Association Between Weight Gain, Blood Parameters, and Thyroid Hormones
and the Development of Ascites Syndrome in Broiler Chickens1
D. Luger, D. Shinder, V. Rzepakovsky, M. Rusal, and S. Yahav2
Institute of Animal Science, Agricultural Research Organization, The Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
ABSTRACT The present study examined the associa-
tion between thyroid hormones and the development of
ascites on one hand and the ability to predict ascites from
growth rate and hematocrit on the other hand. Ascites
syndrome was induced in broiler chickens in two trials
by exposing the chicks to low ambient temperature (Ta)
and by supplying a pellet form of diet. Weight gain, hema-
tocrit, hemoglobin, and plasma thyroxin (T4) and triiodo-
thyronine (T3) concentrations were measured weekly for
each bird, and comparisons were made between birds
that eventually died from ascites and those that did not.
Mortality from ascites amounted to 24.3 and 24.2% in
Trials 1 and 2, respectively. Weight gain did not differ
between ascitic and healthy chickens up to approximately
2 wk before death but was significantly lower in the ascitic
broilers 1 to 2 wk before death. Hematocrit was signifi-
(Key words: ascites, weight gain, hematocrit, thyroid hormone)
INTRODUCTION
Ascites syndrome (accumulation of fluid in the perito-
neal cavity) appears in fast-growing chickens, mostly dur-
ing the winter, and is a considerable cause of mortality
(Wideman, 1988; Maxwell and Robertson 1998). The
pathogenesis of ascites is similar to that of high-altitude
disease, characterized by an imbalance between oxygen
supply and oxygen need, which causes hypoxemia. Hy-
poxemia initiates a cascade of events, including increased
cardiac output, increased pulmonary blood pressure (hy-
pertension), enlargement of the right ventricle, and car-
diopulmonary dysfunction that results in ascites and
death (Julian, 1993, 1998; Wideman and Bottje, 1993; Max-
well et al., 1995). Increased susceptibility of broilers to
ascites has been linked with intensive growth (Maxwell,
1990; Vereijken and Albers, 1990; Owen et al. 1995). How-
ever, Wideman and Kirby (1995, 1996) emphasized that
2001 Poultry Science Association, Inc.
Received for publication November 13, 2000.
Accepted for publication March 13, 2001.
1
Contribution from the Institute of Animal Science, Agricultural Re-
search Organization, The Volcani Center, Bet Dagan, Israel. No. 366/00.
2
To whom correspondence should be addressed: vlyahav@volcani.
agri.gov.il.
965
cantly higher in broilers with ascites with the exception
of ascitic broilers that died at the age of 7 wk (Trial 1).
In ascitic broilers, T4 and T3 concentrations declined sig-
nificantly during the week of death. The present findings
raise the question of whether the association between low
levels of thyroid hormones and the development of ascites
is one of the physiological responses in the syndrome
cascade, or whether the failure to maintain thyroid hor-
mones concentration is one of the triggers of the syn-
drome initiation. This question requires further investiga-
tion. It can be concluded that a high rate of weight gain
is not always a good predictor of ascites development.
Hematocrit and thyroid hormones can provide a good
indication but only during the last week of life, and not
in all cases. None of these parameters, however, can pre-
dict the development of ascites at an early age.
2001 Poultry Science 80:965–971
it is not necessarily the fastest-growing individuals in the
flock that develop ascites.
Ambient temperature (Ta) and dietary energy level are
two factors that are related to the rate of metabolic activity
and, hence, to the amount of oxygen required by the
animal (Kuhn et al., 1984b; Jones, 1994; Buys et al.,
1999a,b). A higher metabolic rate is associated with in-
creased secretion of the hormone thyroxine (T4), which
is deiodinated to triiodothyronine (T3) in the periphery,
mainly in the liver and kidneys. Triiodothyronine is the
main metabolic stimulating hormone (McNabb and King,
1993; Gabarrou et al., 1997). Plasma T3 is associated with
temperature regulation and is an important growth pro-
moter in chickens (McNabb and King, 1993; Carew et al.,
1998; Gonzales et al., 1999; Yahav, 2000); it may thus be
involved in modification of growth rate in response to
environmental temperature. The circulating concentra-
tion of T3 is increased at low temperatures (Hillman et
al., 1985; Kuhn et al., 1984a,b; Yahav et al., 1996) and is
positively correlated to feed intake (Klandorf and Harvey,
1985; Yahav et al., 1995, 1996, 1998). The plasma concen-
Abbreviation Key: Ta = ambient temperature; T4 = thyroxin; T3 = triio-
dothyronine.
966
tration of thyroid hormones may shed light on the associa-
tion between the development of ascites and the ability
of the ascitic chicken to cope with increased metabolic
demands.
Changes in the cardiovascular system to accommodate
oxygen needs have been observed in birds adapted to
