Physiological responses in swine treated with water containing sodium
bicarbonate as a prophylactic for gastric ulcers1,2
J. T. Cole†, R. A. Argenzio*, and J. H. Eisemann†3
Departments of †Animal Science and *Anatomy, Physiological Sciences, and Radiology,
North Carolina State University, Raleigh 27695
ABSTRACT: Maintenance of gastric pH above 4.0
aids the prevention of bile acid–mediated ulcerative
damage to the pars esophageal tissue in pigs. One
means of doing so is the addition of buffering compounds, such as sodium bicarbonate, to the water supply; however, any potential physiological effect of buffer
consumption has yet to be determined. Experiment 1
tested the acute effects of buffer addition to the water
supply on systemic acid-base and electrolyte balance
in swine (BW 40.7 ± 3.0 kg). Consumption of water
calculated to a 200 mOsm solution with sodium bicarbonate for 24 h increased (P < 0.05) blood Na+,
HCO3−, and pCO2, although these effects were all within
physiologically tolerable levels. Urine pH and Na+ excretion increased (P < 0.001) following the consumption
of NaHCO3, with Na+ concentration almost threefold
higher in treated pigs compared with controls. Experiment 2 determined the chronic systemic effects of buffer
consumption by measuring blood and urine variables,
with pigs consuming NaHCO3-treated water throughout. Water consumption increased (P < 0.001) during
buffer consumption, although intake levels remained
within normal ranges. Blood pH levels were not affected
by long-term consumption of dietary buffer; however,
blood HCO3− (P < 0.05), Na+, and pCO2 (P < 0.01) increased. Urine pH and urine Na+ concentration increased (P < 0.01) in buffer-treated compared with control animals. Results indicate that sodium bicarbonate
can safely be added to the water supply for pigs, with
no clinically relevant alterations in acid-base balance
because the animals readily compensate for buffer
intake.
Key Words: Acid-Base Balance, Blood Variables, Gastric Ulcers,
Sodium Bicarbonate, Swine, Water Consumption
2004 American Society of Animal Science. All rights reserved.
Introduction
Gastric ulcers involving the pars esophagea are a
problem among commercial swine operations, with
prevalence between 10 and 17% (Straw et al. 1994;
Eisemann et al. 2002). Several means have been proposed to prevent ulcer formation or enhance mucosal
repair, such as feeding a coarsely ground diet or treating the diet or water supply with buffers to increase
stomach pH (Wondra et al., 1995a,b; Lawrence et al.,
1
Research reported in this publication was funded in part by the
North Carolina Pork Producers Association, the North Carolina Agric.
Res. Serv. (ARS), and the North Carolina State Univ. College of Vet.
Med. The use of trade names in this publication does not imply
endorsement by the North Carolina ARS or criticism of similar products not mentioned.
2
The authors express their appreciation to R. Palmitier, D. Hardin,
and C. McLamb for their excellent assistance.
3
Correspondence: Box 7621 (phone: 919-515-4044; fax: 919-5157780; e-mail: [email protected]).
Received July 21, 2003.
Accepted May 12, 2004.
J. Anim. Sci. 2004. 82:2757–2763
1998; Ange et al., 2000). Wondra et al. (1995b) reported
that a 1% addition of alkaline salts to the feed decreased
gastric ulceration. However, when the ulcer is a secondary condition, induced by anorexia resulting from a
concurrent disease, administering buffers via the water
supply may be a more effective means of preventing
ulcer formation.
The primary cause of ulcerogenesis in swine is bile
and acid reflux into the proximal stomach. Reflux is
enhanced when the contents are made highly fluidic
owing to consumption of a finely ground diet or as time
after feeding increases (Lang et al., 1998). In a normal,
highly acidic stomach, glycocholic acid will primarily
be in the uncharged, protonated form, increasing the
capacity for membrane disruption (Narain et al., 1999).
Ideally, buffer consumption will maintain gastric pH
above 4.0, which Lang et al. (1998) demonstrated to be
the threshold pH for preventing in vitro bile acid damage to the pars esophagea.
