REFERENCES

1. Hinsnaw, L. B., Pace, B, B., Brake, C, M., and
Emerson, T. E., Jx.: Mechanism of Intrarenal Hemo-
dynamié Changes Following Acute Arterial Occlusion,
Am. J. Physiol, 205 :1033, 1963,

2. Hinsuaw, L. B., Emerson, T. E., J8., and Braxe, C. M.
Renal Blood Flow as Influenced by Changes in Arter-
ial, Venous, and Ureteral Pressures, Am. Heart J. 68:
652, 1964. -

3. Braun-Menvez, E., Covian, M. R., and Rapera, CO. E.:
Presencia de Renina en la Sangte Circulante de Ratas

-

e

Normales e Hipertensas, Rev. Soc. Argent. Biol. 23 :131,
1947.

| Pace, I, H., and Heumer, O, M.: A Crystaline Pressor

Substance Resulting from the Reaction Between Renin
and Renin-activator, J. ep. Med, 71:29, 1940.
Hinsuaw, L. B., Day, S. B. and Carrson, C, H.:
Tissue Pressure as a Causal Factor in the Autoregula-
tion of Blood Flow in the Isolated Perfused Kidney,
Am. J. Physiol. 197 :309, 1959.

Scum, H. E., Jr.: Renin, a Physiologic Regulator of
Renal Hemodynamics?, Circulation Res, 11:185, 1962.



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O30% 30-40% 40-50% 50-80% 60-70% 70-00% 100%

© Controt @ Value I post Occlusion Tyee,

4 Value during Occlusion © Volue ot maximum response
Fieure 1. Mean data + standard error showing total
renal vascular resistance (R,), renal artery pressure
(RAP), and renal blood flow (RBF) before, during, and
after a period of partial and complete renal artery occlu-
sion. Groupings represent percent change from control
values. Numbers in parentheses represent number of
experiments in each group.

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4% During Occlusion 0 % 4 4t maximum response

Ficure 2. Total renal resistance (R,), renal artery pres-
sure (RAP), and renal blood flow (RBF) as mean values
depicted as percent change from control.

IV. Discussion.

Autoregulation of blood flow by the kidney was
evident with each step-wise reduction in renal
artery pressure, there being a consistent decrease
in resistance.? At and beyond the apparent critical
range (40% to 50% reduction in pressure), after
the clamp was removed and control pressures re-
gained, the resistance rise exceeded that expected
during autoregulation. This suggested, among
other things, the possibility of the release of
some vasoconstrictor humoral agent, in these de-
nervated organs. The injection of phentolamine
at the peak of the constrictor response had no ef-
fect, thus tending to eliminate catecholamines.
The renin-angiotensin complex is well-known.**
In two additional experiments utilizing a heart-
lung-pump perfused isolated kidney. which has
been previously described,’ antirenin (50 anti-
renin units*) was introduced into the system.
Antirenin, a neutralizing antibody to renin, may
be used to block the renin-angiotensin pressor
system.’ Before the introduction of antirenin,
both organs demonstrated a typical ischemic re-
sponse following a period of partial occulsion.
The same maneuver after the introduction of an-
tirenin into the blood perfusate resulted in re-
active hyperemia, the increase in resistance being
totally obliterated. Angiotensin is then possibly
playing a major role.

Partial renal occlusion, with a reduction in
renal artery blood pressure at or below a critical
level (40% to 50% of control) results in a marked
increase in renal vascular resistance following re-
lease of the obstruction. This is similar to the
results observed following periods of total disrup-
tion of blood flow to the kidney. It is suggested
that the elaboration of renin by the partially
ischemic kidney occurs within a very few minutes
following insult.

*We are indebted to Dr. Herman E. Schmid, Bowman Gray
School of Medicine, for the generous supply of antirenin.