low Ta (Julian et al., 1989; Maxwell et al., 1995; Shlosberg
et al., 1996, 1998; Yahav et al., 1997; Wideman, 2000).
These changes include increases in blood volume, hema-
tocrit, and hemoglobin concentration and are often ac-
companied by compensatory changes in heart weight
(Carey and Morton, 1976; Palomeque and Planas, 1978;
Lubritz et al., 1995; Fedde and Wideman, 1996; Yahav et
al., 1997).
In the present study, we examined the association of
weight gain, hematocrit, hemoglobin, and thyroid hor-
mone concentrations in the development of ascites. The
possibility of using these parameters to predict the devel-
opment of the syndrome was considered.
MATERIAL AND METHODS
Experimental Design
Ascites was induced in broiler chickens in two separate
trials, by exposing the chickens to low Ta and by supply-
ing a pelleted diet. Male chickens (Cobb) were obtained
from a commercial hatchery and raised in a temperature-
controlled room (±1.0 C), under continuous fluorescent
illumination in battery brooders or in cages (up to 3 and
7 wk of age, respectively). At 1 d of age, 200 chicks were
selected from a population of 250, according to body
weight; those with extreme weights were discarded (more
than 2 SD of the mean).
The trials were divided into two treatments: a control
with four replicates of 10 birds each and ascites-induced
treatment with 16 replicates of 10 birds each. Broilers in
the control treatment were raised under regular condi-
tions up to 4 wk of age (Yahav et al., 1996) and then were
exposed to constant 22.0 ± 1 C until 7 wk of age. Chickens
that were treated for the induction of ascites were raised
under standard conditions during the first week of age.
At 7, 14, and 21 d of age, Ta was reduced to 26.0 ± 1.0,
20.0 ± 1.0, and 15.0 ± 1 C, respectively. The lowest Ta was
maintained until the end of the experiment. Water and
feed were provided ad libitum. The feed in pellet form
was formulated according to the specifications of the Na-
tional Research Council (1994).
At weekly intervals, body weights were measured and
blood samples were taken on an individual basis. Whole
blood samples were taken from the brachial vein, and an
aliquot was stored at 4 C for hematocrit and hemoglobin
analyses; the remainder was centrifuged at 3,000 rpm for
10 min to obtain plasma, which was stored at −20 C.
3
Hettich, Tuttlingen, D-78532 Germany.
4
Catalog no. E9133, Sigma Chemical Co., St. Louis, MO 63178-9916.
5
Coat-A-Count, Canine, T4 and T3 kits; Diagnostic products Corpora-
tion (DCP), Los Angelese, CA 90045-5597.
LUGER ET AL.
Hematocrit and Hemoglobin
Blood for hematocrit measurements was collected into
heparinized microcapillary tubes and centrifuged in a
microliter centrifuge3 for 7 min. The hemoglobin concen-
tration was analyzed colorimetrically with Sigma diag-
nostic kit no. 525,4 according to the manufacturer’s in-
structions.
Thyroid Hormones
Radioimmunoassay for T4 and T3 was performed on
plasma samples, using commercial kits5 validated for do-
mestic fowl (Yahav et al., 1998). The T3 assay was charac-
terized by intraassay and interassay variations (CV) of
7.0 and 9.4%, respectively. The T4 assay was characterized
by intraassay and interassay variations (CV) of 5.0 and
7.5%, respectively. The T3 assay was carried out without
modifications, whereas in the T4 analysis, 100-µL samples
were used.
Ascites Diagnosis
During the experiment, all dead chickens were diag-
nosed for ascites according to abdominal fluid accumula-
tion and the ratio of right ventricle to total ventricle
weight. At the end of the experiments, all chickens were
killed for detection of ascites.
Statistical Analysis
The results were analyzed for each of 7 wk for the
following treatment groups: control, healthy chickens
(those treated to induce ascites but did not develop the
syndrome), and chickens that eventually developed asci-
tes and died. All results were subjected to one-way AN-
OVA according to Snedecor and Cochran (1968) and to
Duncan’s multiple-range tests (Duncan, 1955). Means
were considered significantly different at P ≥ 0.05.
RESULTS
Performance and Mortality
Cumulative mortality from ascites syndrome was 24.3
and 24.2% in Trials 1 and 2, respectively, and occurred
between 4 and 7 wk of age, with a maxima of 10 and
8.8% at 5 wk of age in Trials 1 and 2, respectively. None
of the control birds developed ascites. The effects of cold
exposure and the pelleted diet on weight gain are summa-
rized in Table 1. Initial body weights, on Day 1, of the
control and cold exposed groups were similar (54.83 ±
0.06 g and 54.95 ± 0.05 g for Trial 1 and 52.45 ± 0.06 g
and 52.65 ± 0.08 g for Trial 2). Up to 3 wk of age, no
significant differences in weight gain between ascitic and
healthy chickens were observed. Thereafter, a significant
decline in weight gain was observed in the ascitic chickens
prior to death.
 ASCITES, WEIGHT GAIN, BLOOD PARAMETERS, AND THYROID HORMONES 967
TABLE 1. The effect of ascites syndrome development on weight gain
of broiler chickens during life span