Ange et al. (2000) demonstrated that consumption of
200 mOsm NaHCO3 buffer in the water supply maintained gastric pH above 4.0. However, any potentially
2757
2758
Cole et al.
deleterious effects related to consumption of increased
amounts of NaHCO3, which could include toxic levels
of sodium in the blood, severe disruptions of the acidbase balance, and genitourinary problems associated
with elevated urine pH, have not yet been investigated.
Therefore, the present study was conducted to evaluate
systemic acid-base and electrolyte balance and urinary
variables in response to consumption of a buffer treatment through the drinking water.
Materials and Methods
Table 1. Composition of the dieta
Ingredient
Corn
Soybean meal
Lard
Pellet binderb
Defluorinated phosphate
Salt
Limestone
Vitamins and trace mineralscd
%, as-fed basis
70.0
20.6
5.0
1.7
1.8
0.5
0.4
0.2
Particle size before pelleting was 398 ± 2.35 ␮m.
Ameribond (Ligno Tech USA, Greenwich, CT).
c
Supplied per kilogram of diet: vitamin A, 7,815 IU; vitamin D,
1,100 IU; vitamin E, 38.7 IU; vitamin K, 0.86 mg; choline, 959.4 mg;
niacin, 49.5 mg; pantothenic acid, 24.8 mg; riboflavin, 4.4 mg; thiamin,
3.3 mg; vitamin B6, 1.3 mg; and vitamin B12, 26.4 ␮g.
d
Supplied per kilogram of diet: Fe, 125 mg; Zn, 125 mg; Mn, 26
mg; Cu, 12.5 mg; I, 0.26 mg; and Se, 0.3 mg.
a
b
One experiment evaluated the acute effects and the
other evaluated the chronic effects of buffer addition to
the water supply. The North Carolina State University
Institutional Animal Care and Use Committee approved the treatment protocols before the selection of
animals and initiation of both experiments.
Experiment 1
Animals. Eight barrows weighing 40.7 ± 3.0 kg were
obtained from a crossbred herd (Landrace, Duroc, Large
White, Hampshire). Six of the animals were then used
in a single reversal-design experiment, with two treatments. Animals were housed individually in metabolism crates (0.48 m × 1.61 m) fitted with urine drip
trays and fecal screens, in a room with a 12 h light:12
h dark cycle. The animals were weighed immediately
before surgery to determine initial weight, and again
at the completion of the study to determine final weight.
Surgical Procedures. All animals were fitted with jugular catheters to allow repeated blood sample collection.
Animals were fasted a minimum of 12 h before anesthesia, which was induced via injection of ketamine (11.0
mg/kg BW, i.m.) and xylazine (1.5 mg/kg BW, i.m.) and
maintained with isofluorane delivered via mask. To insert the catheter into the jugular vein, a ventral incision
approximately 2.5 cm from the midline of the animal
was made. Blunt dissection exposed the vein; after making a small incision in the vein, the catheter (i.d. 0.102
cm, o.d. 0.203 cm, micro-renathane) was inserted (approximately 10 cm) and sutured into place. A 45-cm
probe allowed exteriorization at the dorsal base of the
neck, where a patch secured the catheter. A minimum
of 10 d was allowed for recovery following the surgical
procedure, before the 24-h period of treatment administration and sample collection.
Water and Diet. Animals were monitored throughout
the day to ensure adequate feed and water availability,
as well as overall health of the animal. Water was available ad libitum and delivered via an Arato water nipple
(Aratowerk GmbH & Co., Cologne, Germany). Individual 25-L Nalgene water containers provided each animal’s water supply. Gravity-fed water flow rate averaged 460 mL/min. Water spillage was collected separately from excreted urine and was quantified to more
accurately estimate each animal’s daily water intake.
In this study of the acute effects of buffer administration, the water containers were weighed before adminis-
tration of the treatment, filled with a measured amount
of fresh or buffered water, and suspended above each
metabolism crate. Following the collection of the last
sample of the 24-h period, the containers were again
weighed, and the water intake determined.
A finely ground and pelleted corn/soybean meal–
based diet was used (Table 1). Before pelleting, particle
size was determined to be 398 ± 2.35 ␮m. Animals were
fed ad libitum; however, feed intake was monitored
daily. Each day at 0800, remaining feed from the previous day was measured and animals were refed at 110%
of each animal’s previous day’s intake. Animals were
fed this diet from the time of catheter insertion to the
completion of the sampling period.
