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Zong-Guang
Zhou, You-Dai Chen,
Department of Hepato-bilio-pancreatic Surgery & Institute of
Microcirculation, West China Hospital, Sichuan University, Chengdu
610041, Sichuan Province, China
Correspondence to: Dr. Zong-Guang Zhou, Department of
Hepato-bilio-pancreatic Surgery & Institute of Microcirculation,
West China Hospital, Sichuan University, Chengdu 610041, Sichuan
Province, China. 258836@mail.guoli.com.cn
Telephone: +86-28-5422484
Received 2001-11-02 Accepted 2001-12-05
Abstract
Pancreatic microcirculatory disturbance plays an important role
in the pathogenesis of acute pancreatitis, and it involves a series
of changes includ ing vasoconstriction, ischaemia, increased
vascular permeability, impairment of nutritive tissue perfusion,
ischaemia/reperfusion, leukocyte adherence, hemorrhe ological
changes and impaired lymphatic drainage. Ischaemia possibly acts as
an initiating factor of pancreatic microcirculatory injury in acute
pa ncreatitis, or as an aggravating/continuing mechanism. The
end-artery feature o f the intralobular arterioles suggests that the
pancreatic microcirculation is highly susceptible to ischaemia.
Various vasoactive mediators, as bradykinin, pla telet activating
factor, endothelin and nitric oxide participate in the developm ent
of microcirculatory failure.
Zhou ZG, Chen YD. Influencing factors of pancreatic microcirculatory
i mpairment in acute panceatitis.World J Gastroenterol
2002;8(3):406-412
INTRODUCTION
Acute pancreatitis remains an important surgical problem with
high morbidity and mortality[1-4]. It is not merely an
injury caused by the activated pan creatic enzymes but also involves
pancreatic ischaemia. Evidences in basic and clinical research
suggest that disturbance of pancreatic microcirculation plays a n
important role in its pathophysiological processes[5-14].
The specific local microcirculatory changes cannot be prevented
merely by adequate fluid therapy. In recent years, studies with
modern molecular biological tools have elucidated that many factors
are involved in the development of pancreatic mi crocirculatory
disturbance. Whether the disturbance of pancreatic microcirculati on
is an initiating factor or as a consequence of progressive
pancreatitis is still debatable. The pathophysiological changes of
pancreatic microcirculatory di sturbance in acute pancreatitis are
complex, they include local release of acina renzymes[15-25],
vasoactive mediators[26-39], vasoconstriction, increase
in vascular permeability, ischaemia[40-41], ischaemia/reper
fusion, leukocyte adherence, intravascular coagulation, capillary
stasis, etc., resulting in pancreatic oedema, hemoconcentration, and
impaired capillary and venous drainage[42-44],
consequently leading to hemorrhagic pancreatic ne crosis[45].
ROLES OF ISCHAEMIA IN PANCREATIC MICROCIRCULATORY DISTURBAN CE
DURING ACUTE PANCREATITIS
Ischaemia as an initiating factor
There is a considerable evidence supporting ischaemia as an
initiating fa ctor of pancreatic microcirculatory injury in acute
pancreatitis[46-48]. As long ago as 1862, Panum induced
hemorrhagic pancreatitis by injection of wax dropl ets into
pancreatic arteries. Later similar changes were noticed by
intra-arterial injection of 8-20μm microspheres, irreversibly
obstructing terminal arte rioles and occluding the capillaries.
While the use of larger particles only res ults in pancreatic oedema,
because there are abundant arcade-like anastomoses b etween the
pancreatic interlobular vessels. There is also evidence suggesting
that microvascular injection of microspheres may progress to chronic
active pancre atitis.
A
clinical report revealed at autopsy that atheromatous thrombi
embolized from t he aorta into the pancreatic arteries were
associated with acute pancreatitis in 10 of 12 cases. The incidence
of pancreatitis in 182 patients died after cardiac surgery was 16%.
