Creatinine analysis was done by the method of
Bosnes and Tausky (9), and PAH by the meth-
od of Smith et ai (10). A Coleman flame pho-
tometer was used to determine sodium and po-
tassium concentration of plasma and urine. His-
tological examinations were carried out on kid-
ney, heart, lung, liver, spleen, adrenals, pan-
creas, brain and intestines.

B. Isolated Kidney Experiments: Six isolated
kidney experiments were prepared as previously
described (11) and perfused with heparinized
blood from the femoral artery of anesthetized
donor dogs. The kidney was transferred without
interruption of blood flow and perfused at the
systemic arterial pressure of the dog. Renal
venous outflow was measured by a graduated /
cylinder and stop watch. Control flows averaged’
3.4 ml/min/gm. The ureter was catheterized for
urine flow measurement. Blood was returned to
the femoral vein from a reservoir via a Sigma
motor pump. Renal arterial pressure was moni-
tored at the kidney inflow tubing. Convulsions
were controlled by immobilizing the animal
with succinylcholine chloride* (0.5 mg/Kg).

*Anectine, obtained from Burroughs Welcome Co.. Tuckahoe.
N.Y.

Respiration was maintained with a Starling res-
pirator using room air. An alcoholic solution
of endrin (25 mg/ml) was added to the blood
reservoir at a rate of 0.5 ml/min.

The adrenergic blocking agent phentola-
mine**, which has little direct vascular effect

**Regitine, obtained from CIBA Pharmaceutical Co.. Sum-
mit, N.J.

(12), was infused into the renal artery of the
kidney before endrin as a control and 70-80
minutes post-endrin, to determine if changes in
renel vascular resistance were due to blood
borne adrenergic agents.

2. CHRONIC EXPERIMENTS:

Chronic studies were carried out on five fe-
male dogs, 14-20 Kg in weight. Two creatinine
and PAH control clearance studies and tubular
maximum (Tmax) determinations were done
on each animal. Injections of endrin were given
five consecutive days each week to each dog.
Weekly clearance studies were carried out dur-
ing the post-endrin period. For each clearance
determination the femoral artery was catheter-
ized by a modification of the percutaneous
method of Seldinger (13). Renal vascular re-

sistance (renal artery pressure/renal blood flow)
was determined from data cbtained from mean
systemic arterial pressure, hematocrit, and PAH
clearance. (The assumption was made that PAH
extraction was complete and that the renal vein
pressure remained low and constant).

Following sacrifice or death of the animals
due to the effects of endrin, tissue samples were
taken as described above.

RESULTS
1. ‘ACUTE EXPERIMENTS:
“A. Intact (in situ) Kidney Experiments

‘(12 animals): The response of these animals

to endrin was widely variable. Most of the meas-
ured parameters showed no consistent change.
The experimental group in which endrin was
injected into the lumen of the intestine did not
develop convulsive signs of endrin poisoning
during the two to four hour post-endrin period.
Changes in renal vascular resistance in ail ani-
mals were widely variable with a mear maxi-
mum change of +178% (range —28 to
+900% ). Glomerular filtration rate (Cc) de-
creased a mean maximum of 46% (rage —7
to —96% ). PAH extraction ratio remained rel-
atively constant. Urine flow was variable and
urine concentration remained in the normal
range (sp. gr. 1.010-1.030). Blood pH was con-
stant and the hematocrit showed no consistent

change (—13 to +8%).

The group receiving endrin intravenously de-
veloped convulsions within ten minutes after
completion of the endrin infusion. Additional
large quantities of sodium pentobarbital ad-
ministered to suppress the convulsions caused
blood pressure changes resulting in erratic kid-
ney function. In order to avoid complications
resulting from excessive pentobarbital adminis-
tration, succinylcholine chloride was used to
control convulsions in subsequent studies.

B. Isolated Kidney Experiments (6 kidneys) :
A marked increase in renal vascular resistance
appeared in most kidneys within ten minutes of
the time endrin infusion was completed. All
kidneys showed an increased resistance within
60-70 minutes post-endrin (fig. 1). Phentol-
amine had very little effect on the renal vascu-
lar resistance when administered pre-endrin (fig.
1A), but caused a significant and sudden drop

—2—


TABLE I

Effect of Chronic Exposure to Endrin on Mean ‘Systemic
Arterial Pressure of Dogs

Dog 1 2 3 4 5
MSAP MSAP MSAP MSAP MSAP
(mm Hg) (mm Hg) (mm Hg) (mm Hg} (am Hg)
Week Pre* Post Pre Post Pre Post Pre Post Pre Post
Infu. Infu.  Infu. Infu. Inu. Infu. — Infu. Infu. — Infu. Inf.
Control