Distribution of ascitic broilers by age at mortality

Age
1 2
(wk) Control Healthy 4 5 6 7
Trial 1
1 119 ± 7.7 116 ± 5.6 121 ± 7.1 121 ± 5.3 124 ± 2.1 115 ± 4.1
2 295 ± 5.7ab 279 ± 5.1ab 268 ± 9.5b 291 ± 6.1ab 300 ± 9.6ab 309 ± 6.1a
3 426 ± 11.0 369 ± 8.5 365 ± 18.3 417 ± 14.7 378 ± 27.0 368 ± 25.0
4 365 ± 23.5ab 428 ± 18.1a 291 ± 39.0b 374 ± 22.3ab 467 ± 25.0a 423 ± 32.9a
5 396 ± 29.8a 386 ± 18.8a 173 ± 46.4c 347 ± 37.6ab 321 ± 29.4bc
6 549 ± 24.5a 506 ± 18.9a 173 ± 90.8b 479 ± 41.3a
7 650 ± 23.0a 626 ± 25.8a 436 ± 67.2b
Trial 2
1 132 ± 3.6 130 ± 2.2 131 ± 3.2 135 ± 5.6 130 ± 4.5 135 ± 7.6
2 337 ± 7.0 320 ± 7.7 336 ± 17.5 339 ± 7.9 316 ± 13.1 325 ± 9.5
3 444 ± 16.2a 303 ± 12.8b 307 ± 17.8b 308 ± 12.8b 330 ± 16.8b 342 ± 20.1b
4 413 ± 13.6ab 459 ± 13.1a 298 ± 30.6c 342 ± 19.6bc 449 ± 14.6a 463 ± 36.3a
5 541 ± 20.1a 507 ± 27.5a 183 ± 64.3b 491 ± 50.1a 473 ± 53a
6 619 ± 45.7ab 654 ± 44.0a 170 ± 88.0c 447 ± 68.0b
7 741 ± 21.2a 515 ± 30.1a 154 ± 161b
Within rows, values with different superscripts differ significantly (P ≤ 0.05).
a–c

n = 40 for control chickens. For chickens exposed to ascites syndrome-inducing conditions n varied with
1

week of age.
2
Healthy = broilers that were exposed to low ambient temperature but did not develop ascites.