There was also evidence for a high susceptibility of the pa ncreas
to ischaemic injury in patients died of shock. A high incidence of
acute pancreatitis shown after cardiopulmonary bypass operations
seemed to be associat ed with intraoperative hypoperfusion in the
splanchnic area.
By
means of intravital microscopy in conjunction with technique of
selected cell s-labeling, direct impairments of pancreatic
microcirculation in the early phas e of acute pancreatitis have been
observed in the experimental ischaemia induced by controlled
haemorrhage or interruption of arterial blood supply to the pancr
eas[49], suggesting the pancreatic microcirculation being
highly suscept ible to ischaemia. This is closely related to the
microvasculature of pancreatic lobule; there is a single
centrally-located intralobular artery as the exclusi ve vascular
supply of each lobule, no anastomosis between the intralobular arter
ies and their branches exists, indicating the cause of its high
susceptibility t o ischaemia[50,51].
Ischaemia as an aggravating and continuing mechanism
Temporary complete or partial ischaemia of pancreas would
not cause hemorrhagic pancreatic necrosis, the slight histological
and functional changes are completely reversible. However, temporary
ischaemia has the potential of being transitio nal from edematous to
necrotizing pancreatitis[52]. While temporary arte rial
occlusion alone does not injure the pancreas following induction of
edemato us pancreatitis by duct ligation[53] with
hyperstimulation, arterial occ lusion for only 15min can result in
parenchymal necrosis, suggesting that isch aemia as an aggravating
factor participates in the development of acute pancreat itis.
Impairment
of microcirculatory perfusion of pancreas is the consequence of the
e ffect of various local factors, such as vasoconstriction, free
radicals, intravascular coagulation, release of vasoactive mediators
taking part in the whole cou rse of acute pancreatitis (see below).
Recently, ischaemia/reperfusion is consid ered one of the important
causative factors for development of acute pancreatitis after
pancreatic transplantation. It has been repeatedly demonstrated that
change of pancreatic perfusion is an early event in experimental
acute pancreatitis , and microcirculatory impairment in human
pancreas also correlate well with the degree of ischaemic injury.
These findings support the hypothesis that the micr ovasculature is
the primary target of reperfusional injury after ischaemia.
CHANGES OF PANCREATIC MICROCIRCULATION IN ACUTE PANCREATITIS
Many indirect methods have been applied to assess the changes of
panc reatic microcirculation during acute pancreatitis in previous
studies[54]. Recently, intravital fluorescence microscopy
combined with the technique of separate labeled-cells and
computerized image analysis system has been successf ully used in
the studies of pancreatic microcirculation in acute pancreatitis. M
any important phenomena as vascular permeability change,
vasoconstriction, capil lary blood flow, functional capillary
density, leukocyte-endothelium int eraction, etc., have been
continuously and directly observed during the course o f acute
pancreatitis. It is now believed that microcirculatory changes is
import ant as well as early feature in the pathophysiology of acute
pancreatitis[55].
Vasoconstriction
The first step in the sequence of microcirculatory events in
pancreatitis is the constriction of interlobular vessels, especially
in the proximal segments of th e interlobular arterioles and venules[56,57].
The vasoconstriction occu rring in the early phase of acute
pancreatitis may cause ischaemia and stasis of the microcirculation[58],
which can be prevented by the radical scaveng ers, superoxide
dismutase and N- (2-mercaptopropionyl)glycine in sodium tauroc
holate-induced pancreatitis, suggesting that vasoconstriction might
be induced by free radicals. There is also great support for the
concept that solutions inj ected into the pancreatic duct to induce
biliary pancreatitis exert their effect via the interstitial route.