Treatments. Treatments consisted of either unaltered
water (control) or water containing sodium bicarbonate
to produce a 200 mOsm solution (BUF). Treatments
were initiated at 0800 on the day of the experiment,
which lasted 24 h.
Blood and urine samples were taken throughout the
24-h period. The experimental design allowed animals
receiving the treated water in the first period to receive
the control in the second period and vice versa. The six
animals selected for experimentation were randomly
separated into two groups of three, which went through
the protocol sequentially for logistical reasons. Each
group was randomly divided into two subgroups, designated to receive buffer-treated or control water, and
then switched between periods to the other treatment,
so that all six pigs would receive both treatments. Between periods, all animals received untreated water for
48 h to eliminate any carryover effect from consuming
buffer-treated water.
Sample Collection. Blood samples were taken at 0730,
0900, 1000, 1200, 1400, 1600, and 0730 the following
day. The initial samples collected at 0730 determined
the baseline values and were taken before administration of the treatment. Before each collection, a blood
volume equivalent to twice the catheter volume was
drawn and discarded to prevent contamination of the
ensuing sample by the solution used to seal the catheter
2759
Acid-base response to buffer consumption
between samplings. At each collection, 3 mL of blood
was collected and sealed immediately to prevent atmospheric exposure and subsequent alteration of blood
gas values. Samples were immediately placed on ice
and transported to a blood gas analyzer (GEM Premier
Plus; Instrumentation Laboratory, Lexington, MA),
which quantified pO2, pCO2, HCO3−, K+, Na+, and hematocrit. Samples were analyzed within 60 min of collection. Voided urine was collected at 1030, 1230, 1430,
1630, and the following day at 0830. The entire amount
voided was immediately weighed and a pH value determined using a pH meter (Acumet; Fischer Scientific,
Pittsburgh, PA). Subsamples (∼50 mL) were frozen for
later determination of Na+, Cl−, and K+ on an electrolyte
content analyzer (Hitachi 912; Roche Diagnostics, Indianapolis, IN).
Experiment 2
Animals, Water, and Diet. Ten crossbred barrows
weighing 33.8 ± 3.0 kg were obtained and fitted with
jugular catheters. Eight of the animals were used in
the experiment, which had a single reversal design,
although this experiment lasted for 10 d. Barrows were
from the same herd as those in Exp 1. They were
housed, fed, and watered as described above, with the
same procedure used to determine intake of both feed
and water. The animals were weighed immediately before surgery to determine an initial weight, and again at
the completion of the study to determine a final weight.
Surgical Procedures. Animals were fitted with jugular
catheters, as described for Exp. 1, with the following
exceptions. Anesthesia was induced by injection of Telazol (a combination of tiletamine and zolazepam, 3 mg/
kg BW), instead of ketamine/xylazine. Anesthesia was
maintained with isofluorane administered via orotracheal intubation.
Treatments. Treatments were initiated at 0800 of d
1 and consisted of either untreated water (control) or
water containing sufficient sodium bicarbonate to obtain a calculated 200 mOsm solution. The experimental
design allowed the animals to receive one of the two
randomly assigned treatments in the first period and
then receive the other treatment in the second period.
Periods lasted 10 d, with all animals receiving untreated water for 72 h between periods. This allowed
elimination of any carryover effect from consumption
of treated water in the previous period. Additionally,
the animals were randomly divided into two groups,
which went through the protocol sequentially.
Sample Collection. Blood was collected for analysis
on d 5 and 10 of each period at 1100, 1300, 1500, and
1700. Blood samples were collected and analyzed as
described above. Urine samples were collected daily,
following the morning feeding. Samples were weighed
and pH was measured. Subsamples were taken and
stored for analysis as described above. Water samples
were taken daily and frozen for later analysis, as described above. Aliquots of the daily water samples for
each animal were later pooled, combining an equal
amount of water from each day on which the animal
received the buffer treatment, and, separately, received
the control treatment. Thus, two samples were measured, in duplicate, for each pig: one untreated sample
and one treated sample. These aliquots were then analyzed for osmolality (Micro-osmette; Precision Instruments, Natick, MA).
