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The relationship between level of triglycerides in plasma and number of basophils in blood
The Relationship between Level of Triglycerides in Plasma and Number of Basophils in Blood By H. BRAUNSTEINER, S. SAILERAND In normal persons and patients with varying concentrations of triglycerides a good positive correlation (p < 0.001) was found between the level of triglycerides in plasma and the number of basophils. Cholesterol correlated to the number of basophils only at the 5 per cent level of significance, between the free fatty acids resp. phospholipids no
S
INCE
observed
IIAIIN’
hyperlipemic
effect
state,
and in particular
important
question
arises,
phenomenon
for the clearing
effect,
conditions
without
effect
deal of work
its relationship
pharmacologic
correlation was demonstrable. These findings give further evidence of the physiologic role of basophils, resp. heparin in metabolism of triglycerides. In 7 cases of essential hyperlipemia the number of basophils was much lower than expected from their high triglyceride level. (Metabolism 14: No. 10, October, 1071-1075, 1965)
clearing
the
a great
whether
this
effect
an endogenous
which
the
lil)ase.2
Furthermore,
a positive
an endogenous heparin,
A method direct
exhibits
in plasma
important
has
influences
as a
which
been
only
is responsible
was found
which
of the activity
the normal seem
and Braunsteiner
in Japan.
et al.!’ were
basophils
in hyperthyroids
increased.
After successful
phils can be observed.
able
treatment
In addition,
and James3
of basophils
of
lipase.” play
permits
this method,
higher
and/or
diseases
States
and Thumb”
a diminished the number a normal
30
nutritional
in the United
Braunsteiner
the Code
as approximately
racial
to demonstrate in myxedema
in maturity-onset
level
might
which
Using
some
Inagaki,’
of these
in
by endogenous-
heparina
value in adults
Braunsteiner
the
lipoprotein
activated
chamber.
to exist
Further,
whereas,
between
contain
the mean values were somewhat than
activity
lipoprotein
of this enzyme.
by Moore
in a counting there
lipase
of postheparin
lipasc is probably
developed
However,
lipoprotein
of this endogenous
leukocytes,
of basophils
because
aIld Scandinavia
in the number
correlation
lipoprotein basophil
et al.” were the first to define basophils/cmm.
regarded
be
lipase,
characteristics
and the activity
role in the control
counting
this The
also plays a role under physiologic and pathophysiologic method injection of heparin. Using a microtitration
to demonstrate
an
concerning
of triglycerides.
prior
plasma
Since
must
or if this lipoprotein
in an alimentary
done
to the metabolism
hum:m
ly liberated
of heparin
has been
we vverc able
triglycerides
F. SANDHOFER
number of was greatly
value of baso-
and ThumbX found an increase diabetes.
They
hypothesized
that
From the Department of Jletlicirrv, Unicersit~y of Innsbruck, All.s$ricl. Rcceiced for yubZication July 20. 1965. HERBERT BRAUNSTEISEH, h1.D.: Profe.v.!or, Hcd of t/w Dcpartmcnt of Internal Medicine, ?dcdicaZ %‘hooZ, Uniuersit!y of Innshrcrck, Austria. SICUHD SAILER, X1.D.: Assistant Professor, Dcpwtment of lnterwl Medicine. Metabolism Lnborcrtory, I7tlirersity of Innsbruck, Austria. FRIEDRICII SAXDHOFER, hl.D.: Sertior Re.sidcnt, Depurtmcnt of Interrud Xfdicinc~,
~letnbolism
Laboratory,
tinker&y
of Znnxbrwk,
1071
Ardricl.
BRAUNSTEIXER,
1072 Table BXZO-
phils
cmm
Cho-
erides
lesterol
mg
“VT.
‘:
Are
Ma. s.
F
20
31
GO
212
760
25R
Diab.
Ki. J.
M
71
44
110
860
:365
291
Occlusive
Wa.
F
76
24
134
1x2
1040
1X3
Diabetes Myocarditis
Diagnosis mell.,
disease
mellitus
B1. S.
M
17
67
182
260
450
258
M
55
53
194
265
627
310
Diabetes
Ra. J.
