Use of Renal Blood Flow
Although the kidneys receive almost one fourth of the cardiac
output and extract relatively little oxygen, there is a marked discrepancy between
cortical and medullary blood flow and oxygen delivery and consumption. The apparent
overabundance of blood flow to the cortex is designed to maximize flow-dependent
functions, such as glomerular filtration and tubular reabsorption. In the medulla,
blood flow and oxygen supply are restricted by a tubulovascular anatomy specifically
designed for urinary concentration. There appears to be a physiologically important
reason for the paucity of blood flow and, consequently, the oxygenation in the medulla.
[176]
The tubules carrying blood to the medulla
are arranged in a hairpin-loop pattern to allow a countercurrent exchange of solute
between the ascending and the descending limbs of the hairpin loop. In this way,
urine in the tubule becomes highly concentrated. The osmotic gradient in the deeper
portions of the medulla requires active transport of sodium in the thick ascending
loop of Henle and limited blood flow through the medullary vessels to prevent washout
of the solutes in those deeper tubules. To maintain this concentration gradient
in the thick ascending limb, high energy demand (i.e., active sodium transport)
must be coupled with low oxygen delivery. The ambient partial pressure of oxygen
in the medulla ranges from 10 to 15 mm Hg. The high metabolic requirement of the
thick ascending loop of Henle in a hypoxic environment makes it especially vulnerable
to injury associated with an imbalance in oxygen supply and demand.[177]
[178]
Hypoxic perfusion of an isolated kidney preparation
has demonstrated that the cells of the thick ascending limb of the loop of Henle
in the medulla are extremely vulnerable to hypoxic damage.[69]
This damage is patchy and is most evident in tubules farthest from a vessel. The
selective vulnerability of the cells in the thick ascending loop of Henle is thought
to result from their high oxygen consumption. Blood flow is approximately 90% to
95% to the cortex, compared with 5% to 10% to the medulla. Average blood flow is
5.0 mL/g/min and 0.03 mL/g/min for the cortex and medulla, respectively, and the
oxygen extraction ratio (i.e., oxygen consumption over oxygen delivery) is 0.18 and
0.79 for the cortex and medulla, respectively. Normally, the partial pressure of
oxygen is about 50 mm Hg in the cortex and 8 to 15 mm Hg in the medulla, making the
thick ascending loop of Henle most vulnerable to tissue hypoxia. Severe hypoxia
may therefore easily develop in the medulla if total renal blood flow is inadequate.
The initial response to decreased renal blood flow is an increase
in sodium absorption in the ascending loop of Henle, which increases oxygen demand
in the regions most vulnerable to decreased oxygen delivery. Ischemic renal damage
may reflect hypoxic injury deep in the medulla to the metabolically active cells
of the ascending loop of Henle. The normal response to systemic hypoperfusion is
active sodium and water reabsorption, a metabolic response that demands oxygen at
the time of greatest hypoxic vulnerability. To compensate, sympathoadrenal mechanisms
cause cortical vasoconstriction and oliguria, which redistributes blood flow away
from the outer cortex to the inner cortex and medulla. Determination of total RBF
does not provide a reliable predictive index of organ function after an ischemic
insult or surgery. Another compensatory mechanism, increased sodium delivery to
the macula densa, results in afferent arteriolar constriction. With afferent arteriolar
vasoconstriction, glomerular filtration decreases, after which solute reabsorption
in the loop of Henle and oxygen consumption are reduced. In a hypoperfused kidney
preparation, oxygen-enriched perfusion reduced cellular damage, hypoxic perfusion
increased it, and complete cessation of perfusion (i.e., glomerular filtration equal
to zero, preventing ultrafiltration) was associated with less cellular injury than
hypoxic perfusion.[68]
The severity of cellular
injury appears related to the degree of imbalance between cellular oxygen supply
and demand. Afferent arteriolar vasoconstriction may be a normal protective response
to acute tubular injury. By reducing ultrafiltration, further energy expenditure
by already ischemic medullary tubular cells is prevented, even at the cost of retaining
nitrogenous waste.
Theoretically, therapeutic intervention designed to prevent renal
insufficiency should be focused on preserving renal blood flow and oxygen delivery.
Continuous monitoring of urinary oxygen tension has been examined as a method for
assessing renal function during the perioperative period.[179]
[180]
[181]
[182]
[183]
[184]
[185]
[186]
Urinary oxygen tension (PuO2
)
decreases with clinical shock and dehydration. It has been demonstrated that PuO2
decreased when renal blood flow decreased or PaO2
decreased and that PuO2
increased when
PaO2
increased. Changes in PuO2
,
however, are relatively insensitive to oxygen content compared with changes in PaO2
.
Because urinary oxygen tension depends on renal perfusion and renal oxygenation,
it may be a useful tool for predicting renal cell injury, but it is not yet clinically
practical to measure PuO2
. Urine samples
obtained from bladder catheters provide artificially high PuO2
values because samples are easily contaminated with the oxygen in room air. Another
problem with measuring urinary oxygen tension or saturation is that bladder measurements
may be different from ureteral measurements. Ureteral measurements also may not
reflect accurately the regional use of oxygen in the renal cortex versus the renal
medulla or the renal pelvis. Interpreting the physiologic significance of changes
in urine oxygen tension or saturation requires knowledge of where the oxygen comes
from and its relationship to other physiologic variables.
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