Even at a low injection pressure of 40cmH2O, rupture of
the ducto-acinar junction is detectable with subsequent fluid
extravas ation in the interstitial space, where they gain access to
the pancreatic microv asculature precipitating vascular spasm. It
has been noticed that segmental cons triction of pancreatic arteries
occured in bile-induced pancreatitis, and of me senteric arteries
directly exposed to diluted bile. There is also pronounced dam age
to the pancreatic vessels resulting in haemorrhage, endothelial
detachment and thrombosis, as has been shown with the taurocholate,
trypsin, and trypsin-di gested blood vessels. The vasotoxic effect
of these substances was further subst antiated by the demonstration
that interstitial injection into the omentum preci pitates similar
changes at the injection site. The finding that stress and shock can
convert oedematous to hemorrhagic experimental pancreatitis suggests
that c atecholamines mediators might participate in the process.
Therefore, pancreatic vasoconstriction in acute pancreatitis might
be relevant to a variety of factors .
Changes of permeability
The intravital microscopic findings of immediate leakage of
the macromolecular plasma marker (FITC-Dextran 70) from the
microvasculature into the interstitial tissue, and the scanning
electron microscopic evidence of leakage of the cast ma terial
through the capillary membrane in the early phase of acute
experimental p ancreatitis suggest that presence of increased
permeability during the disease process. Further experiments
demonstrate that permeability changes precede stasis and stasis
precedes leukocyte adherence[59], suggesting that
increased vascular permeability and ischaemia are the initial
microcirculatory lesions in acute pancreatitis induced by sodium
taurocholate leading to haemorrhagic necros is. The non-specific
detergent effect of sodium taurocholate and bile acids in general
seems to be responsible for the initial changes due to the direct
dissol ution of cellular membranes.
Changes of nutritive tissue perfusion
Acute pancreatitis is characterized by impairment of
nutritive tissue perfusion as a consequence of gradually decreased
capillary blood flow and functional capi llary density[60].
Reduction of capillary infusion volume and of functio nal capillary
density has been observed with intravital microscopy and
laser-Doppler flowmetry in the experiments of acute pancreatitis. In
such experiments, c apillaries are progressively excluded from
perfusion starting 30min after the induction of pancreatitis, and
with only few capillaries remaining perfused after 3h. At the same
time, flow through the preferential pathways is maintained.
Measurements of pancreatic blood flow during acute pancreatitis have
ever yielde d conflicting results. Some found no change or even
increased blood flow, but most experiments have repeatedly
demonstrated decreased total blood flow in acute pancreatitis. The
perfusion values with an initial increase followed by a sharp
decrease have been observed. Increased pancreatic blood flow is
considered as a consequence of vasodilatation in acute inflammation.
Because of the tremendous d istributional disturbances of the
microcirculation in the pancreas, however, mea surements of total
blood flow of the pancreatitis do not reflect proportionately the
pathological status of different local regional perfusion within the
pancre as. The pathological states, both the hyperemia and ischaemia,
can be found at t he same time in the different regions within the
pancreas, thus emphasizing the importance of capillary blood flow
measurement for accurate evaluation of microc irculatory blood flow
changes. In most of the studies the degree of pancreatic h
ypoperfusion was found to be disproportionately more severe than the
decrease in cardiac output at comparable intervals. Moreover it has
been shown that a decre ase in pancreatic perfusion cannot be
prevented by adequate fluid therapy using Ringer's solution even
though cardiovascular parameters are stabilized at the ba seline
level, proposing a specific mechanism of local microcirculatory
ischaemic impairment[61-63].
Impairment of ischaemia/reperfusion and leukocyte adherenc e
Ischaemia/reperfusion of the pancreas with impairment of the
microcirculation ha s attracted attention both in experimental and
clinical studies of acute pancrea titis[64-73]. Ischaemia/reperfusion
leads to the adherence of leukocyte s to the vascular endothelium.