Statistical Analysis
In both Exp. 1 and 2, data were analyzed using the
Proc Mixed procedure of SAS (SAS Inst., Inc., Cary,
NC). The repeated factor used was (TIME), representing the time at which each sample was collected. Blood
variables were analyzed using a model consisting of
treatment, animal(treatment), time, time × treatment,
day × treatment, as well as day, and treatment × time
× day in Exp. 2 only. In Exp. 1, the initial 0730 samples
were analyzed separately from those collected after
treatment initiation. Variables were analyzed via the
same methods, excepting time inclusive statements.
The fixed effects were treatment, time, and day. Random effects included animal within treatment and the
interactions. Each animal was an experimental unit.
Urine and water variable analysis used the same model,
without the time terms. Significance was declared at P
< 0.05.
Results
Experiment 1
Initial body weights of the pigs were 40.7 ± 3.0 kg,
whereas final body weights measured 54.3 ± 4.2 kg.
Initial weights were taken the day before the surgery,
and the final weights were taken the morning of the
final sample collection. Weights were taken 22 d apart.
One pig’s catheter came out after the first period, so
no data were obtained from that pig in the second period. This pig received the control water treatment in
the first period, and did not receive the treated water
in the second period. Therefore, there were only two
animals on the treated water in the second period, leaving only five animals to receive the buffered water treatment, compared with six consuming the untreated
water.
Water intake was not affected by treatment. Pigs
consuming water treated with bicarbonate consumed
4.34 ± 1.35 kg of water in 24 h, whereas those receiving
untreated water consumed 5.05 ± 1.20 kg. Feed intake
was monitored from the day animals were acquired
until the completion of the study, to assist monitoring
the health status of the animals following surgery.
From the day the animals were obtained until the conclusion of the study, barrows consumed 1.72 ± 0.20 kg/d;
during the two sampling periods the barrows consumed
1.63 ± 0.34 kg/d.
Despite being assigned randomly to treatment
groups, pigs in the BUF group demonstrated elevated
2760
Cole et al.
Table 2. Blood and urine variables in pigs in Exp. 1 measured during 24-h consumption of either buffer-treated
(200 mOsm NaHCO3) or untreated (control) watera
Item
Blood variables
pH
HCO3−, mmol/Lc
pCO2, mmHgc
K+, mmol/L
Na+, mmol/Lc
Hematocrit, %
Urine variables
Na+, mmol/Ld
pHd
Controlb
7.43 ± 0.01
34.51 ± 0.92
51. 5 ± 1.23
4.53 ± 0.06
142.09 ± 0.52
36.55 ± 1.06
61.62 ± 2.29
7.60 ± 0.10
Bufferb
7.45
38.31
55.0
4.44
143.64
37.79
±
±
±
±
±
±
0.01
1.00
1.34
0.07
0.58
1.16
177.94 ± 7.16
8.61 ± 0.11
a
For each variable and treatment, values are main effect means ±
SEM representing six sampling times for the blood variables and five
sampling times for the urine variables over a 24-h period.
b
Control, n = 6; buffer, n = 5. The effects of sampling time (P = 0.14)
and the time × treatment interaction (P = 0.32) were not significant.
c
Means within a row differ: P < 0.05.
d
Means within a row differ: P < 0.01.
values (P < 0.05) for blood pH, HCO3−, and pCO2 before
receiving any treatments (data not shown). In pigs consuming the buffer-treated water, pH remained constant, whereas mean values for HCO3− and pCO2 were
increased (Table 2; P < 0.05). Blood sodium measurements showed an effect (P < 0.05) of treatment, with
higher levels seen in BUF pigs (Table 2). However,
the magnitude of these changes is clinically irrelevant
because it did not exceed normal ranges for these variables (Nagai et al., 1994). Blood potassium and hematocrit (Table 2) were not affected by treatment.
Both urine sodium and urine pH values showed a
rapid response to the consumption of NaHCO3-treated
water. For both variables, there was an increase in
mean levels (Table 2, P < 0.01) in pigs consuming
treated water compared with pigs receiving untreated
water. Urine sodium concentration was almost threefold higher in BUF pigs than in control pigs.