AM 65-27

INTRARENAL HEMODYNAMIC CHANGES FOLLOWING
ACUTE PARTIAL RENAL ARTERIAL OCCLUSION

Charles M. Brake
Dale Reins
Lorenz E. Wittmers
Lerner B. Hinshaw

Approved by Released by
J. Roserr ‘Dure, M.D. P. V. Srecer, M.D.
Cuter, Civ, A®rROMEDICAL FeperaL Arr SurcEon
INstITuTE

October 1965

FEDERAL AVIATION AGENCY
Office of Aviation Medicine



FOREWORD

The work described in this report was performed by members of the Envi-
ronmental Physiology Branch, CARI, and the Department of Physiology,
University of Oklahoma School of Medicine, Oklahoma City, Oklahoma. It
was supported in part by a grant-in-aid from the American Heart Association
and the Tulsa County (Oklahoma) Heart Association.

Qualified requestors may obtain Aviation Medical Reports from Defense Documentation
Center. The general public may purchase from Clearinghouse for Federal Scientific and
Technical Information, U.S. Dept. of Commerce, Springfield, Va. 22151.


INTRARENAL HEMODYNAMIC CHANGES F OLLOWING
ACTIVE PARTIAL RENAL ARTERIAL OCCLUSION

I, Introduction.

Both an increase and a decrease in total renal
vascular resistance, following a period of total
renal artery occlusion, have been reported from
this laboratory. The duration of the occlusive
period and the height of the perfusion pressure
were found to prescribe consistently the hemody-
namic response. The present study was under-
taken to determine if a similar renal vascular
response occurred after a period of partial renal
artery occlusion. Results indicate that following
a period of partial occlusion, in a critical range
of renal artery pressure, intrarenal hemodynamic
changes mimicked those seen after total obstruct-
ion of blood flow. Reactive hyperemia was not
observed.

II. Methods.

Experiments were performed on adult mongrel
dogs of both sexes, weighing from 15 to 19 kg.
Surgical anesthesia was produced and maintained
with sodium pentobarbital, the initial dose being
30 mg/kg. The left kidney was exposed through
a flank incision. The vessels of the renal pedicle
were dissected free of the surrounding tissues, in-
cluding stripping away of all visible nerve fibers.
The renal venous effluent, measured at intervals
with an appropriately sized polyethylene tube.
with a graduated cylinder and stop watch, was
collected in a reservoir, thence through a sigma-
motor pump returned to the femoral vein of the
dog. Anticoagulation was insured by the ad-
ministration of 3 mg of Heparin per kilogram of
body weight. A screw clamp was positioned on
the exposed renal artery. Renal artery pressure
was continuously monitored and recorded on a
Sanborn direct-writing instrument, a needle be-
ing inserted in the vessel distal to the screw
clamp. The systemic arterial blood pressure was
recorded in the usual fashion from the cannu-
lated femoral artery.

Adjustments of the screw clamp resulted in a
step-wise decrease in renal artery pressure. Pres-
sure-flow relationships were observed at each
level, and at intervals after removal of the clamp,
a “steady-state” condition being prerequisite to
each maneuver. A final period of total occlusion
was produced in each experiment. In some in-
stances, an adrenergic blocking agent, phentola-
mine (Regitine, Ciba) was employed in an at-
tempt to characterize any released humoral
agents, ~

III. Results.

Renal blood flows in a total of 10 experiments
averaged 2.6 ml/min/gm of kidney (range 1.6 to
3.3), at a mean arterial pressure of 121 mm Hg.
Systemic arterial blood pressure was constant.
The duration of the times of partial renal artery
occlusion was varied from 5 to 30 minutes. Fol-
lowing these spans of time there was a consistent
increase in total vascular resistance, The results.
are depicted in Figures 1 and 2. The total renal
resistance, renal blood flow, and renal artery
pressure values are arranged by groups based on
the percent of change from control values accord-
ing to the tension produced by the adjusted screw
clamp. Beyond a 30% reduction of mean control
renal artery pressure, a persistent fall in renal
vascular resistance occurred during the period of
partial occlusion. Significant alteration in total
renal vascular resistance did not occur until renal
artery pressure had been reduced to a critical
range of from 40% to 50% of the control value.
Greater reduction in pressure resulted’ in an in-
crease in magnitude of the response. Renal blood
flows returned to or very near control values with-
in 8 to 11 minutes following release of the con-
striction. One minute after release of a total
occlusion reactive hyperemia was noted, followed
by a greater increase in resistance.