Blood Variables Thyroid Hormones

Hematocrits were significantly higher in ascitic broilers
1 to 2 wk before death as compared to healthy birds.
During the week of death, ascitic broilers had extremely
high hematocrits as compared to controls and healthy
broilers of the same age. However, at 7 wk of age, ascitic
and non-ascitic broilers exhibited similar hematocrit val-
ues (Table 2, Trial 1). In Trial 1, hemoglobin concentration
approximately 2 wk before death tended to be higher in
the ascitic broilers than in the healthy ones, whereas in
Trial 2, it was significantly higher (Tables 2 and 3).
Plasma T4 concentration was significantly higher in the
control chickens than in the treated ones, throughout the
experiment (Tables 4 and 5). Exposure to low Ta resulted
in a decline in plasma T4, followed by immediate or
slower recovery in the control or healthy chickens, respec-
tively; whereas in the ascitic chickens, no such recovery
was demonstrated. Plasma T4 concentration was signifi-
cantly reduced in the ascitic chickens 1 wk before death.
Plasma T3 concentration increased as a result of cold expo-
sure and was significantly higher in the healthy chickens

TABLE 2. The effect of ascites syndrome development (Trial 1) on hematocrit and hemoglobin
concentrations in broiler chickens at 3 to 7 wk of age

Distribution of ascitic broilers by age at mortality

Age
1 2
(wk) Control Healthy 4 5 6 7
Hematocrit (%)
2 33.7 ± 0.47b 33.6 ± 0.4b 36.9 ± 0.58a 35.2 ± 0.49ab 35.0 ± 0.77ab 32.7 ± 0.64b
3 33.6 ± 0.67b 34.1 ± 0.51b 39.3 ± 1.4a 36.6 ± 0.83ab 35.5 ± 1.0ab 34.3 ± 0.91b
4 31.9 ± 0.64d 38.3 ± 0.68c 47.2 ± 1.7a 45.4 ± 1.67ab 40.3 ± 2.0bc 37.4 ± 1.6cd
5 34.2 ± 0.8c 39.2 ± 0.62bc 51.9 ± 2.4a 44.7 ± 2.3b 41.7 ± 2.0b
6 33.5 ± 0.9b 38.1 ± 0.75b 51.3 ± 2.6a 38.8 ± 2.0b
7 35.5 ± 0.84ab 36.1 ± 0.74ab 38.1 ± 2.3a
Hemoglobin (g/dL)
2 9.7 ± 0.33a 9.0 ± 0.17ab 9.4 ± 0.16ab 9.8 ± 0.26a 9.7 ± 0.10a 8.3 ± 0.35b
3 9.6 ± 0.31b 9.7 ± 0.46b 10.7 ± 0.45ab 10.1 ± 0.39ab 11.8 ± 0.55a 10.3 ± 0.59ab
4 9.7 ± 0.69b 11.6 ± 0.49ab 11.6 ± 0.43ab 11.8 ± 0.39ab 12.0 ± 0.45a 10.8 ± 0.77ab
5 9.4 ± 0.67b 11.0 ± 0.32ab 13.3 ± 0.70a 11.9 ± 0.45ab 11.9 ± 0.29ab
6 10.9 ± 0.93 11.2 ± 0.52 12.9 ± 0.58 11.7 ± 1.46
7 8.8 ± 0.38 9.5 ± 0.36 10.2 ± 0.71
a–d
Within rows, values with different superscripts differ significantly (P ≤ 0.05).
1
n = 10 for control and healthy chickens. For chickens with ascites, n varied with week of age.
2
Healthy are broilers that were exposed to low ambient temperature but did not develop ascites.
968 LUGER ET AL.
TABLE 3. The effect of ascites syndrome development (Trial 2) on hematocrit and hemoglobin
concentration in broiler chickens at 3 to 7 wk of age