Experiment 2
Initial body weights of the pigs were 33.6 ± 3.21 kg.
Final body weights, taken 43 d later at the completion
of the study, were 81.9 ± 8.59 kg. Feed intake was not
altered by water treatment; BUF pigs consumed 2.35
± 0.27 kg/d, and control pigs consumed 2.36 ± 0.38 kg/d.
Bicarbonate was added at a calculated osmolality of
200 mOsm; however, the measured osmolarity of the
treated water was 176.6 mOsm/L compared with 6.1
mOsm/L for the untreated water. Water intake (Figure
1) was monitored daily. Due to a system to divert and
account for spillage, water consumption was quantified
accurately. Pigs receiving the BUF treatment consumed more (P < 0.001) water (10.10 ± 0.23 kg/d) than
the control pigs (6.95 ± 0.23 kg/d).
Blood pH (Table 3) was not affected by treatment or
time, with neither treatment demonstrating a discernible trend in blood pH values across collection times on
Figure 1. Water intake in pigs in Exp. 2 during 10-d
consumption of either buffer-treated (200 mOsm
NaHCO3) or untreated (control) water. Treatments were
begun at 0800 on d 1. Values are daily means ± SEM.
Average water intake was higher (P < 0.001) in pigs consuming buffer-treated water. No day × treatment interactions were observed (P = 0.46).
the sampling days (data not shown). Consumption of
bicarbonate-treated water did generate an increase in
circulating HCO3− (P < 0.05), as well as an increase in
pCO2 (P < 0.01; Table 3). Across treatments, the average
pCO2 concentration was higher (P < 0.05) on d 5 than
d 10 (data not shown).
Mean blood sodium (Table 3) was higher (P < 0.01)
in pigs receiving the BUF treatment than in pigs receiving the control treatment. Blood potassium concentrations (Table 3) were unaffected by treatments. The
mean hematocrit (Table 3) decreased (P < 0.01) in pigs
consuming NaHCO3-treated water compared with control, suggesting an increase in extracellular fluid
volume.
Urine electrolyte concentrations (Na+, K+, Cl−), pH,
and output were also analyzed, with the aim of determining the fate of the excess Na+ intake, or any pH
alterations attributable to the bicarbonate treatment.
Consumption of NaHCO3 caused an increased urine
Na+ concentration within 24 h of treatment initiation
(Figure 2). Overall mean sodium concentration in urine
was higher (P < 0.01) in pigs consuming bicarbonatetreated water than in control animals. Overall mean
urine K+ concentration (Figure 3) was lower (P < 0.01) in
pigs consuming the BUF treatment. The total amount of
potassium excreted was unchanged; BUF pigs excreted
10.8 ± 2.8 g K+/d; control pigs excreted 11.7 ± 3.2 g K+/d.
Overall mean urine pH values (Figure 4) were higher
(P < 0.01) in pigs fed the NaHCO3 treatment compared
with those receiving the control. Overall mean urine
volume (Figure 5) increased (P < 0.05) in pigs consuming NaHCO3 compared with the animals receiving untreated water.
2761
Acid-base response to buffer consumption
Table 3. Blood variables in pigs in Exp. 2 measured during 10-d consumption of either buffer-treated (200 mOsm
NaHCO3) or untreated (control) water. Mean values across sampling time on d 5 and 10. The overall value is the
mean of all samples collecteda
HCO3−, mmol/L
pH
Item
Day 5
Day 10
Overallb
SEM
pCO2, mmHgc
K+, mmol/L
Na+, mmol/L
Hematocrit, %
Control
Buffer
Control
Buffer
Control
Buffer
Control
Buffer
Control
Buffer
Control
Buffer
7.42
7.42
7.42
0.001
7.43
7.43
7.43
0.001
37.5
37.0
37.2*
0.30
40.1
38.7
39.4*
0.30
57.4
56.4
56.9**
0.50
59.9
57.9
58.4**
0.50
4.38
4.39
4.38
0.03
4.36
4.29
4.33
0.03
141.9
142.0
142.0**
0.20
143.3
142.4
142.8**
0.20
34.9
34.6
34.8**
0.31
33.8
33.3
33.1**
0.31
a
For each variable and treatment, values are treatment means representing four sampling times on each sampling day. The effect of
sampling time (P = 0.12), the time × treatment interaction (P = 0.24), and the day × treatment interaction (P = 0.35) were not significant.
b
For each variable, means within a row differ: *P < 0.05; **P < 0.01.
c
Mean values for pCO2 across treatment were higher (P < 0.05) on d 5 than 10.
