. 1963; Campbell and Fell 1964; Fell et al. 1964; Long 1969; Lichtenberger and Trier 1979b.

Growth of the stomach during the reproductive cycle has been evaluated mainly by ~norphological and his- tological techniques. Fell et al. (1963) found that Iacta- tion was associated with hypertrophy, as they observed increases in organ weight and hypertrophy of parietal cells examined histologicaIly. Crean and Rurnsey 4 B 97 1 ) found hyperplasia of the gastric mucosa as evid- enced by increases in fundus weight and total parietal and peptic cell populations.

This staldy was designed to reevaluate the phenome- non of gastric fundus growth by means of biochemical criteria not only during lactation bait also during pregnancy and after weaning. An evaluation of fundus DNA contents, concentrations and contents of pepsin, protcin, and RNA was perfomcd to distinguish between hyperpIasia and (or) hypertrophy of the gland.

his work was siapported lay the Natural Sciences and Engi- neering Research Council of Canada, grant No. A-6369.

A reirnt11.s A population of baby female Sprague-Dawley rats from

our own colds~~y was selected at birth and grown until they were 3 months old. At this age sotrae females were selected at random for itrapregnation and the others were ciesignatcd as their iannaated controls. Each female and hcr control were then allocated according to a predetermined random order to one of' nine sample groups which were killed at weekly intervals corresponding to different stages of the pregnancy and Iracta- tion of the impregnated rat. The anaimals in cach group were caged by pair in the same cage throughoa~t the experiment except for the period extending Srorn 1 week before parturition until the end of the period of lactation when the darn was housed in a separate large plastic cage with her pups. After parturition the nunaber of rats per titter was reduced or corn- plctecf to 10 as previously described by L,arose and Mc~risset (1977).

Between 10 and 13 pairs of rats were selected in each sample group. For the purpose of mating. six females were hoiased in a single Iarge cage with one fertile male. Vaginal smears were examined each tnorning and i~npregnatiasn was considered to have occupretl on the day that spermatozoa werc first c~bserved. In this experiment lactatidsr~ was pem-nitted fur 2 8 days following delivery. All anlrr~als were fasted overnight before sacrifice. 'I'heir final body weight was rccorated just before death; in the case of the pregnant animrals (i.e., those in groups 2 and 3) final body weight was estimated as the difference between their body weight before death aaad the wet

0008-42 1218 1 /020096-06$0 1 .00/0 "'1981 National Research Cobancil c~f Ciae~ada/Gonseil tlational de recherches du Canada

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Page 2: Effects of gestation and lactation on rat gastric fundus

TARI.E 1 . Effects of pregna~~cy and lactation on gastric Rnndus weight and total DNA content in rats

- Gastric fundus weight, ang Total DNA, ralg

Ilnrnated Mated C/c IJn~a~ated Mated (h Periods Weeks females femalc5 dafference females females difference

Pregnancy I '7

Postlactation I 2 3

NOTE: Results are given as mean values with their standard errors. Values significantly greater than i~nrnated control: *P ( 0.05; t P -: 0.01; :bP <: 0.(301. Values in parentheses are the number of animals in each group.

weight of the uterus and its contents which were removed and from 232 to 278 g. Body weights of the mated females weighed immediately after the 5acrifice: no al8ow:ince was were \ig~sificantly increased over their respective con- made for the weight of the uterus in any of the other groups trols by l ( , t x after the 2nd week (pf gestation alrd hq a5 it was under 100 mg. l4(X1 after thc 3rd week of gestation; for all the other

Assaj3 'Fhe W ~ C P I C ston~ach was removed aftcr death anti cut open

along the greater curvature; the antrum and rumen were then separated frorn the gastric fundus by cutting along the appro- priate junction with fine scissors. The gasrric fanndus including sanooth muscle was cleaned with water, swabbed dry, and weighed. The organ was placed in I5 1n1, of 0. I M sodium phosphate buffer, pH 6.9: and homogenizcd with a PoIytro~a (IT 20, Brinkman Instrument). SarnpIes s f the homogenate were precipitated in 2.1 N percl2lsric acid (PCA) for RNA and DNA determinations.