M
56
100
515
239
403
129
Coronary
Ga. A.
F
77
31
112
217
670
263
Pulmonary
Ob. C.
F
19
56
126
311
330
Hypertension
Lu.
H.
M
50
:35
194
:332
/ 560
256
Myocardial
Ra.
M.
F
54
23
92
274
620
273
NCJllnal
Eb. H.
hyyertbyroidism
arterial
St. A.
Ki. E. Au. W. Wi. A. Hi. E. Wo. E. Ku. A. Re. H. St.. D. Ra. A. Mu. M. Do. 0. MO. J. Me. J. St. J. Ju. S. Fe. M. Wi. J. Ra. A. Ha. A.
SANDHOFER
PhosuhoFFA h&./L.
Sex
%
AND
I
Pat.
A.
per
Triglyc-
SAILER
mellitus insufficiency heart
disease*
infarction
F
59
68
237
293
501
294
Hypertension
M
17
29
70
132
421
162
Duodenal
M
50
113
287
221
334
259
Congestive
M
46
101
493
343
695
Y19
C”ronaty
F
22
45
9x
205
620
159
Normal
M
6R
22
84
220
450
174
N”W~al
M
35
50
135
249
647
2 08
Myocsrdial
iniarction
M
44
53
157
293
630
2RO
Myocardial
infarction
F
64
12
69
172
670
159
Hyperthyroidism
F
41
0
57
223
73.5
234
Blanchogenic
M
38
54
I 5x
154
1x7
Hyperthyroidism
1400
ulcel heart
F
15
52
123
129
550
200
Tonsillitis
M
63
65
136
818
595
267
Latent
F
17
41
17
162
836
170
Hypuchromic
F
58
52
117
159
740
193
Normal
F
54
2Y
73
134
650
151
Normal
F
69
2
82
226
XtiO
237
Pneumonia
M
49
51
292
269
935
317
Myocardial
F
76
26
12x
226
x10
226
Normal
M
40
22
208
189
750
221
Myocardial
Table S.-Patients Pat
He. R.
SW
Age
Ijasophils per cmm
?Vl
46 30 s7 45 40 45 47
20 34 12 45 32 60 63
SC. G.
;\I
Ha. W.
hl
Se. N.
hl
St. A.
hl hl RI
Br. A. Se. R.
with Essential
the augmented
blood
of basophils. The present
lipids
carcin”ma
diabetes
mellitus anemia
infarction infarction
Hyperlipemia Phosphw lipids mg. ‘,:
Triglycerides
mg.r; 750 920 1680 1660
433 673 575
1095
511 35” 888
and diabetes
designed
670 970 990 ,590 830 ,570 17%
511
975 3300
in myxedema
study was therefore
failure
insufficienry
caused
38Fi 310 4.38 300 .51x Xl” 660
the elevation
to test the hypothesis
of Rraun-
Steiner and Thumb’ by comparing the number of basophils with the level of triglycerides, free fatty acids, phospholipids, and total cholesterol in plasma and in patients
with varying plasma lipid levels. METHODS
Ptiients. 1)
ns well
fasting.
Normal
persons and
as patients
with
patients
essential
with
varying
hyperlipemia
levels
(table
2)
of plasma were
triglycerides
studied
after
(table
overnight
TRIGLYCERIDESIN
1073
PLASMA
,
I
r*
I
100
200
I
300
Triglycerides.
I
I
400
500
A
mg9o
Fig.
l.- The concentration of tryglycerides in mg. per cent (abscissa) is plotted There is a positive correlation the number of basophils/ccm. (ordinate). between triglycerides and basophils. In addition, the regression line and the 95 per cent confidence limits are drawn.
against
Cktr~kc~l
Determirutions.