(2 Wk. Ave.) 135 142 105 118 105 138 110 116 80 106

1 145 149 130 124 90 130 95 120 75 105
2 i15 134 80 125 125 126 90 125 85 101
3 90 122 80 101 105 151 85 111
4 90 151 80 136 90 151 75 94
5 105 136 90 126
6 95 149 80 80
7 95 131
8 85 86
*Pre Infusion = Value Prior t» Infusion of Clearance Solution.
TABLE II

Effect of Chronic Exposure to Endrin on Glomeruler Filtration
Rate in Dogs

Dog Tr 2 3 4 5
GFR GFR GFR GFR GFR
Week alli} fell pnins pentru {alin} onl pais
Control

(2 Wk. Ave.) 3.10 4.1 2.7 3.5 3.6
1 2.5 4.3 3.0 3.9 2.8
2 48 3.4 3.4 4.5 48
3 3.9 3.7 2.5 4.6
4 3.2 3.8 3.0 2.2
5 4.3 4.2
6 3.5 4.0
7 6.2
8 6.4


Under the conditions of these experiments
only mild pathological changes were seen in the
kidney, liver, spleen, adrenal gland, and lungs.
The appearance of protruded segments of prox-
imal convoluted tubules is reported by Mayer
and Ottolenghi (14) as occurring in apparently
normal dogs. However, Wachstein and Meisel
(15) and Waugh and Beschel (16) associated
this phenomenon with ischemic damage to the
kidneys. Reflux of tubular epithelium was ob-
served occasionally in cases of acute toxicity
but was apparently absent in chronically pois-
oned dogs. This is in agreement with the find-

ings of Waugh and Beschel (16) with serotonin
induced ischemia. Congestion of the liver, lungs,
and adrenals did not appear to be of long dur-
ation and may have been associated with the
terminal drop in blood pressure.

Dysphagia in chronic animals leading to star-
vation and dehydration appeared to account for
systemic hypotension (i7) which was reversed
at first by infusion but in the moribund state
became irreversible. There was no consistent
change in renal function as 4 result of the de-
velopment of hypotension (tables I, V).

ACKNOWLEDGEMENT

The authors wish to express their appreciation to Dr. B. L. Glenn of
Oklahoma State University for his assistance as consulting pathologist.

BIBLIOGRAPHY

1. T. E. Emerson, C. M. Brake and L. B.
Hinshaw

CARI Report 63-16

2. J. F. Treon, and F. P. Cleveland
J. of Ag. and Food Chem. 3, 402, 1955

3. J. R. Busvine
Practitioner 188, 267, 1962

4. J. B. DeWitt
J. of Ag. and Food Chem. 3, 672, 1955

5. A. Bell *
Med. j. of Australia 2, 698, 1960

6. E. J. Spiota
A. M. A. Arch. Ind. Hyg. 4, 560, 1951

7. E. Nelson
Rocky Mt. Med. J. 50, 483, June, 1953

8. B. E. Conley
J. A.M. A. 158315, 1364, August 13, 1955

9. R. W. Bosnes and H. H. Tausky
J. Bioi..Chem. 158, 581, 1945

10. W. W. Smith, N. Finkelstein and H. W.
Smith
J. of Biol. Chem. 135, 231, August, 1940
11. L. B. Hinshaw, G. M. Bradley and C. H.

Carlson
Am. J. Physiol. 196, 1127, 1959

12. H. D. Hohnson, H. D. Green and J. T. La-
nier
J. of Pharmacol. and Exp. Ther. 108, 144
1953

13. S. I. Seldinger
Acta Radiologica 39, 368, January-June,
1953

14. E. Mayer and L. A. Ottolenghi
Anatom. Rec. 99, 477, 1947

15. M. Wachstein and E. Meisel
J. Histochem. and Cytochem. 5, 204, 1957

16. D. Waugh and H. Beschel
Amer. J. Path. 39, 547, 1961

17. C. M. Wilhelmj, A. J. Carnazzo and H. M.
McCarthy
Am. J. of Phys. 191:1, 103, 1957


in renal resistance when administered post-en-
drin (fig. 1B). The renal artery tubing was par-
tially constricted in three experiments to lower
renal artery pressure to control levels. In these
animals injection of phentolamine caused the
renal resistance to return to near control value.
In the other animals the renal artery tubing
was not constricted and injection of phentol-
amine caused a drop in renal resistance but to
some level above control value. Dogs immobil-
ized with succinylcholine chloride: showed a
consistent hypertension in response to endrin
and occasionally an increased urine flow. Hy-
pertension was also seen when convulsions ap-
peared in the non-anectinized animal. No at-
tempt was made to establish a diuresis in these
kidneys and it was noticed that occasionally
there was a complete cessation of urine flow.
Addition of mannitol solution to the blood res-
ervoir caused an almost immediate response by
re-establishing a urine flow.

