Biomedical Engineering Reference
In-Depth Information
a
TABLE 8.14
Clinical Chemistry Reference Values for
M. fascicularis
Parameter
GD 25
(Range)
GD 50
(Range)
GD 75
(Range)
GD 100
(Range)
Cl (mM/l)
110
2
(108e113)
109
2
(105e112)
109
3
(106e114)
109
3
(107e114)
TCO
2
(mM/l)
24
2
(20e27)
24
5
(16e30)
22
5
(12e28)
20
3
(16e24)
K (mM/l)
4.8
0.4
(4.1e5.4)
5.0
0.6
(4.3e5.9)
4.7
0.5
(4.1e5.7)
4.9
0.5
(4.2e5.9)
Na (mM/l)
146
2
(144e148)
146
3
(143e153)
146
3
(143e151)
144
1
(142e147)
Alb (g/dl)
4.0
0.3
(3.7e4.5)
3.5
0.3
(2.8e3.8)
3.1
0.4
(2.4e4.0)
3.2
0.3
(2.7e3.8)
BUN (mg/dl)
21
6
(11e29)
21
6
(15e31)
21
5
(16e32)
18
3
(14e22)
Glucose (mg/dl)
62
9
(46e76)
48
11
(30e64)
46
13
(31e70)
49
6
(40e59)
TP (g/dl)
7.8
0.4
(7.1e8.2)
7.3
0.5
(6.5e7.9)
6.9
0.6
(6.3e8.2)
6.9
0.4
(6.4e7.4)
ALT (U/l)
47
16
(22e76)
54
34
(15e132)
51
30
(21e112)
50
31
(18e117)
ALP (U/l)
175
49
(114e290)
166
51
(119e275)
123
41
(86e212)
145
31
(104e199)
Ca (mg/dl)
10.0
0.4
(9.5e10.8)
10.0
0.6
(9.2e11.1)
9.7
0.5
(9.0e10.3)
9.2
0.4
(8.8e9.9)
Cr (mg/dl)
0.9
0.1
(0.8e1.0)
0.9
0.1
(0.8e1.1)
0.8
0.1
(0.6e1.0)
0.8
0.1
(0.7e0.9)
P (mg/dl)
3.9
1.1
(1.7e4.7)
3.3
0.8
(1.7e4.5)
2.7
0.8
(1.4e4.3)
3.6
0.6
(2.4e4.3)
Note:
Cl, chloride; TCO
2
, total carbon dioxide; K, potassium; Na, sodium; Alb, albumin; BUN, blood urea nitrogen; TP, total protein; ALT, alanine amino-
transferase; ALP, alkaline phosphatase; Ca, calcium; Cr, creatinine; P, phosphorus.
a
Gestational days (GD) 25e100 (n
ΒΌ
10; mean
SD).
From
Hendrickx and Dukelow (1995)
.
deprivation during pregnancy results in maternal as well as
fetal mortality in this species (
Kohrs et al., 1976
). The
effects of experimentally induced diabetes mellitus on fetal
metabolism and well-being have also been examined in
rhesus monkeys (
Mintz et al., 1972
). Administration of the
pancreatic
b
cell cytotoxin streptozotocin before concep-
tion and during the first trimester of pregnancy was asso-
ciated with a 27%mortality rate during the second and third
trimesters. The drug effects included fetal hyper-
insulinemia, enhanced pancreatic islet cell responsiveness,
enlarged placentas, and polyhydramnios.
Both spontaneous and experimentally induced maternal
infections are important factors in reproductive failure in
a variety of nonhuman primate species (
Hendrickx and
Binkerd, 1980
). The following infections have been
implicated as causative agents in abortions or stillbirths:
Chagas' disease (Trypanosoma cruzi-like) in marmosets;
T-strain mycoplasmas in talapoins and patas monkeys;
measles virus in rhesus monkeys (
Renne et al., 1973
);
rubella virus in long-tailed monkeys and baboons; and
mumps virus in rhesus monkeys.
Observations in rhesus monkey colonies indicate that
maternal psychological factors may be as important for
fetal viability as maternal physiological conditions during
pregnancy. The high level of abortion (50
e
70%) among
pregnant animals captured in a native environment and
shipped to the USA for experimental purposes may be
partially attributable to the high degree of stress associated
with handling techniques (
Myers, 1972
). Experiments
carried out in rhesus monkeys to study the effect of
maternal stress on pregnancy indicate that excitability and
discomfort associated with labor and delivery may have
deleterious effects on the fetus. Brief episodes of experi-
mentally induced stress in near-term rhesus monkeys cause
fetal deterioration in the form of fetal bradycardia and
decreased arterial oxygenation (
Morishima et al., 1978
)
or fetal asphyxia and concomitant disturbances in the
acid
e
base balance as a result of impaired uteroplacental
circulation.
Boot et al. (1985)
have also demonstrated that
housing conditions (i.e. cage size and density) can
adversely affect the pregnancy outcome and may be related
to stress.
Changes in the mother's environment during pregnancy
(e.g. social change, location change) have been noted to
influence pregnancy outcome in several nonhuman primate
species. A variety of reproductive deficiencies were noted
ranging from poor infant survival to a complete inhibition
of ovulation and infertility. Specific hypothalamic factors
(i.e. suppression of GnRH or LH/FSH) have been suggested
as
the mechanism responsible
for
these
changes