Hrparinized bloocl samplrs were collected and cellular ckhy centrifugation at 4 C. xt 3000 r.p,n~. for 10 min. Lipids ww and triglycerides,” total extracted acuxcling to Folch et al. lo as modified hy Carl~on,~’ ch010strrol,12 free fatty acids, 13 and phosphalipids (lipid phosphorus T 35 = phospholipids) ‘-I were estimated. mc’rrts rcmovecl
promptly
C’c~rr~fiflg of Basoplti/s. Basophil mcthotl of hloore and James.~
lenkocytcx
were
counted
in tluplicatc
according
to tht,
RESULTS
In figure 1 the concentration plotted
agtinst
the
number
of triglycerides of basophils/cmm.
in mg. per cent (abscissa) is (ordinate). The values in the
figure are derived from individuals described in table 1. The figure shows that there is a good positive correlation between the concentration of triglycerides in plasma and the number of basophils: n = 30, r = +0.780, p < 0.001. In addition the 95 per cent confidence limits are drawn. The correlation between the concentration of total cholesterol and the number of basophils is significant only at the S per cent level (n = 30. r = f0.410, p < 0.05). No correlation can be demonstrated between the concentration of free fatty acids (n = 29, r = --0.189, p > O.l), resp. the concentration of phospholipicls (n = 30, r = f0.234, p > 0.1) and the number of basophils. Figure 2 shows the regression line of the number of basophils upon the concentration of triglycerides and the confidence limits as shown in figure 1. The values for each of the 7 individuals with essential hyperlipemia as ckscribed in table 2 are far helow the confidence limits.
BRAUNSTEINER,
1074
SAILER
AND SANDHOkTR
.
2000 Triglycerides,
with essential Fig. 2.- In patients below the confidence limits as cakulated
mg%
the
hyperlipemia for figure 1.
number
of hasophils
lies
DISCUSSION Inagaki’
and
pathologic basophils
Braunsteiner
al.” studied
et
the number
states. They were able to demonstrate in hyperthyroids whereas, in myxedema
was increased.
As the latter
levels and as basophils
diseases
contain
of basophils
a diminished and diabetes
are accompanied
heparinl
which
by high
is regarded
in various number of the number triglyceride
as an integral
part
Braunsteiner and Thumbs supposed th:it of the lipoprotein lipase system.” there might be a relationship between the number of basophils in blood and the metabolism phils
of fat. The
positive
and the concentration
esis. It seems strated
to be important
only for triglycerides
Recently
a good
positive
plasma and endogenous that the level dogenous Together a marked
with
that
such
which
between in plasma
a good
are the
correlation
lipoprotein
of triglycerides
lipoprotein
correlation
of triglycerides
correlation
substrate
between
the number confirms
seems
can
of
the level to control
ho-
lwpotl~-
be demon-
for lipoprotein
lipase was demonstrated.”
in plasma
this
lipasc.
of triglycerides
in
It was suggcstctl the activity
of H-
lipase.
the observation
degranulation
of Juhlin
of the basophils
and
Shelley’”
after a fatty meal,
who
demonstrated
the following
con-
trol mechanism is suggested: ( 1) the increased level of triglycerides seems to cause an elevation in the number of basophils; (2) by elevation of the number of basophils and their degranulation more heparin is liberated for the activntion of lipoprotein lipase. The
correlation
between
the number
of basophils
and triglycerides.
hog-
ever, does not apply to those cases of essential hyperlipemia with very high triglyceride level that we have so far investigated. Since there is no absolutcl lack of basophils, a primary insufficiency of the basophihc system is not vvr!. probable.
An exhaustion
of the
basophilic
system
as a result
of the
over-
TRIGLYCERIDES
1075
IN PLASMA
demand caused explanation.
by the high
triglyceride
level
seems
to be the most
logical
ACKNOWLEDGMENT We are indepted nical
to Ch.
Cornploy.
Ch.
Rinderer
and
Ch.
Zcch
for their
excellent
tech-
assistance.
REFERENCES 1. Hahn,
P. F.: Abolishment
of alimentary
hpemia following injection of heparin. Science 98:19-20. 1943. 2. Sandhofer. F., Sailer, S., and BraunSteiner, H.: Endogene Lipoproteidlipaseaktivit$t in menschlichem Plasma. Dtsch. med. Wschr. 89:426-429, 1964. 3. Sailer, S.. Sandhofer, F., and BraunSteiner, H.: Stcuerung der endogcnen Lipoproteicl-Lipase-Aktivitlt im Plasma bei Normalpersonen uncl Patienten mit essentieller HyperlipLmie. Dtsch. med. Wschr. 90:863-868, 196.5. 4. Bchrens, M., and Tauhert, 51.: Der
9.