Distribution of ascitic broilers by week of mortality

Age
1 2
(wk) Control Healthy 4 5 6 7
Hematocrit (%)
2 30.1 ± 0.4 31.7 ± 0.95 33.7 ± 0.75 30.3 ± 0.76 32.4 ± 0.77 30.8 ± 0.91
3 31.5 ± 0.5c 37.3 ± 0.67b 40.6 ± 0.7a 39.9 ± 0.76ab 39.1 ± 0.73ab 40.4 ± 0.68ab
4 30.8 ± 0.89d 34.0 ± 0.56cd 42.4 ± 1.66a 40.6 ± 0.93ab 37.1 ± 0.91bc 35.6 ± 0.8c
5 30.2 ± 0.83d 34.1 ± 0.87c 46.1 ± 1.82a 38.6 ± 1.0b 36.0 ± 1.28bc
6 31.9 ± 0.99b 33.2 ± 0.95b 41.6 ± 2.6a 40.7 ± 1.9a
7 30.1 ± 0.83b 31.9 ± 1.1b 44.1 ± 3.6a
Hemoglobin (g/dL)
2 10.3 ± 0.18 10.6 ± 0.71 9.3 ± 0.22 9.4 ± 0.58 9.3 ± 0.38 9.2 ± 0.70
3 9.4 ± 0.14b 10.8 ± 0.25a 10.97 ± 0.21a 10.7 ± 0.30a 11.4 ± 0.33a 11.5 ± 0.32a
4 10.2 ± 0.94c 11.5 ± 0.94bc 14.3 ± 0.37 a
14.4 ± 0.84a 14.3 ± 0.48a 13.8 ± 1.10ab
5 10.5 ± 0.53c 12.9 ± 0.79bc 16.2 ± 0.62a 14.7 ± 0.55ab 13.6 ± 0.75b
6 11.3 ± 0.50b 10.7 ± 0.63b 12.5 ± 0.71ab 13.9 ± 0.70a
7 9.9 ± 0.42ab 11.1 ± 0.41a 13.9 ± 0.70b
a–d
Within rows, values with different superscripts differ significantly (P ≤ 0.05).
1
n = 10 for control and healthy chickens. For chickens with ascites, n varied with week of age.
2
Healthy = broilers that were exposed to low ambient temperature but did not develop ascites.

than in the control ones. In general, a decline in hormone
concentration was observed with age. In addition, T3 was
significantly lower in the ascitic birds 1 wk before death
as compared to the healthy broilers.
DISCUSSION
The unique feature of the present study lies in the
possibility of determining the changes in each parameter
during an individual’s life span. A severe induction of
ascites was demonstrated. It was achieved by a combina-
tion of cold exposure early in life (2 wk of age) and by
supplying a pelleted diet, as demonstrated previously (Da
Silva et al., 1988; Bendheim et al., 1992; Nir et al., 1995).
One criterion for susceptibility to ascites is rate of
growth. Increased susceptibility of broilers to ascites has
previously been linked with high growth rate (Dale and
Villacres, 1988; Maxwell, 1990; Vereijken and Albers,
1990). However, in the present study, we demonstrated
that during the 7-wk life span of the broilers, either the
weight gain of the individuals that suffered from the
syndrome was similar to that of the control and the
healthy chickens or it was significantly lower during
the last week of life. These results were in agreement with
those of Wideman (2000) who emphasized that broilers
susceptible to ascites do not have to be the fastest growing
members of the flock as long as their rate of weight gain
exceeds the rate at which their pulmonary vascular capac-
ity increases to accommodate cardiac output. Ascites syn-
drome causes a significant deterioration in the perfor-
mance of the broilers (Julian, 1993; Griffin and Goddard,
1994) when in its critical stage (close to death).