Protein was deterrnined by the method of L,owry et al. (1951) with bovine selxna albumin as a standard. RNA and DNA were extracted according to Mainz et 31. ( 1973). RNA was hydrolyzed overnight in 0.3 N KOH at 37'C and measured by determining absorbance at 260 nnl crf the final 0.1 A' PCA extract. An absorbance of 1.000 was assumed to equal 32 p g RNA/mL, of extract (Munro and Flect 1966). DNA was n~casured by the naethod of Volkin and Cohn (1954) after its extraction into 0.5 N PC,% for I 5 min at 90°C; calf thyrnus DNA was used as a standard. Pepsin was assayed according to Lanoe arad Dunnigan (1978) and the unit was elefiwed as the amount of enzyme that catnsed an increase in optical density at 280 nrn of 0.001 per minante of incubation. Data were analyzed by Student's t-test.

In this study increases in DNA content were used as an index of hyperplasia and increases in the ratios of gastric fundus weight (cellular mass), RNA, protein, rand pepsin coal-

periods body weights were cirnparable hetween mated arad unmated fensales.

Gastric fundus weight increased significiintiy in nmated females after the 2nd week of gestation (Table 1); thereafter constant rises were okse~~red reaching a maxi- rnurrs of 48.9% over control at the cnd of the lactation period. AAcr weaning a sharp drop to 1'7.5% greater than control was oktained within :a week, although the gastric funsdaac of the mated fcn~alcs remained larger than those of the controls even 3 weeks postlactation. The weight of the gastric fu~ndus of the inns sated females increased by 19.656 from the I st week until eke end of the 6th weck, this being ascribcd to normal grsstvth of the organ.

Although the weight of the gastric fundus increased regularly from the beginning of pregnancy until the end of the lactation period, total fundic DNA of the matcd females increased slightly halt Inever significantly, mainly during lactation and the first 2 weeks after weaning (Table 1).

The cellular mass (gastric fundus weight per DNA) was significantly increased by 9% after the 2nd week of gestation and by 22 and 34% after the Bast 2 weeks of lactation. After weaning it returned to control values (Table 2). Total WNA eontents were also significantly augmented after eke 2nd week of gestation, after each

. .

tents to DNA content as irndices of kypcrtrophy. of &he 3 weeks of lactation. and the 2nd week after weaning (Table 2). Total pepsin contents were signifi-

Results cantly increased by 48%~ only after the %st week sf As the control females grew older over the 9 weeks gestation but were significantly decreased by 39% after

of experimentation, their mean body weight ismcreased the 3rd week, just before parturition (Table 3).

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Page 3: Effects of gestation and lactation on rat gastric fundus

TABLE 2. Effects of pregnancy and lactation on gastric %'undus cellular mass and total RNA content

- - - -

Gastric fundus weigkt/800 pg DNA 'Fatal WNA

Unmated Mated % Unmated Mated 5%) Periods Wecks females females difference females females difference

Pregnancy 1 2 3

NOTE: Results are given as Inem values with their standard eprors. WNA is expressed in mi l l igm~s . Values significantly greater than lin~nated control: *P < 0.05; i'P < 0.02: SF < 0.01. Values in parentheses are the musrnber of rats in each group.

TABLE 3. Effects of pregnancy and lactation on gastric fundus pepsin and protein contents

- - - -- - - --

Total pepsin Total protein

Un~amatt'd Mated $1, Unrnated Mateai %I Periods Firecks felxmales females difference fernales females difference

Lactation 1 2 3

NOTE: Results are given as mean values with their staradard errors. Values significantly greater than unmated control: *P <: 0.05; t P .: 0 ~ 0 2 ; $P <r 0.01; #IJ < 0.001. Pepsin is expressed in kilounits and protzin in milligrams. Values in parentheses are the number of rats in each group.

Thereafter ncs significant changes were obseived. Total prcatei1.a contents did not change during the gestation period but were significantly increased during lactation and thc first 2 weeks after weaning; a return to control values was observed 3 weeks after weaning (Table 3).