10.
11.
Nachweis von Heparin in den h:lsophilen Leukozyten. Klin. \Vsrhr. 30: 76-78, 1952. 5. hloore, J. E., and James, G. W.: A simple direct method for absolute basophi1 leucocyte count. Proc. SW. Exp. Biol.. N. Y. 82:601-603, 1953. 6. Code, C. F., Mitchell. R. G., and Ken-
12.
nedy, J. C.: The effect of cortisone on the number of circulating bxsophils and eosinophils: is there a relation between these cells? Proc. Staff. Meet. Mayo Clin. 29:200-204,
14.
1954. 7. Inagaki, S.: The relationship between the level of circulating basophil leucocytes and thyroid function. Acta endocrinol. 26:477-488, 1957. 8. Braunsteiner, H., and Thumb, N.:
13.
15.
16.
Quantitative Veranderungen drr Bhzthasophilrn und ihre klinische Bedelltung. Acta hnemat. 20:339-349, 19-58. -, Hijfer, R., Thumb, N., and Vetter, H.: Untersuchungen iiber dir basophilen Leukozyten bei Schilddriiscnerkrnnkungen. Min. Wschr. 37:250252, 1959. Folch, J. hl., Lees, Ivl., and Slo:mcStanley, G. H.: A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chcm. 226:497-509, 1957. Carlson, L. A.: Determination of serlun triglycerides. J. Atheroscler. Res. 3: 334-336, 1963. Searcy, R. L.. Bergquist, L. hl., and Jung, R. C.: Rapid ultramicro rstimation of serum total cholesterol. J. Lipid Res. 1:349-351, 1960. Dole, V. P., and hleinertz, H.: Microlong-chain fatty dcterniination of acids in plasma and tissues. J. Biol. Chem. 233:2595-2599, 1960. Bartlett, G. R.: Phosphorlls assay in chromatography. J. Biol. column Chem. 2343466-468, 1959. Robinson. D. S., and French. J. E.: Heparin, the clearing factor lip:lse, and fat transport. Pharmacol. Rev. 12:241-263, 1960. Juhlin, L., and Shelley, W. B.: II?granulation of the basophil of man induced by lipemia. Amer. J. Med. Sci. 242:211-222, 1961.
S
INCE
observed
IIAIIN’
hyperlipemic
effect
state,
and in particular
important
question
arises,
phenomenon
for the clearing
effect,
conditions
without
effect
deal of work
its relationship
pharmacologic
correlation was demonstrable. These findings give further evidence of the physiologic role of basophils, resp. heparin in metabolism of triglycerides. In 7 cases of essential hyperlipemia the number of basophils was much lower than expected from their high triglyceride level. (Metabolism 14: No. 10, October, 1071-1075, 1965)
clearing
the
a great
whether
this
effect
an endogenous
which
the
lil)ase.2
Furthermore,
a positive
an endogenous heparin,
A method direct
exhibits
in plasma
important
has
influences
as a
which
been
only
is responsible
was found
which
of the activity
the normal seem
and Braunsteiner
in Japan.
et al.!’ were
basophils
in hyperthyroids
increased.
After successful
phils can be observed.
able
treatment
In addition,
and James3
of basophils
of
lipase.” play
permits
this method,
higher
and/or
diseases
States
and Thumb”
a diminished the number a normal
30
nutritional
in the United
Braunsteiner
the Code
as approximately
racial
to demonstrate in myxedema
in maturity-onset
level
might
which
Using
some
Inagaki,’
of these
in
by endogenous-
heparina
value in adults
Braunsteiner
the
lipoprotein
activated
chamber.
to exist
Further,
whereas,
between
contain
the mean values were somewhat than
activity
lipoprotein
of this enzyme.
by Moore
in a counting there
lipase
of postheparin
lipasc is probably
developed
However,
lipoprotein
of this endogenous
leukocytes,
of basophils
because
aIld Scandinavia
in the number
correlation
lipoprotein basophil
et al.” were the first to define basophils/cmm.
regarded
be
lipase,
characteristics
and the activity
role in the control
counting
this The
also plays a role under physiologic and pathophysiologic method injection of heparin. Using a microtitration
to demonstrate
an
concerning
of triglycerides.
prior
plasma
Since
must
or if this lipoprotein
in an alimentary
done
to the metabolism
hum:m
ly liberated
of heparin
has been
we vverc able
triglycerides
F. SANDHOFER
number of was greatly
value of baso-
and ThumbX found an increase diabetes.
