RICHARD V. EBERT, CRAIG W. BORDEN, WENDELL H. HALL and ...

380 SHOCK DUE TO BACTERIAL TOXIN
TABLE 2.—Effect of Hemonhage (10 ml. per Kg.) on
Hypotension Produced by Meningococciis Toxin
DOE
5
6
S
12
Cardiac Output
L./Kg./Min.
Before
.716
.315
.134
.105
After
.060
.077
.065
.071
Total Periphera
Mean Arterial Resistance
Pressure mm. Hg dynes/seconds/
cm." 1
Before
97
74
S6
75
After
56
55
4S
50
Before
7594
1971
4916
6260
After
S623
5957
5658
6595
.factor for the hypotension induced by the
toxin.
The effect of reduction of blood volume on
the hypotension produced by toxin was
studied. Four animals were given toxin intravenously.
After the maximum decline in
arterial pressure had occurred, blood in the
amount of one per cent of the body weight
was removed. The observations were repeated
ten minutes later (table 2). The further decline
in arterial pressure was principally associated
with a marked further reduction in cardiac
output in all four animals consequent to
further impairment of venous return by the
hemorrhage. Calculation of the T.P.R., which
showed a marked increase in one experiment
(dog 6), and probably insignificant increases
in the three others, supports this contention.
A hemorrhage of this magnitude in the normal
animal would have relatively little permanent
•effect on cardiac output and arterial pressure.
Inasmuch as the hypotension and reduction
in cardiac output following the administration
of toxin was accompanied by a reduction in
Don
1
2
4
6
7
10
13
15
16
22
systemic and pulmonary venous pressure, an
experiment was performed to determine the
effect of increasing the blood volume on the
circulation. Hypervolemia was produced by
the intravenous infusion of 6 per cent dextran
in 0.85 per cent saline. Toxin was first administered
to the animals. When a maximum
decline in arterial pressure had occurred,
dextran solution in the amount of 30 ml. per
Kg. was administered. Observations were
made immediately before and after the infusion
of dextran. The results on 10 animals
are given in table 3. The right atrial pressure
and the cardiac output increased after dextran
infusion to above the control level, while the
increase in arterial pressure was of a lesser
degree. This was apprently due to the fact
that there was a marked decline in total
peripheral resistance after administration of
dextran in the majority of experiments.
The effect of levarterenol on the arterial
pressure and cardiac output was studied in
eight animals. Observations on the effect of
levarterenol prior to the administration of
toxin revealed that a moderate pressor response
was produced by infusion at the rate of 20
tig. per min. A marked pressor response was
produced by infusion at the rate of 40 ^g- per
min. Following administration of toxin and
development of hypotension, a larger quantity
of levarterenol was required to produce a
pressor response in some of the animals. The
course of a typical experiment is shown in
figure 1. The amount of levarterenol required
to produce a rise in arterial pressure of 20
TABLE 3.—Effect of Dextran (SO ml. per Kg.) on Hypotension Produced by Meningococciis Toxin
Mean Arterial Pressure
mm. Hg
Before
76
73
53
74
64
42
55
65
55
78
After
129
130
102
S2
6S
63
125
104
91
107
Right Atr al Pressure
mm Hg
Before
-0.2
-1.5
-2.0
-2.5
-0.5
-0.2
-2.6
-0.6
-4.0
-3.S
After
+0.5
+ 14.3
+2.0
+0.2
0
0
-0.2
+0.5
+0.5
+0.7
Before
.116
.128
.144
.315
.077
.063
.OSO
.057
.045
.128
Cardiac output
L./Kg /min.
After
.218
.410
.318
.274
.103
.200
.280
.322
.364
.305
Total Peripheral Resistance
dynes/ seconds/cm."*
Before
5475
7113
4196
1971
6647
6274
504S
7113
10723
5874
Downloaded from
http://circres.ahajournals.org/ by guest on November 28, 2012
After
4955
3969
3650
2504
5275
2997
3290
2025
21S5
3423