TABLE 4. The effect of ascites syndrome development (Trial 1) on plasma thyroxine (T4) and
triiodothyronine (T3) in broiler chickens at 3 to 7 wk of age

Distribution of ascitic broilers by week of mortality

Age
1 2
(wk) Control Healthy 4 5 6 7
T4 (ng/mL)
2 10.9 ± 0.49a 5.02 ± 0.47b 4.50 ± 0.56b 4.60 ± 0.58b 3.98 ± 0.22b 5.19 ± 0.129b
3 5.37 ± 0.68a 3.33 ± 0.21b 3.61 ± 0.32b 3.20 ± 0.35b 2.58 ± 0.21b 3.62 ± 0.19b
4 4.75 ± 0.36a 367 ± 0.16ab 2.53 ± 0.21c 2.65 ± 0.11bc 2.89 ± 0.11b 3.37 ± 0.51b
5 5.89 ± 0.85a 3.14 ± 0.17b 1.19 ± 0.10c 1.04 ± 0.18c 3.26 ± 0.21b
6 6.95 ± 0.72a 4.51 ± 0.19b 2.26 ± 0.17c 2.68 ± 0.38c
7 7.67 ± 0.65a 5.70 ± 0.44b 2.93 ± 0.38c
T3 (ng/mL)
2 1.06 ± 0.59b 1.64 ± 0.71ab 1.61 ± 0.11ab 1.85 ± 0.112ab 2.03 ± 0.45a 1.68 ± 0.30ab
3 1.38 ± 0.58b 1.83 ± 0.50a 1.66 ± 0.93a 1.74 ± 0.84a 1.77 ± 0.72a 1.75 ± 0.71a
4 1.68 ± 0.11bc 2.17 ± 0.84ab 1.21 ± 0.11c 1.86 ± 1.00b 2.59 ± 0.21a 2.00 ± 0.15b
5 0.94 ± 0.73b 1.52 ± 0.67a 0.93 ± 0.14b 0.51 ± 0.18b 1.23 ± 0.23ab
6 0.92 ± 0.45b 1.55 ± 0.65a 0.67 ± 0.13b 088 ± 0.19b
7 0.84 ± 0.51b 1.40 ± 0.72a 0.89 ± 0.22b

Within rows, values with different superscripts differ significantly (P ≤ 0.05).

a–c
1
n = 10 for control and healthy chickens. For chickens with ascites n varied with week of age.
2
Healthy = broilers that were exposed to ambient temperature but did not develop ascites.
 ASCITES, WEIGHT GAIN, BLOOD PARAMETERS, AND THYROID HORMONES 969
TABLE 5. The effect of ascites syndrome development (Trial 2) on plasma thryoxine (T4) and
triiodothryonine (T3) in broiler chickens 3 to 7 wk of age

Distribution of ascitic broilers by week of mortality

Age
1 2
(wk) Control Healthy 4 5 6 7
T4 (ng/mL)
2 13.2 ± 0.5a 4.96 ± 0.9b 5.27 ± 0.5b 4.92 ± 0.7b 4.94 ± 0.45b 5.26 ± 0.4b
3 6.47 ± 0.7a 1.68 ± 0.3b 1.73 ± 0.4b 2.06 ± 0.4b 1.45 ± 0.3b 2.57 ± 0.7b
4 6.92 ± 0.7a 3.91 ± 0.6b 2.92 ± 0.4bc 2.45 ± 0.2c 2.92 ± 0.3bc 4.1 ± 0.4b
5 4.07 ± 0.6a 5.12 ± 0.5a 1.71 ± 0.2b 2.83 ± 0.4b 2.93 ± 0.4b
6 6.99 ± 0.8a 5.26 ± 0.55b 1.27 ± 0.4c 3.41 ± 1.1bc
7 3.89 ± 0.5a 4.95 ± 0.6a 2.07 ± 0.8b
T3 (ng/mL)
2 0.95 ± 0.1b 3.7 ± 0.4a 3.54 ± 0.2ab 3.6 ± 0.4ab 3.64 ± 0.2a 3.31 ± 0.1ab
3 2.08 ± 0.1b 3.59 ± 0.1a 3.67 ± 0.2a 3.27 ± 0.4a 3.58 ± 0.2a 3.42 ± 0.2a
4 2.82 ± 0.2bc 3.82 ± 0.2a 3.28 ± 0.3abc
2.39 ± 0.3c 3.79 ± 0.2ab 3.83 ± 0.4a
5 2.59 ± 0.2a 2.92 ± 0.1a 1.48 ± 0.2b 2.57 ± 0.2a 2.82 ± 0.3a
6 1.75 ± 0.2bc 2.44 ± 0.1a 1.12 ± 0.2c 1.81 ± 0.2b
7 2.08 ± 0.2b 2.71 ± 0.2a 1.35 ± 0.4b
Within rows, values with different superscripts differ significantly (P ≤ 0.05).
a–c
1
n = 10 for control and healthy chickens. For chickens with ascites n varied with week of age.
2
Healthy = broilers that were exposed to low ambient temperature but did not develop ascites.