They
hypothesized
that
From the Department of Jletlicirrv, Unicersit~y of Innsbruck, All.s$ricl. Rcceiced for yubZication July 20. 1965. HERBERT BRAUNSTEISEH, h1.D.: Profe.v.!or, Hcd of t/w Dcpartmcnt of Internal Medicine, ?dcdicaZ %‘hooZ, Uniuersit!y of Innshrcrck, Austria. SICUHD SAILER, X1.D.: Assistant Professor, Dcpwtment of lnterwl Medicine. Metabolism Lnborcrtory, I7tlirersity of Innsbruck, Austria. FRIEDRICII SAXDHOFER, hl.D.: Sertior Re.sidcnt, Depurtmcnt of Interrud Xfdicinc~,
~letnbolism
Laboratory,
tinker&y
of Znnxbrwk,
1071
Ardricl.
BRAUNSTEIXER,
1072 Table BXZO-
phils
cmm
Cho-
erides
lesterol
mg
“VT.
‘:
Are
Ma. s.
F
20
31
GO
212
760
25R
Diab.
Ki. J.
M
71
44
110
860
:365
291
Occlusive
Wa.
F
76
24
134
1x2
1040
1X3
Diabetes Myocarditis
Diagnosis mell.,
disease
mellitus
B1. S.
M
17
67
182
260
450
258
M
55
53
194
265
627
310
Diabetes
Ra. J.
M
56
100
515
239
403
129
Coronary
Ga. A.
F
77
31
112
217
670
263
Pulmonary
Ob. C.
F
19
56
126
311
330
Hypertension
Lu.
H.
M
50
:35
194
:332
/ 560
256
Myocardial
Ra.
M.
F
54
23
92
274
620
273
NCJllnal
Eb. H.
hyyertbyroidism
arterial
St. A.
Ki. E. Au. W. Wi. A. Hi. E. Wo. E. Ku. A. Re. H. St.. D. Ra. A. Mu. M. Do. 0. MO. J. Me. J. St. J. Ju. S. Fe. M. Wi. J. Ra. A. Ha. A.
SANDHOFER
PhosuhoFFA h&./L.
Sex
%
AND
I
Pat.
A.
per
Triglyc-
SAILER
mellitus insufficiency heart
disease*
infarction
F
59
68
237
293
501
294
Hypertension
M
17
29
70
132
421
162
Duodenal
M
50
113
287
221
334
259
Congestive
M
46
101
493
343
695
Y19
C”ronaty
F
22
45
9x
205
620
159
Normal
M
6R
22
84
220
450
174
N”W~al
M
35
50
135
249
647
2 08
Myocsrdial
iniarction
M
44
53
157
293
630
2RO
Myocardial
infarction
F
64
12
69
172
670
159
Hyperthyroidism
F
41
0
57
223
73.5
234
Blanchogenic
M
38
54
I 5x
154
1x7
Hyperthyroidism
1400
ulcel heart
F
15
52
123
129
550
200
Tonsillitis
M
63
65
136
818
595
267
Latent
F
17
41
17
162
836
170
Hypuchromic
F
58
52
117
159
740
193
Normal
F
54
2Y
73
134
650
151
Normal
F
69
2
82
226
XtiO
237
Pneumonia
M
49
51
292
269
935
317
Myocardial
F
76
26
12x
226
x10
226
Normal
M
40
22
208
189
750
221
Myocardial
Table S.-Patients Pat
He. R.
SW
Age
Ijasophils per cmm
?Vl
46 30 s7 45 40 45 47
20 34 12 45 32 60 63
SC. G.