Ratios of contents of gastric fundus constituents to contents of DNA as indices of hypertrophy are shows irm Table 4. From thesc data it seems that hypertrophy was present above all after the 3rd week of Iactatiols as three of the four indicative parameters were simultaneously and significantly increased tiuring that period.

Discussion Ncw Pindirags frcam this study are that, during gcsta-

tion and lactation, under our experimental conditions, the rat gastric fundus ((1) did not exhibit important intra- cellular cornponerat rnodificaticans, (b) showed mild hypertrophy late during the lactation period, ( c ) did not modify its pepsin content and concentraticll~s un- like those of RNA and protein, and (d) did not exhibit major signs of sis.;ue hyperplaasia during the whole reproductive cycle.

The progressive increase in gastric fundus ~veight

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Page 4: Effects of gestation and lactation on rat gastric fundus

SOELC<)EUR E'I' Al,.

T,mr t 4. Effects of pregnancy and lactation on ratiob of total gastric fundus weight,RNA, pepsin, and protein to DNA content

- .-

Gastric fundub Period\ Weeks weight WNA Pepsin Protein

Pregnancy 1 1.02 0.98 1.30* 0.96 2 1.09'" 1.07 1.15 0.96 3 1 . 1 1 0.94 0.61 t 1.02

Postlactation 1 1.05 0.99 0.73 0.98 2 % .07 1.03 0.93 1.07 3 1.08 0.99 0.77 0.96

Nore: Values are ratios of mated female groups to un~niited fernale gmups. Data are pre- sented on basis of I00 p g DNA; they represent total gastric firndus weight, RNA, pepsin, and protein in rnilligrarns or units. Values sig~~ifYcantiy greater than 1 .O and therefore significantiy greater ehnn unrnated fe~nales: " P <: 0.05; t~ < 0.01.

observed from the beginning of pregnancy until the end of the lactation period was quite comparable to that pre- vicxisly reported by Crean and Rumsey (1 87 1 ), Cripps and Williams ( 1975), and L,ong ( 1969). Indeed thcse different i~nvestigators observed ~naxianum increases in total stomach or gastric fundus weights at the end of the 2nd or 3rd week of lactation. Each study also agreed on a return of gastric fundus weight towards control value after weaning but the time periods at which it occurred were slightly different. In the first two strldles it was evident within a week where the present data iindicabe that the gastric fundus weights were still signil'icantly higher than those of the controls 3 weeks after weaning.

In this study growth of the gastric fundus has beela evaluated exclusively from biochenraical criteria allow- ing a distinction to be esaahlished between hyperplasia and hypertrophy whereas in others (Crean and Ru~nsey 194 1 ; Fell et a1. 1963) anorphological and histological parameters were chosen. For this reason coi~~parisons are difficult to establish and the different experimental approaches may explain some of the discrepancies observed. For example, Crean and Rumsey (197 1) observed hyperplasia of the fundic nnucosa following significant increases in total parietal and peptic cell pc~paslations late during pregnancy and carly during lac- tation. While measuring total DNA contents, increases were noticed during the entire lactation period and the first 2 weeks after weaning but they were not signifi- cant. Moreover, in this study smooth muscles of the gastric fundus were included in all the biochemical assays and it is not known what happens to this portion of the gland during the reproductive cycle.

A factor that could have restrained hyperplasia of the gastric fundus is somatostatin. Iindeed soinatostatin cells are present in the antsal and oxyntic mucosae of

the rat stomach (Alumets et al. 19'79) and sc)matostatin was shown to be secreted in the cat antral lumen under vagal stimulation (Uvnas-Wallensten et al. 1977) and into the circulation from the dog stomach during the intestinal phase of a meal (Schuscizian-a et al. 1979). This hormone has also been shown to inhibit gastric secretion and gastrin release in rraan (Raptis ct al. 1975), gastric secretion iia dog (Konturek et al. 1977), and serum gastrin concentration followiiag vagal denerva- tion and fundectomy in rats (Alumets et al. 1979). The cffect of somatostatin in coiatrolli~ag DNA content of the gastric fundus might be indirect, as a result of a decrease in gastrin release, or direct, with somatostatin acting as an inhibitor of DNA synthesis as shown by I,ehy et al. (1979) in rat fundic and antral rnucosae following gastrin stimulation.