Discussion
Expected normal water intake values in pigs are difficult to estimate owing to water spillage during consumption, as well as normal variation owing to environmental temperature, physiological state, dietary characteristics, quality of feed or water, and health of the
animal. However, several researchers have presented
information that can be used to calculate an estimated
normal intake. A report by the ARC (1981) indicated
that the relationship of water intake to diet consumption ranged from 3.9 to 5.0 L water/kg diet. Based on
these values, expected daily water intake was calculated to determine excessive consumption in the treated
animals. The animals in the first experiment can be
Figure 2. Urine sodium levels in pigs in Exp. 2 during
10-d consumption of either buffer-treated (200 mOsm
NaHCO3) or untreated (control) water. Treatments were
begun at 0800 on d 1. Values are daily means ± SEM.
Average urinary sodium concentration was higher (P <
0.01) in pigs consuming buffer-treated water. No day ×
treatment interactions were observed (P = 0.41).
expected to consume between 4.75 to 5.80 kg water/d
based on feed intake. The control pigs consumed 5.05 ±
1.20 kg water/d, with the treatment slightly decreasing
water intake (4.35 ± 1.35 kg water/d), and both values
being within the normal ranges.
In Exp. 2, the expected water intake based on feed
consumption ranged from 9.13 to 11.7 kg/d. Control
animals consumed 6.95 ± 0.42 kg water/d and the BUF
pigs consumed 10.10 ± 0.86 kg water/d. The intake values in the second experiment were higher than those
in the first experiment owing to the greater feed intake
and growth rate of the animals. At the completion of the
second experiment, the animals were approximately 27
kg heavier than at the completion of the first experiment. In comparison, Ange et al. (2000), using pigs
of weights similar to those in the second experiment,
reported water disappearance levels for a 200 mOsm
water treatment of 13.56 kg/d; however, wastage was
not quantified in that study.
Figure 3. Urine potassium concentrations in pigs in
Exp. 2 during 10-d consumption of either buffer-treated
(200 mOsm NaHCO3) or untreated (control) water. Treatments were begun at 0800 on d 1. Values are daily means
± SEM. Average urinary potassium concentration was
lower (P < 0.01) in pigs consuming buffer-treated water.
No day × treatment interactions were observed (P = 0.25).
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Cole et al.
Figure 4. Urine pH levels in pigs in Exp. 2 during 10d consumption of either buffer-treated (200 mOsm
NaHCO3) or untreated (control) water. Treatments were
begun at 0800 on d 1. Values are daily means ± SEM.
Average urinary pH was higher (P < 0.01) in pigs consuming buffer-treated water than in pigs consuming untreated water. No day × treatment interactions were observed (P = 0.16).
The increase in water intake by pigs consuming the
BUF treatments may be due to numerous factors. Possibly, the consumption of 200 mOsm water may increase
plasma osmolarity, activating hypothalamic thirst sensors, and stimulating increased intake (Vander, 1991).
An alternative explanation may be due to a “salt appetite, thirst analogue.” In addition to having a regulatory
Figure 5. Urine output (kg) in pigs in Exp. 2 during
10-d consumption of either buffer-treated (200 mOsm
NaHCO3) or untreated (control) water. Treatments were
initiated at 0800 on d 1. Values are daily means ± SEM.
Pigs consuming buffer-treated water micturated a greater
amount (P < 0.05) of urine than did pigs consuming untreated water. No day × treatment interactions were observed (P = 0.22).
appetite for salt to ensure adequate intake, many mammalian species have a hedonistic appetite causing ingestion of much higher salt quantities than is required
to meet their physiological needs (Vander, 1991).
The decrease in hematocrit following NaHCO3 administration suggests an extracellular fluid volume
expansion owing to Na+ retention. However, this increase is within normal values and thus of limited clinical relevance (Nagai et al., 1994).