In parallel with reduction of functional capillar y density, an
increase of heterogeneity of capillary perfusion has been noted. P
rimary capillary perfusion failure after onset of reperfusion is a
characteristi c microcirculatory feature of ischaemia and is called
no-reflow phenomenon. Among various stimuli promoting
leukocyte-endothelium interaction are ischaemi a/reperfusion and
formation of oxygen free radicals leading to rolling and adher ence
of leukocytes, the latter provoking the “reflow/paradox”
phenomenon with loss of endothelial integrity and macromolecular
leakage as an end result. E nhanced generation of oxygen radicals
elicits ischaemia/reperfusion-induced leu kocyte infiltration in the
tissue, which is instrumental in the progression of a cute
pancreatitis. Degree of endothelial cell dysfunction and severity of
leukoc yte adherence is dependent upon the duration of ischaemia and
reperfusion. Compl ete ischaemia/reperfusion of the pancreas induces
extensive capillary stasis,i.e. pancreatic microcirculatory failure.
Effect of hemorrheological changes
Since blood viscosity is the inherent resistance of blood to
flow, it is probabl e that the hemorrheological changes might be
important to acute necrotizing panc ratitis[74-84]. 188
Wistar rats were studied by measuring hemorrheologi cal and
stereological parameters of pancreatic microvasculature. The results
showed that increased blood viscosity, causing red blood cell
aggregation with roul eaux formation, and decreased erythrocyte
deformability are responsible for panc reatic microcirculatory
disturbances and play an important role in the transitio n of
oedematous pancreatitis to necrosis.
It
has been noticed that the time points in the course of experimental
acute pan creatitis are extremely variable. This can be explained as
investigators with va rious pancreatitis models, different infused
substance, concentration, volume as well as intraductal pressure,
the latter may be more important than the others. The high
intraductal injection pressure results in an increased leakage of
bile and a more generalized distribution in the interstitial space,
even immediate h emorrhagic pancreatic necrosis, thus emphasizing
the pathophysiological signific ance of experimental models in acute
pancreatitis. In the low-pressure ductal p erfusion model the
etiological factor and the pathophysiological course are simi lar
to those associated with the disease clinically.
VASOACTIVE MEDIATORS IN ACUTE PANCREATITIS
Bradykinin
Bradykinin
probably exerts its influences upon microvessels via several
pathways involving endothelial cells, including stimulating the
formation and release of NO, arachidonic acid metabolites and
tackykinins. Microcirculatory responses to bradykinin are biphasic:
at low concentrations it causes vasodilatation, while at higher
concentrations it causes vasoconstriction.
The
role which bradykinin plays in microcirculatory impairment of acute
pancreat itis is controversial. It was noticed that in sodium
taurocholate-induced pancr eatitis, the number of perfused
capillaries was increased and capillary flow pre served and the mean
venular leukocyte adherence decreased and histopathological change
improved in icatibant(a B2 receptor antagonist)-treated rats; kinase
II inhibitor captopril or exogenous bradykinin in addition to an
otherwise effectiv e dosage of icatibant resulted in
microcirculatory stasis, extensive venular leu kocyte adherence and
severe histological damage, indicating that bradykinin may aggravate
the microcirculatory disturbance[85,86]. But another
study showed that B2 receptor antagonist increased the severity of
acute pancreatitis, w hile lys-bradykinin substituting bradykinin
didn't[87].
Platelet-activating factor(PAF)
PAF acts on microvasular diameter, permeability and
leukocyte rolling, adhesion and migration through different
mechanisms, including synthesis and release of N O and arachidonic
acid metabolites, and upregulated expressions of ICAM-1 and C
D11/CD18. Actions of PAF on microvasculature have the following
features: constr iction response of venules to PAF is stronger than
that of the arterioles; its a ction on arteriolar diameter is
biphasic.
It
was observed that treatment with PAF receptor antagonist improved
pancreatic capillary blood flow, reduced the severity of
pancreatitis-associated endotheli al barrier compromise and
pancreatic leukocyte recruitment, suggesting that PAF is
proinflammatory in pancreatitis[88-92].