;\I
Ha. W.
hl
Se. N.
hl
St. A.
hl hl RI
Br. A. Se. R.
with Essential
the augmented
blood
of basophils. The present
lipids
carcin”ma
diabetes
mellitus anemia
infarction infarction
Hyperlipemia Phosphw lipids mg. ‘,:
Triglycerides
mg.r; 750 920 1680 1660
433 673 575
1095
511 35” 888
and diabetes
designed
670 970 990 ,590 830 ,570 17%
511
975 3300
in myxedema
study was therefore
failure
insufficienry
caused
38Fi 310 4.38 300 .51x Xl” 660
the elevation
to test the hypothesis
of Rraun-
Steiner and Thumb’ by comparing the number of basophils with the level of triglycerides, free fatty acids, phospholipids, and total cholesterol in plasma and in patients
with varying plasma lipid levels. METHODS
Ptiients. 1)
ns well
fasting.
Normal
persons and
as patients
with
patients
essential
with
varying
hyperlipemia
levels
(table
2)
of plasma were
triglycerides
studied
after
(table
overnight
TRIGLYCERIDESIN
1073
PLASMA
,
I
r*
I
100
200
I
300
Triglycerides.
I
I
400
500
A
mg9o
Fig.
l.- The concentration of tryglycerides in mg. per cent (abscissa) is plotted There is a positive correlation the number of basophils/ccm. (ordinate). between triglycerides and basophils. In addition, the regression line and the 95 per cent confidence limits are drawn.
against
Cktr~kc~l
Determirutions.
Hrparinized bloocl samplrs were collected and cellular ckhy centrifugation at 4 C. xt 3000 r.p,n~. for 10 min. Lipids ww and triglycerides,” total extracted acuxcling to Folch et al. lo as modified hy Carl~on,~’ ch010strrol,12 free fatty acids, 13 and phosphalipids (lipid phosphorus T 35 = phospholipids) ‘-I were estimated. mc’rrts rcmovecl
promptly
C’c~rr~fiflg of Basoplti/s. Basophil mcthotl of hloore and James.~
lenkocytcx
were
counted
in tluplicatc
according
to tht,
RESULTS
In figure 1 the concentration plotted
agtinst
the
number
of triglycerides of basophils/cmm.
in mg. per cent (abscissa) is (ordinate). The values in the
figure are derived from individuals described in table 1. The figure shows that there is a good positive correlation between the concentration of triglycerides in plasma and the number of basophils: n = 30, r = +0.780, p < 0.001. In addition the 95 per cent confidence limits are drawn. The correlation between the concentration of total cholesterol and the number of basophils is significant only at the S per cent level (n = 30. r = f0.410, p < 0.05). No correlation can be demonstrated between the concentration of free fatty acids (n = 29, r = --0.189, p > O.l), resp. the concentration of phospholipicls (n = 30, r = f0.234, p > 0.1) and the number of basophils. Figure 2 shows the regression line of the number of basophils upon the concentration of triglycerides and the confidence limits as shown in figure 1. The values for each of the 7 individuals with essential hyperlipemia as ckscribed in table 2 are far helow the confidence limits.
BRAUNSTEINER,
1074
SAILER
AND SANDHOkTR
.
2000 Triglycerides,
with essential Fig. 2.- In patients below the confidence limits as cakulated
mg%
the
hyperlipemia for figure 1.
number
of hasophils
lies
DISCUSSION Inagaki’
and
pathologic basophils
Braunsteiner
al.” studied
et
the number
states. They were able to demonstrate in hyperthyroids whereas, in myxedema
was increased.
As the latter
levels and as basophils
diseases
contain
of basophils
a diminished and diabetes
are accompanied
heparinl
which
by high
is regarded
in various number of the number triglyceride
as an integral
part
Braunsteiner and Thumbs supposed th:it of the lipoprotein lipase system.” there might be a relationship between the number of basophils in blood and the metabolism phils
of fat. The
positive
and the concentration
esis. It seems strated
to be important
only for triglycerides
Recently
a good
positive
plasma and endogenous that the level dogenous Together a marked
with
that
such
which
between in plasma
a good
are the
correlation
lipoprotein
of triglycerides
lipoprotein
correlation
of triglycerides
correlation
substrate
between
the number confirms
seems
can
of
the level to control
ho-
lwpotl~-
be demon-
for lipoprotein
lipase was demonstrated.”
