‘THE DEVELOPMENT OF REVERSIBLE HEMATURIA AND OLIGURIA
FOLLOWING ELEVATION OF RENAL VENOUS PRESSURE
E. Emerwn,
‘B. Hinshaw
M. Brake .
Tampletro

ui

i

ie .
te

uaa
r Hee
ii i ie

|
85
Ht

noel

vice (range I
proximal to the
case, a number 27 gauge
oe
vein with
+ the

tubing and’ pressure monitored

bing

1
pat

tw

iis 1 ae ules
wee [3 i Ht
alba Ane



ii ite

.: i

Hin i
Hea

233 su234823

iE
ft

i!

ini
et

PPP LELEEE

>

a


Tawz 1

EFFECT OF INCREASED RENAL VENOUS PRESSURE ON THE KIDNEY*
HEART-LUNG-KIDNEY PREPARATION

Exp. No.

amon

*
/°Mi

Hematuria

tet te

% RBC in

Urine
15
09
Ol
10
18

Urine Flow Renal LVP*
(Sof Control)

10
6
87
wv
86

INTACT DOG KIDNEY PREPARATION

+e et

+
+

Increase in Large Vein Pressure Required to Elicit Hematuria

05
05
06
10
01
02

-3—

.

Sot?

S@erea

(mm Hg)

RBSRAB

2288R888


rates were measured as described above. Mean
systemic arterial pressure was monitored from

-a catheterized femoral artery and registered

on a Sanborn direct-writing recorder.

Urine samples were collected in centrifuge
tubes during a five or ten minute period and
1 cc samples of each collection period were
centrifuged in Wintrobe tubes for urine hema-
tocrit determination.

Resuits. The experimental data are sum-
marized in Table 1. Results hema-
turia was present in all experiments following
venous pressure elevation. The volume of red
blood cells present in the urine is seen to be
small and variable (0.1-1.8%). Urine flow
rate decreased in all

7
E

crease in urine flow rate for a wide range of
renal venous pressures expressed on a percent-
age basis. Hematuria was not observed in
either group until the urine flgw rate was sig-
nificantly reduced, (mean of both groups: 44%
of control). ‘y
rf

Discussion. Results show that gross hema-*
turia, including red'blood cells and hemoglobin,
appears when a relatively high pressure
is produced. If the pressure is f elevated,
the degree of hematuria’ in and is sus-
tained until contro] venous pressure is restored,
at which time it disappears. Hemoglobinuria,
present in the isolated kidney, was not present
in the intact organ under conditions of in-
creasgd renal venous pressure. Although ab-
sent at low venous pressures in the isolated
organ, the subsequent appearance of hemo-
globinuria at elevated pressures could be ac-
counted for by increased levels of plasma hem-

oglobin (due to the perfusion pumps) or
decreased tonicity of urine (due to the absence
of ADH).

There are at least three possible sites of en-
branes for red blood cells nto the urine. One
possible region is the peritubular capillaries.
Swann described these as being “leaky” and
suggested that a free communication exists be-
tween these vessels and the interstitial space
(5). Evidence for the existence of large pores
in the peritubular capillaries is given by elec-
tron microscopy studies (6). However, a mech-
anism for getting the red cells into the urine
from the interstitial has not been pro-

cells is through
by virtue of an increased glomerular pressure,
although it seems unlikely that venous pressure
transmissions would be effective in increasing
transmural pressure at the glomerular mem-
brane (7). A factor opposing the glomeruli
as the site of entrance is that renal venous

walls of blood vessels bordering the renal pel-
vis which could be temporarily opened, allow-
ing for passage of red cells into the urine.

absorption of water from the tubules (11) and
increased back pressure with decreased glom-
eruler filtration rate (2, 12-14).


—

—

Ea

BEFERENCES

1. Bull, G. M, Clie, Sct, 1948, v7, 77.
2 Winton, F. R, J. Physiol, 1931, v72, 49.

a Hindey, Te

JF Phyl, 1966, 106,
s Swain, H. G., Taxes Rpta, Biol. Med., 1900, vi, 60.
6 Peace, D.C, Anat, Rec., 1955, v121, 701.
‘1. Winton, F. R., Physiol. Rev., 1937, v17, 408.
& Gottschalk, C. W., Mylo, M., Am. J. Physiol, 1058,

v185, 430.

a Eiamem Fo Leo Brown, BK, JAM-A, 1994, vat

10, Polish, HC, Shges FL, f Ut, 1947 v5T, 834

11. Blake, W. D., Wegria, R., Keating, R. P., Ward, HP.
‘Am. J. Physiol, 1949, v157, L

12, Selaut, E. E, Hall, P. W., Spencer, M. P, Am. J
Physio., 1949, v157, 40.

13. French, D. M., Moland, P. A, Brooker, W. M, Fed
Proc., 1948, v7, 38.

14. Bradley, S. E., Bradley, G P., J. Clin. Incest, 1947
v28, 1010.

Snr


e

|

‘ inn Ht ill |
5 pe SWS
iy”

AND OLIGURIA
FOLLOWING ELEVATION OF
RENAL VENOUS PRESSURE

TIA
ahes mute)

7
ape WB |
L a
t ped

u aS

bee
ms .

be

FEDERAL AVIATION AGENCY
AVIATION MEDICAL SERVICE

ESEARCH DIVIEION
CIVIL AEROMEDICAL RESE/
OKLAHOMA CITY, OKLAHOMA

JANUARY 1963


fa

URINE FLOW (% Change)

URINE FLOW (% Change)

° ISOLATED
1 PERFUSED
KIDNEY
-204
+
-407
-604
4
-60
-100 fara 4

D | sy, en ree ee
! to «0 | © 0
RENAL VENOUS PRESSURE (mm Hg)

Ficuns 1. The effect of increasing renal venous pressure
on the urine flow rate, The vertical lines indicate the
total range at the various pressures.

-4-


it 4 | |
i
Hil eat
iin HU ty
Hla Gadi
itt WG FL
We aL ge ngine
DEL Ee

v



Fe

THE DEVELOPMENT OF REVERSIBLE HEMATURIA AND OLIGURIA
FOLLOWING ELEVATION OF RENAL VENOUS PRESSURE

T. E, EMERSON

} L. B. HINSHAW

C. M. BRAKE

: P. F. IAMPIETRO

| with the technical assistance of
F, Masucei

Environmental Physiology Branch

yf : 4

4.


a3 a3
iis ty
Hu vu

ay #73 7 as ils Anh
S25 232%
Bl pig it ; Fay i ii aie

: ‘Elf abel ke! ahi
i a i ee, Eby fa
ha i i fe jase
Be I til lie ta
a

i: if

age a say Uae

. ate ut
et ae
oe ae
fee li nH

i

he] Hi ghsetaa

2 it i a i i]