Endothelin(ET)
There are three kinds of endothelins, and endothelin-1 is
predominantly expressed by vascular endothelial cells. There are
three types of endothelin receptors, and ETA receptor is
endothelin-1 selective, and found mainly on vascular smooth muscle
cells, mediating vasoconstriction; ETB is nonselective and expressed
by endothelial cells; it mediates vasodilatation through the release
of NO and pro stacyclin. The action of endothelin-1 on microvessels
is biphasic: at low conce ntration, it causes vasodilatation; at
higher concentration, it causes sustained vasoconstriction.
Several
experiments demonstrated that endothelin-1 was involved in the m
icrocir culatory disturbance and in the development and progression
of acute pancreatiti s[93-99]. Administration of
endothelin-1 after the caerulein injection decreased pancreatic
blood flow significantly, aggravating microcirculatory disturbance.
Topically superfused endothelin-1 induced pancreatic microvascular
de terioration and acinar cell injury similar to that induced by
intraductal infusi on of sodium taurocholate in rats[100].
Studies also showed that ETA rec eptor antagonist is protective in
microcirculatory disturbance of acute pancreat itis[101].
Nitric oxide(NO)
NO is formed from L-arginine by NO synthase(NOS).
cNOS(constitutive form) catalyzes formation of NO of physiological
level. Catalytic activity of iNOS(inducibl e form) is stronger and
lasts longer than that of cNOS, and NO of higher than ph ysiological
level is produced by iNOS. NO dilates blood vessels, but at higher
concentrations it is cytotoxic.
Pancreatic
NO level in acute pancreatitis may be decreased[102] or
signi ficantly elevated in different experiments. Intravenous
administration of L-arginine to rats with hemorrhagic pancreatitis
improved pancreatic blood flow and a meliorated the severity of
pancreatitis in a dose-dependent manner, while nitro -L-arginine
infusion to the rats with edematous pancreatitis caused a decrease
in pancreatic blood flow and exacerbated pancreatitis, indicating
that NO is pr otective[103-106]. However, some
experiments showed that NO was not inv olved in the progression from
edematous to hemorrhagic pancreatitis.Even microc irculatory changes
were significantly alleviated in caerulein-induced pancreati tis
pretreated with nitro-L-arginine, suggesting NO may be
proinflammatory [107]; it was found that L-arginine
improved the pancreatic microcirculatio n but worsened the
microscopic alterations within the pancreas[108,109] .
Adhesion molecules
Leukocyte-endothelial interaction is an important step in
the development of ac ute pancreatitis. It was demonstrated by
experiments that levels of ICAM-1, PEC AM-1 and ELAM-1 were
upregulated, and expressions of P- and E-selectin enhan ced, and
leukocytes became CD18-positive in acute pancreatitis[110,111] .
Immunoneutralization of adhesion molecules was proven effective in
the treat ment of acute pancreatitis[112]. Administration
of monoclonal antibody a gainst ICAM-1 to rats with acute severe
pancreatitis significantly enhanced cap illary blood fow in the
pancreas, reduced leukocyte rolling and stabilized capil lary
permeability[113].
PATHOGENESIS OF MICROCIRCULATORY FAILURE IN ACUTE PANCREATITIS
The pancreatic microcirculation is impaired in acute
pancreatitis[114-124 ]. Capillary stasis may be due to a
variety of mechanisms including hemoconce ntation and intravascular
coagulation, generation of oxygen free radicals in the
microenviroment of the pancreatic ducto-acinar complex, increase in
interstiti al pressure, increase in leukocyte-endothelium
interaction[125], and lo cal reduction of endothelial
derived relaxation factor (nitrous oxide)[126 ]. An
acinar abnormality may be the initiating factor arising from a
combinat ion of ductal obstruction and exocrine hypersecretion
followed by an increase in intraductal pressure and leakage of
enzymes into the pancreatic interstitium with release of zymogen and
lysozymes.