in plasma
this
lipasc.
of triglycerides
in
It was suggcstctl the activity
of H-
lipase.
the observation
degranulation
of Juhlin
of the basophils
and
Shelley’”
after a fatty meal,
who
demonstrated
the following
con-
trol mechanism is suggested: ( 1) the increased level of triglycerides seems to cause an elevation in the number of basophils; (2) by elevation of the number of basophils and their degranulation more heparin is liberated for the activntion of lipoprotein lipase. The
correlation
between
the number
of basophils
and triglycerides.
hog-
ever, does not apply to those cases of essential hyperlipemia with very high triglyceride level that we have so far investigated. Since there is no absolutcl lack of basophils, a primary insufficiency of the basophihc system is not vvr!. probable.
An exhaustion
of the
basophilic
system
as a result
of the
over-
TRIGLYCERIDES
1075
IN PLASMA
demand caused explanation.
by the high
triglyceride
level
seems
to be the most
logical
ACKNOWLEDGMENT We are indepted nical
to Ch.
Cornploy.
Ch.
Rinderer
and
Ch.
Zcch
for their
excellent
tech-
assistance.
REFERENCES 1. Hahn,
P. F.: Abolishment
of alimentary
hpemia following injection of heparin. Science 98:19-20. 1943. 2. Sandhofer. F., Sailer, S., and BraunSteiner, H.: Endogene Lipoproteidlipaseaktivit$t in menschlichem Plasma. Dtsch. med. Wschr. 89:426-429, 1964. 3. Sailer, S.. Sandhofer, F., and BraunSteiner, H.: Stcuerung der endogcnen Lipoproteicl-Lipase-Aktivitlt im Plasma bei Normalpersonen uncl Patienten mit essentieller HyperlipLmie. Dtsch. med. Wschr. 90:863-868, 196.5. 4. Bchrens, M., and Tauhert, 51.: Der
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Nachweis von Heparin in den h:lsophilen Leukozyten. Klin. \Vsrhr. 30: 76-78, 1952. 5. hloore, J. E., and James, G. W.: A simple direct method for absolute basophi1 leucocyte count. Proc. SW. Exp. Biol.. N. Y. 82:601-603, 1953. 6. Code, C. F., Mitchell. R. G., and Ken-
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nedy, J. C.: The effect of cortisone on the number of circulating bxsophils and eosinophils: is there a relation between these cells? Proc. Staff. Meet. Mayo Clin. 29:200-204,
14.
1954. 7. Inagaki, S.: The relationship between the level of circulating basophil leucocytes and thyroid function. Acta endocrinol. 26:477-488, 1957. 8. Braunsteiner, H., and Thumb, N.:
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Quantitative Veranderungen drr Bhzthasophilrn und ihre klinische Bedelltung. Acta hnemat. 20:339-349, 19-58. -, Hijfer, R., Thumb, N., and Vetter, H.: Untersuchungen iiber dir basophilen Leukozyten bei Schilddriiscnerkrnnkungen. Min. Wschr. 37:250252, 1959. Folch, J. hl., Lees, Ivl., and Slo:mcStanley, G. H.: A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chcm. 226:497-509, 1957. Carlson, L. A.: Determination of serlun triglycerides. J. Atheroscler. Res. 3: 334-336, 1963. Searcy, R. L.. Bergquist, L. hl., and Jung, R. C.: Rapid ultramicro rstimation of serum total cholesterol. J. Lipid Res. 1:349-351, 1960. Dole, V. P., and hleinertz, H.: Microlong-chain fatty dcterniination of acids in plasma and tissues. J. Biol. Chem. 233:2595-2599, 1960. Bartlett, G. R.: Phosphorlls assay in chromatography. J. Biol. column Chem. 2343466-468, 1959. Robinson. D. S., and French. J. E.: Heparin, the clearing factor lip:lse, and fat transport. Pharmacol. Rev. 12:241-263, 1960. Juhlin, L., and Shelley, W. B.: II?granulation of the basophil of man induced by lipemia. Amer. J. Med. Sci. 242:211-222, 1961.