The only criteria we can refer to as indices of hyper- trophy are the increases in tissue weights observed by Crean and Rumsey 4 197 1 ) and Long 6 1969) and those of total nitrogen contents obsemcd by Caralpbell and Fell 61964) and Fell et al. (19631. Data presented in the present study indicate a mild hypertrophy of the gastric faindus only after the 3rd week of lactation as estab- lished by simultaneous increases in cellailar mass, as well as contents and concentrations of WNA and pro- tein. At this particular time increases in cellular mass were in the order of 36.2% (Table 2) whereas those of RNA and protein concentrations were 27% (Table 4). The difference between the increases in cellular mass and those of RNA and protein concentrations could be accounted for by increases in water content as Long ( 1 969) and Cripps and Williams ( 1 977%) have shown that the proportion of water in the wall of the stomach was increased during lactation.

This is the first study to examine pepsin variations

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Page 5: Effects of gestation and lactation on rat gastric fundus

1 001 CAN. J . PHYSHOL. PHARMACQL. VOL. 59, 1981

during a complete reproductive cycle. Long (1 9691, however. demonstrated slight decreases in pepsin con- centration of the gastric juice during the first 2 weeks of lactation. This observation does not contradict our findingc (Table 3) .

Once tissue enlargement has occurred it becomes iampo~tant to search for potential initiators; a homonal control in this case seems appropriate because of the known trophic effects of gastrin on the stomach but it has to be re~nembered that these growth effects of gastrin or pentagastrin were observed following chronic treatments, conditions which are quite different from the physiological situaticsa~s that are experienced in this study.

Chronic injections of pentagastrin, 4 mg/day for 3 weeks, were associated with a 33% increase in gastric fundus wcight (Crean et al. 1969) which is comparable to the 36% increase noticed after 2 weeks of lactation (Table I ). In antrec~ornized rats, pentagastrin restc~red gastric ~nucosal %Q%\IA content to 90%) of its control valuc but failed to increase DNA content (Johnson and Chandler 1973). These findings argrlc for a hyper- trophic rather than a hyperplastic action of pentagastrin on the fundus which was also observed above all during the lactation period.

The difference between the increases in cellaalar mass and those of WNA and protein concentrations could be ascribed, as discussed previously, to increases in water contents of the stonaach. Unfortunately, to our knowledge no study has been reported on the effects of gastrin or pentagastrin c~n gastric fundus water con- tent. The only data available indicate that pentagastrin increased the volume of the fundus mucosa (Grean et al. 1969), parietal cells (Helander 16378), and partially resttsred the reduced glandular rnucosal volume observed after antrectomy (Capofem and Nygaard 1973).

As mentioned earlier in this discussion, somatostatin might be a pcjssible fractor controlling stomach growth under physiological conditions; its antitrophic effect, I~owever, could be less important in the course of chrc~nic gastrin or pentagastrin treatments as penta- gastrin was shown tc~ be a weak releaser of gastric sc~matostatin froin petiused rat stonlach whelm compared with secretin and bornbesin (Chiba et al. 1980). This observation may explain why DNA contents were increased in the oxyntic gland rnucosa following chro- nic pentagastrin treatment (Dembinski and Johnson 1980).

As evidenced in this study. the rat gastric fundus remained quite stable during the whole reproductive cycle showing slight ilmcrea~es in DNA contents during lactatic~n and after weaning and mild hypertrophy at the end of the Iactation period. Gastrin could be partially rcspoaasible for these changes as antral and serum

gastrin concentrations increased during lactation (Lichtenberger et al . 1976; Lichtenberger and Trier 1979). However the antral hormone is not believed to be the only growth factor as duodenal growth occurred during lactation even after antrectc~rny (Lichtenberger and Trier 1979) when semm gastrin concentrations remained comparable to those of the unrnated female. Also, stomach growth occurs during pregnancy when semm gastrin csi.acentrations also remained at control levels. Other hormones such as cholecystokinin or prolactin might also interact alone or in synergy with gastrin: this remains to be studied.