Hemoconcentration
and intravascular coagulation play an additional role in the d
evelopment of pancreatic ischaemia in acute pancreatitis. The
increased capillar y permeability is the initial feature of
experimental biliary pancreatitis, resu lting in loss of fluid and
cells into the pancreatic interstitium induced by osm olarity shifts
either in the duct or extracellular fluid[127]. Local hem
oconcentration takes place at the site of plasma sequestration, even
if the syst emic hematocrit is maintained at the initial level. In
conjunction with the impa irment of endothelium, intravascular
coagulation occurs and causes a further dec rease of blood fluidity.
These changes are aggravated by a systemic hypercoagula rity in
acute pancreatitis, probably due to thromboplastic material and
activate d trypsin gaining access to the systemic circulation.
The
mechanism of oxygen free radical is important in acute pancreatitis
of any c auses[128] and is a direct sequel of
biliopancreatic reflux at the onset of acute biliary pancreatitis.
Besides disintegration of cell membranes by lipi d peroxidation,
free radicals trigger the extravasation of granulocytes into the
surrounding parenchyma representing an early lesion in acute
experimental pancr eatitis. The initial margination of granulocytes
in the capillaries may be a con tributing factor in endothelial
injury and impairment of capillary perfusion. Ox ygen radicals
mediate depletion of pancreatic sulphydryl compounds with changes in
both lipid peroxide and oxygen radical scavengers. Serum
concentrations of vi tamin C, a potent antioxidant, are depleted in
acute pancreatitis so that synthe tic ascorbic acid derivatives have
been used as a free radical scavenger.
Postischemic
intensive adherence of leukocytes to the endothelium of the venules
and adhesive leukocytes forming plaques partially occluding the
lumen of the ve nules have been observed within the reperfusional
period in the experimental acu te pancreatitis. This adhesive
interaction is largely confined to postcapillary venules. And it is
determined by a variety of factors such as expression of adhe sion
molecules on leukocytes and/or endothelial cells, products of
leukocyte (su peroxide) and endothelial cell (nitric oxide)
activation and physical forces gen erated by the movement of blood
along the vessel wall[129,130]. The fir m adhesion of
leukocytes that take place within postcapillary venules may increa
ses the postcapillary pressure more than 200 folds, cause the
passive dilatation of the capillaries and microcirculatory stasis.
Many studies show that some com pounds appear to be effective in
reducing or abolishing leukocyte-endothelial cell adhesion, whereas
some classical anti-inflammatory drugs such as indomethac in and
aspirin actually promote leukocyte adhesion in the venules.
There
may also be relation to lymphatic drainage[131]. Increase
in local interstitial pressure as a consequence of obstructed lymph
drainage further interferes with pancreatic microperfusion due to
the venous outflow impairment. In the early period of acute
experimental pancreatitis, dilated lymphatic vessels a re visible
macroscopically, and further progress of oedema with consequent
focal hemorrhagic pancreatic necrosis is possible in case of
insufficient lymphatic d rainage. Experiment demonstrates that an
increase of thoracic duct lymph flow fo llowed by a pronounced and
prolonged reduction. Erythrocytes originating from pa ncreatic
interstitial hemorrhages were shown to enter and obstruct the
microlymp hatics.
CONCLUSIONS
Recent advances in experimental research have helped witness the
pathophysiology of acute pancreatitis. The phenomena of
microcirculatory changes observed in ac ute experimental
pancreatitis during the past few years gradually underlie the d
isturbance of the local microcirculation in acute pancreatitis, but
several chal lenges remain. Still some questions remain unexplained
concerning the mechanisms :(1)Which is the first event in the
pathogenesis of acute pancreatitis? (2)Which factor determines the
edematous or hemorrhagic necrotizing pancreatitis in a gi ven
experimental or clinical situation? (3)What is the role of impaired
distribu tion of blood supply in early steps of acute pancreatitis?
The potential vasoact ive mediators responsible for the progression
of the disease severity have large ly remained subjecting to
speculation and debate.
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