2. Chronic Experiments (5 dogs): The
first noticeable sign of endrin poisoning was
dysphagia. Muscle twitches of the tongue and
throat made it difficult for the animals to eat.
Most dogs developed hypotension within two
weeks after initiation of endrin poisoning (table
I). Glomerular filtration rates were variable
(table II). A decrease in renal resistance was
seen in some dogs (table III). Sodium and po-
tassium absorption showed no consistent change
(table V).

PATHOLOGICAL CHANGES:

Acute Studies: Renal tubular necrosis was
seen in only one dog. There was a mild to mod-
erate degree of protein precipitation in Bow-
man’s space and in the tubules. An occasional
glomerulus was observed in which a reflux of
epithelium from the proximal convoluted tubule
into Bowman’s space had occurred.

The spleen exhibited moderate to severe con-
gestion with early degenerative changes and a
mild degree of necrosis in the reticular cells as-
sociated with the germinal centers. The degen-
erative changes were more prominent in the
large active germinal centers. Mild to moderaie
congestion and irregularly distributed cloudy
swellings were present in the liver. The lungs
were slightly congested and contained occasion-

al areas of hemorrhage, but the heart, pancreas,
and intestine appeared normal.

Chronic Studies: No definite tubular
changes were detected in the kidneys. The spleen
exhibited a mild degree of inactivity of the
germinal centers. There appeared to be some
lipid depletion in the adrenal gland which show-
ed mild to moderate congestion more pronoun-
ced near the cortico-medullary junction. In some
dogs a moderate degree of passive congestion
was seen in the liver. Mild congestion and occa-
sional hemorrhage were found in the lungs of
most animals. No significant pathological
changes were seen in the brain, pancreas, lungs,
heart, or intestine.

DISCUSSION

The constancy of the PAH exiraction ratio in
the acute studies of in situ kidneys suggests that
endrin has no direct effect on the kidney in the
first two to four hours after administration. In-
creased renal resistance and the effect demon-
strated by phentolamine on the dog-pump per-
fused isolated kidney suggest action on the sym-
pathoadrenal system. The increase in renal vas-
cular resistance was not completely due to adre-
nergic agents since there was a small drop in
renal vascular resistance when the renal artery
pressitre was reduced to control level in three
kidneys. When phentolamine was administered,
renal resistance returned to control levels. In
other kidneys the ariery was not clamped to
reduce the pressure and the renal vascular re-
sistance did not return completely to control
level when phentolamine was administered but
to some level above it. This difference from con-
trol values apparently represents the fraction
of resistance change due to autoregulation with-
in the kidney. The diuresis occasionally seen in
acute endrin poisoning may be due to an in-
creased resistance in the efferent arterioles. Ad-
ministration of mannitol to re-establish urine
flow in those animals with complete cessation
of urine flow may indicate a form of treatment
when this occurs in humans. The effect of man-
nitol in acute studies suggests that the infusion
necessary for clearance studies constituted a
form of treatment. It is a most significant ob-
servation that no evidence was obtained for
renal failure due to chronic endrin poisoning.

—3—



_PHENTOLAMINE PRE-ENDRIN PHENTOLAMINE POST-ENDRIN

ols

Tle

els

a pe — "a
it

RENAL RESISTANCE

TIME IN MINUTES
FIGURE I-A FIGURE 1-B

Ficure 1A. Changes in renal vascular resistance in isolated kidneys with phentolamine only

Froure 1B. Changes in renal vascular resistence in isolated kidneys with phentolamine 70-80
min. after endrin.

—6—



ff! (—

LEN ACUTE AND CHRONIC
Ue al EFFECTS OF THE

X . “Se ff INSECTICIDE ENDRIN ON
N \ A RENAL FUNCTION AND
= Kp ae = RENAL HEMODYNAMICS
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FEDERAL AVIATION AGENCY
AVIATION MEDICAL SERVICE
AEROMEDICAL RESEARCH DIVISION
CIVIL AEROMEDICAL RESEARCH INSTITUTE
OKLAHOMA CITY, OKLAHOMA

[ere nn fre

| JUL 14 1964
0

DDC-IRA C



TABLE V

Effect of Chronic Exposure to Endrin on Sodium and Potassium

Reabsorption of Dogs

Dog

Week

Control
(2 Wk. Ave.)

wa bk wn

aon

Na
(%)
(reab.)

98.6
99.5
99.2
99.4
98.6

99.0 |
98.7

98.8
99.4

K
(%)
(reab.)