A~rr~b,as , J. , M. EKEI L,'WD, H. ,A. Er, rvfr:Ns~ru, R. H~KANSCBN, 1. I,CPHPEW, and F. SUNDLLR. 1979. Topography of somatostatin cell5 in the stomach of the rat: po~siblc functional significance. Cell T~ssue Wes. 26112: 177- 188.

CP~MPBELI~, R. M., and B. F. FELL. 1964. Gastro-intestinal hypertrophy in the lactating rat and its relation to food intake. 9. Pknysiol. (London), 171: 90-97.

CAPOPERRO, R., and K . NYGAARI). 1973. Effects of antrec- tomy on the gastric mucissa of the rat. Scand. J . Gastroen- terol. 8: 347-352.

C~rrsa. T., T. T A M I N A ~ O , S. KALIOWAKI, Y. I N O B ; ~ , K . MCBRI, Y . SEINC), H. ABE, K. CHIHAKA, S. MATSB:KI:RA, T. FUJBTA, and Y . G o ~ a . 1980. Effccts of variou\ gastrointestinal peptides on gastric somatostatin release. Endocrinology, 106: 145- 149.

CWEAN, G. P., M. W. MAWSIIAI L, and R. D. E. RCJMSLY. 1969. Parietal cell hyperplasia induced by the administra- tion of pentagastrin (ICH 50, 123) to rats. Gartroenterology, 57: 147-156.

CKEAN, G. P., and R. 14. E. R ~ - M ~ E , Y . 1971. Hyperplasia of the gastric mucosa during pregnancy and lactation in the rat. J. Physiol. (London), 215: 181 - 197.

CRIPPS, A. E., and V. J. Wrr~r~hfs. 1975. The effect of pregnancy and lactation on food intake, gastrointestinal anatomy and the absorptive capacity of the srnall intestine in the albino rat. Br. J . Nutr. 33: 17-32.

DEMBINSKB, A. B., and 1,. R. JOHNSON. 1980. Stimulation of pancreatic growth by secretin, caeruiein and pentagastrin. Endocrinology, 106: 323 - 328.

FELL, B. I;., W. M. CAMPBEIL, and R. B O ~ N F . 1964. $her- vations on the n~orph(blogy and nitrogen content of the alimentary canal in breeding hill sheep. Res. Vet. Sci. 5: 175- 185.

FEI I , , B. F., K. A. S ~ ~ I I ~ I , and W. M. CAMPBFLB . 1963. Hypertrophic and hyperplastic changes in the alia-nen- tary canal of the lactating rat. J. Pathol. Bacteriol. 85: 179-1823.

HELAND~R, H. F. 1978. Effects of chronic pentagastrirl stimulation on parietal cc11 size in rat gastric mucora. Acta Physiol. Scand. Suppl. 19- 23.

JEI~-INSC)N, Id. R., and A. M. CIIANDLH.,R. 1973. RNA and DNA of gastric duodenal mucow in antrectonnized and gastrnn-treatcd rats. Am. J . Physiol. 224: 937 -940.

KONTIJREK, S. J . , J . TASLLR, R. KRCBH~, ,4. DEMRINSKII. D. H. COY, and A. V . SLI-IALLY. 1974. Effect of soma-

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Page 6: Effects of gestation and lactation on rat gastric fundus

JOLICOEUR E'I' AL. BOI

tostatin analog 011 gastric and pancreatic secretion. Proc. Soc. Exp. Bic11. Med. 155: 519-522.

LAY^^, J. , and J . DITNNIGAN. 1978. Imprc~ven~ents of the Anron assay for measuring proteolytic activities in acidic pH range. Anal. Bimhern. $9: 461 -471.

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