The intensive selection of broilers for maximal body
mass has resulted in anatomical and physiological limita-
tions of blood flow through the lungs, with consequent
insufficient oxygenation of the tissues (Julian, 1993). Ex-
posure to cold conditions enhances the imbalance be-
tween oxygen supply and oxygen needs, and changes in
the cardiovascular system have been observed to accom-
modate the needs for oxygen under those conditions.
Increases in blood volume, hematocrit, and hemoglobin
concentration have been observed in broilers acclimated
to low Ta (Yahav et al., 1997; Wideman et al., 1998).
In the present study, exposure to cold was acute and
induced changes that included increases in hematocrit
and in hemoglobin concentration. The changes in hemato-
crit and the less significant changes in hemoglobin con-
centration accumulated as the syndrome developed and
appeared at 3 wk of age. These results are in agreement
with those of Owen et al. (1995). The patterns of increase
of hematocrit and hemoglobin in ascitic broilers differed
between experiments. The differences could be related to
differences between flocks in their physiological re-
sponses to the acute cold exposure, which may be ex-
pressed as differences in erythrocyte production, in fluid
permeability between the blood system and the interstitial
fluid, or both. An exception was exhibited in the group
of broilers that died from the syndrome at 7 wk of age
(Trial 1 only). Throughout the life span, these chickens
exhibited hematocrit values similar to those recorded in
control and healthy broilers. It may be suggested, there-
fore, that there is not always an association between the
ascites syndrome and hematocrit, as was found by Shlosb-
erg et al. (1996, 1998).
The pattern of thyroid hormones was monitored care-
fully to elucidate its association with the development
of ascites. Plasma T4 concentration of the control group
declined, whereas that of T3 increased at the age of 4 wk
(Tables 4 and 5) as a result of transferring chickens from
battery brooders to temperature-controlled rooms where
Ta was 22 C. For healthy broilers the plasma T4 concentra-
tion then increased continuously to the level recorded
before the exposure to 22 C. In healthy broilers that were
exposed to 26 C from the age of 7 d, a significantly lower
T4 concentration was measured, most probably as a result
of a dramatic increase in peripheral deiodination (Rudas
and Pethes, 1986). Thereafter, recovery of T4 production
was observed in these birds also. However, chickens that
developed ascites could not produce T4 at a sufficient rate
to make up for the reduction caused by cold exposure.
This reduction in T4 coincided with a significantly lower
T3 concentration. Such a decline in T4 concentration, but
with no change in T3 concentration, was demonstrated
in ascites-susceptible broilers (Buys et al., 1999a).
Thyroid hormones are involved in controlling meta-
bolic rate, and the concentration of circulating T3 is posi-
tively correlated with oxygen consumption in broilers
(Bobek et al., 1977; Gabarrou et al., 1997). However, in
the ascitic broilers, although they were exposed to cold
and, therefore, had high oxygen demands, the T3 concen-
tration was significantly lower. This finding raises the
question of whether the low levels of these hormones
are part of the events during the development of the
syndrome or the result of a failure of the thyroidal axis,
which may be one of the triggers initiating the syndrome.
This question requires further investigation.
It can be concluded that a high rate of weight gain
is not always a good predictor of ascites development.
Hematocrit and thyroid hormones may be good indica-
tors, but only during the last 2 wk of life and not in all
cases. None of these parameters, however, can predict
the development of ascites at an early age.
ACKNOWLEDGMENTS
This study was supported by a grant from the Egg and
Poultry Board of Israel. We wish to thank V. Bresler for
technical assistance.
970 LUGER ET AL.
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