93.8
93.1
82.8
91.6
92.2
94.0
91.9
81.4
98.3

oD
(reab.)

06.8

96.9
96.4
95.2
95.0
96.8
98.5

K
(%)
(reab.)

78.1
83.0
86.2
90.5
98.1
89.6
95.9

Na
(%)
{reab.)

(

K
(%)

reab.)

918
2.8
88.0
$1.6

i

Na
(%)
(reab.)

96.8
97.1
97.8
97.4
97.7

K
(%)
(reab.)

92.8
86.9
91.5
95.4
75.0

Na
(%)
(reab.)

96.1
97.1
98.3

)
(reab.)

87.0
94.2
96.8

U.S. GOVERNMENT PRINTING OFFICE : 1964 onney

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FIGURE {

Ficuae ). Changes in renal vascular resistance in isolated kidneys after administration of endrin.

—5—


ACUTE AND CHRONIC EFFECTS OF THE INSECTICIDE
ENDRIN ON RENAL FUNCTION AND RENAL
HEMODYNAMICS

D. A. Reins
D. Holmes
B. Hinshaw

ABSTRACT

Chronic and acute effects cf the insecticide endrin on renal function were studied in dogs.
Animals were exposed to endrin chronically by intramuscular injection and acutely by intra-
venous infusion. In acute studies dogs developed systemic hypertension and increased renal
vascular resistance attributable to a sympatho-adrenal action. Basic renal autoregulation
was not impaired by endrin but was masked by effects of blood borne adrenergic agents. Changes
in renal function were minimal. In chrenic studies dogs developed progressive systemic hypo-
tension with variable changes in renal function and terminal renal vasodilation in some in-
stances. Pathological findings were minimal and could be #elated to hemodynamic alterations
in the peripheral vasculature. Results from this investigation provide no evidence for renal

failure due to chronic insecticide poisoning.

Biological effects of chlorinated hydrocarbon
insecticides have been described (1, 2, 3). En-
drin, the most toxic member of this group (2, 4)
was chosen to be the subject of the present in-
vestigation. The effect of endrin on renal hemo-
dynamics has not been described, but impair-
ment of rena] function has been noted in some
cases of chlorinated hydrocarbon poisoning (5,
6, 7). Pathological changes in the kidney have
been reported by Treon et al (2), although
Cenley (8) reports postmortem changes as non-
specific. The present studies were designed to
determine if endrin has a direct action on renal
hemodynamics and renal tubular function, as
indicated by pressure flow relationships and
changes in glomerular filtration rate, effective
renal plasma flow, and tubular transport.

METHODS

Three types of experiments were carried out
on adult mongrel dogs: acute endrin poisoning;
chronic endrin poisoning; isolated perfused
kidneys receiving blood from animals acutely
poisoned with endrin.* Animals were anesthe-
tized with sodium pentobarbital, 30 mg/Kg.

*Endrin, obtained from Nutritional Biockemicals Corp., 21010
Miles Ave., Cleveland 28, Ohio.

Dogs in acute studies received a lethal dose of
endrin (10 mg/Kg) in alcohcl, while those in
chronic experiments were given intramuscular
injections of endrin in cotton seed oil (1 mg/
Kg). Systemic arterial pressures were measured
from cannulated femorai arteries with Statham
pressure transducer connected to a Sanborn di-
rect writing recorder.

A priming solution of mannitol, PAH, and
creatirine was administered intravenously and
blood levels were maintained by intravenous in-
fusion. Dogs were infused until a urine flow of
1.5 to 2.0 ml/min was established.

1. ACUTE EXPERIMENTS:

A. Intact Kidney (in situ) Experiments: The
left renal vein was catheterized for blood sampl-'
ing. Four studies were carried out in which an
alcoholic solution of endrin (25 mg/ml) was
injected into the lumen of the small intestine.
Eight additional animals were infused with en-
drin via the femoral vein. Endrin was admin-
istered after control clearance determinations.
Clearance periods were carried out at haif hour
intervals for two to four hours. Blood pH and
hematocrit determinations were alsc made.

—1—


ACUTE AND CHRONIC EFFECTS OF THE c

INSECTICIDE ENDRIN ON RENAL FUNCTION
AND RENAL HEMODYNAMICS

D. A. REINS
D. D. HOLMES
L. B. HINSHAW

Renal Physiology Section
Environmental Physiology Branch

63-26

FEDERAL AVIATION AGENCY
CIVIL AEROMEDICAL RESEARCH INSTITUTE
AERONAUTICAL CENTER
OKLAHOMA CITY, OKLAHOMA

OCTOBER 1963


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