Biochernical Society Transactions ( 1 993) 21
Permeability of the respiratory membrane in healthy, non-smoking
controls and patients with sarcoidosis and chronic obstructive lung
disease
Table 1. Values for the determined parameters in control group and
patients with sarcoidosis and chronic obstructive pulmonary
disease (COPD) (mean +SE)
ARZU SEVEN', REMISA SENGUL', GULDEREN $AHIN**,
GclLDEN CANDAN', NILCJFER ESEN'*, FIRUZ CELIKOGLU***,
TUNCER KARAYEL'.' and SEYHAN CELIKOGLU"'
* Dcpartmcnt of Biochemistry, Ccrrahpasa Medical Faculty, Istanbul
University, Istanbul, Turkey
* * Department of Physiology, Cerrahpasa Medical Faculty, IJtanbul
University, Istanbul, Turkey
* * * Department of Pncumology, Internal Medicine, Cerrahpap Medical
Faculty, Istanbul University, Istanbul, Turkey
I n pulmonary and/or bronchial circulatory systems the exudation of
plasma proteins to lung compartments may be due to increased
pcrnieatiility of the respiratory membrane[ 1,2]. Epithelial and endothelial
cells DI !lie alveolar lcvcl arc joined by tight junctions in the lungs of
normal healthy people. These tight junctions form a barrier to prevent
protein cxudation[3]. The permeability of the epithelial layer to proteins
is less than that of the endothel layer]3]. In pathologic cases, high
nioleculer weight proteins can pass the endothelial barrier easily through
the intcrcndothelial gaps[3,4\.
Biopsy material taken from the airway mucosa of patients with asthma
showed increased epithel obstruction, enlargement of the basal
nienibranc, protein exudation and increased permeability of respiratory
membrane[S]. There is a strong correlation between respiratory
membranc permeability and airway hypcrresponsiveness and airway
inflammation[5-7]. Airway hyperresponsiveness is the obstructive reaction
of the bronchioles to cold, allergens. dangerous respiratory irritants, fog,
dust and occupational exposures[X]. On the other hand the unbalance
between the contracting and relaxing effects of adrenergic and cholinergic
systems on muscle tonus constitutes another factor[6,9]. The activation of
parasympathetic nervous system leads to a release of mediators from
mast cells and leukocytes[7-9]. Hypercholinergic response plays an
important role in the local bronchial inflammatory reaction. Increased
airway epithelial destruction and increased permeability of respiratory
membrane occur as a result of neurogenic inflammation[9, lo].
In the recent years the permeability of the respiratory membrane is
determined by the concentration gradient of proteins between the serum
and the bronchoalveolar lavage fluid (BALF) to understand the
pathogenesis of various pulmonary diseases[l1-13]. High molecular
weight proteins not formed in the lungs are specially chosen for
determination111-13].
We examined in this study the permeability of the respiratory
membrane in healthy, non-smoking controls (n= ll), patients with
sarcoidosis (n = 19), and patients with chronic obstructive pulmonary
disease (COPD) (n= 12).
Venous blood was obtained from each individual and BALF was taken
from the right nicdiuni lobe by means of a fiber optic broncoscope.
Serum and BALF saniplcs were analyzed for albumin (alb), total
protein (Tpr) and urea. Albumin and lotal protein analyses were done by
the Fulin-Lowry methodl 141 and urea by the enzymatic methodllS].
From the biochemical data: The concentration gradient across the
respiratory membrane
(protcinl in BALF
and
0 protein = IlHNl x
[protcinl in serum
distribution coelllclcnt(DC)
=
[protcinl in plnsma/[total protein] in plasma
[protein] in BALF/[total protein] in BALF
wcrc calculated using the ahove stated formulae[l1,12].
Unpaired Student's t test was used to compare the difl'erences
hetween the study groups.
A significant difference was not found among serum Tpr, alb and urea
values between the patient and control groups. The BALF (Tpr) values of
the p;iticnts with sarcoidosis was found significantly higher than that of
thc cuntrol group (Table I), 0 (Tpr) values of the sarcoidosis group was
signilirantly highcr than that of the control group (Table 1). There was
not a significant difl'crcncc bctwccn the BALF (alb) values of the above
309s
BALF total protein(mg%)
BALF albumin(mg%)
BALF urea(mg%)
Serum tntal protein(g%)
Serum albumin(g%)
Serum urea(mg'7n)
Q total protein
Q albumin
Conlrol
Sarcoidosis
COPD
(n=Il)
(n=19)
78.84i12.2'
43.92i13.5
2.92i0.7
8.12i 1.a
4.4nio.34
41.53i3 62
9.29iI.l*
9.4i2.31
1.24~0.13
(n=12)
57.31i12.3
32.19i7.3
19.5t12.2
i.m..77
4.79i0.65
50.1 1i7.69
6.27i I 41
7.67i 1.8
1.41i0.23
45.83i4.9
20.06i1.74
2.63t0.71
7.89i0.55
4.17t0 35
40.07i3.89
5.71i0.86
5.35t0.80
127t0.18
DC
*p<0 05 for sarcoidosis group compared with control group
*p<O 05 for sarcoidosis group compared w i t h COPD group
stated groups. When the control group was compared with the COPD
group; only BALF ( a h ) values were found significantly higher in the
COPD group. There was not a significant difference among the other
parameters in the above mentioned groups. Q (Tpr) was found
significantly higher in the sarcoidosis group when compared with the
COPD group. BAL (urea) values were found lower in the sarcoidosis
group when compared with COPD group. No significant difference was
obtained between the control and patient groups in the distribution
coefficient, calculated from albumin and total protein values in each
group.
In conclusion the results demonstrate the increased permeability of
respiratory membrane of patients with sarcoidosis when compared with
the control and COPD's patients. The significant increase in Q (Tpr) in
sarcoidosis group unaccompanied with a significant increase in Q (alb)
makes us think that other proteins besides albumin may have interferred
in BALF. The normal permeability of respiratory membrane in chronic
obstructive lung disease group may be due to the duration and severity of
the disease. Our results indicate that bronchial hyperresponsiveness and
inflammation has not formed in this group.
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