It was theorized that the consumption of such high
levels of NaHCO3 (in some cases more than 100 g/d)
may alter blood acid-base balance and induce a mild
alkalosis. In neither experiment did the BUF treatment
result in an increase in blood pH, indicating rapid compensation for excess base intake. Hannon et al. (1990)
reported a mean venous pH value for healthy, untreated
pigs of 7.42, with a range of 7.38 to 7.48. The values
obtained in this study in pigs consuming NaHCO3 for
10 d (7.43 pH) were well within physiologically tolerable ranges.
Despite the consumption of large quantities of
NaHCO3, neither blood K+ concentration nor urine K+
excretion levels were altered. Urine concentration of K+
decreased with the BUF treatment, but, owing to the
increased urine output, the total amount of K+ excreted
did not change.
Comparison of blood HCO3− levels between Exp. 1
and 2 showed a similar pattern, with the bicarbonateinduced increase being greater in Exp. 1 than in Exp.
2, indicating physiological adaptation. In a study characterizing various blood variables in pigs, Hannon et
al. (1990) observed venous HCO3− levels of 31 mEq/
L, which is much lower than even the control pigs in
these trials.
Acid-base balance in mammals is regulated primarily
by two mechanisms: 1) respiratory control of blood pCO2
and 2) urinary HCO3− excretion (Rose, 1989). Blood pH
is maintained at an optimal level by a 20:1 ratio of
HCO3− to CO2 (Hannon et al., 1990). In these studies,
the BUF treatment elevated circulatory HCO3− levels,
with no alteration of blood pH. To maintain the optimal
20:1 ratio, the animals hypoventilated, thereby increasing pCO2 levels. Calculating the Henderson-Hasselbach
equation, pH = 6.1 + log[HCO3−]/[CO2], using values
obtained in this study confirm that the consumption of
large amounts of NaHCO3 did not cause any disturbance in acid-base balance because the 20:1 ratio was
maintained.
Despite the consumption of nearly 25 g/d of Na+ from
both feed and water intake, there was little effect on
blood levels. Values never approached a concentration
of 150 mEq/L, which is considered the minimal threshold for hypernatremia (Fraser et al., 1991). Pigs consuming 20 g of Na+ from the BUF treatment, in addition
to the approximately 5 g/d of Na+ intake in the diet,
excreted almost 19 g of Na+ daily in the urine.
As these studies indicate, the consumption of moderate levels of buffer (NaHCO3) may induce a short-term,
clinically insignificant alkalotic state, for which the
Acid-base response to buffer consumption
body rapidly compensates. One concern with the elevated urine pH is the development of uroliths. To the
best of the authors’ knowledge, the only report of uroliths in swine was by Manning and Blaney (1986). In
other species with this problem, such as cats, castration
and increased urine pH (typically secondary to bacterial
infection) are the two primary risk factors for the development of uroliths (Osborne et al., 1990). Normal urine
pH levels in swine range from 5.5 to 7.7 (Schenkman
et al., 1999). During the 10-d study, both groups of
animals produced urine with an elevated pH; however,
animals consuming NaHCO3 generated more alkaline
urine, with a maximal value of 9.1 seen at d 9. Although
this would seem to put the typical commercial animal
at risk for the development of urinary tract problems,
the increase in urine output following consumption of
buffer-treated water, should decrease the likelihood of
urinary tract problems associated with increased urine
pH. Additionally, if the buffers are used prophylactically during anorexigenic illness, the short-term consumption of buffers would likely eliminate the possibility of urolith formation.
Implications
Previous research in this laboratory and others has
demonstrated the efficacy of adding buffers to the water
or feed supply in maintaining proximal gastric pH
above 4.0, the threshold for epithelial damage. However, until this study, the systemic effects of consumption of high levels of sodium bicarbonate had not been
determined. The studies described here show no clinically significant physiological disturbance to the acidbase homeostasis. Should an economically feasible
means of delivering buffer-treated water be developed,
it may prove possible to decrease ulcerative damage
following unrelated disease, such as herd outbreaks of
respiratory illness, or any condition involving anorexia.
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