NEUROENDOCRINOLOGY
LETTERS
including
Psychoneuroimmunology, Neuropsychopharmacology,
Reproductive Medicine, Chronobiology
and Human Ethology, ISSN 0172–780X
OBJECTIVES:
Angiogenesis comprises two different mechanisms: endothelial
sprouting and intussusceptive microvascular growth. The sprouting
process is based on endothelial cell migration, proliferation
and tube formation. Intussusceptive microvascular growth divides
existing vessel lumens by formation and insertion of endothelial
columns into the vessel lumen. The morphological features
of microvessels of cerebral cortex and neurohypophysis were
evaluated in a model of the cerebral traumatic injury.
METHOD:
The observations were conducted seven days after induction
of cortical trauma. Traumatic injury was induced in the fronto-temporal
region of cerebral cortex in general anesthesia with 20mg/kg
ketamine hydrochloride.
RESULTS:
Seven days after traumatic brain injury in sections from cerebral
cortex and neurohypophysis we can observe morphological features
of angiogenesis. Endothelium of the cerebral cortex possesses
high endotheliocytes tightly connected and enveloped by amorphous
basement membrane-like material. Transcapillary pillars tightly
connected with neighbouring endothelial cells split the newly
formed vessels and branching takes place. In neurohypophysis
we can observe all stages of non-sprouting angiogenesis: proliferation
endothelial cells on the inside mother vessel, splitting newly
formed blood vessels by transcapillary pillars directed into
the vessel lumen, maturation of endothelium and network formation.
CONCLUSION:
The mechanical injuries directly induced angiogenesis not
only in cerebral cortex, but also in neurohypophysis. Our
studies show that mechanism of angiogenesis is not the same
as observed previously in neurohypophysis after focal cerebral
ischemia (Neuroendocrinology Letters 2001; 22:
87–92). This study indicates that mechanism of angiogenesis
can depend on kind of induction.
* * *
Introduction
Vessel
formation can occur by a number of different processes [1].
Early in development, vessel formation takes place in a process
referred as vasculogenesis, in which endothelial cells differentiate
and proliferate in situ within a previously avascular tissue,
and then coalesce to form a primitive tubular network. Angiogenic
remodelling refers to the process by which this initial network
is modified to form the interconnecting branching patterns characteristic
of the mature vasculature. During this time, vessel walls also
mature, as endothelial cells integrate tightly with supporting
cells such as pericytes, smooth muscle cells and surrounding
matrix [2].
A different process, referred to as angiogenic sprouting, involves
the sprouting from existing vessels into a previously avascular
tissue. In some cases, it seems as mature vessels must first
be destabilized to allow for subsequent sprouting [3]. The vessels
formed by sprouting are initially immature and must further
develop. The recent explosion in identifying and characterizing
physiological regulators of blood vessel growth demands reevaluation
of therapeutic efforts aimed at regulating blood vessel growth-whether
it be promoting vascular ingrowth to replenish ischemic tissue
or repairing damaged and leaky vessels during inflammation or
other pathological setting [4]. Therapeutic angiogenesis may
ameliorate vascular insufficiency and may also provide direct
beneficial effects on neural integrity, indicating a new paradigm
for the treatment of neural disorders. An improved understanding
of the mechanisms underlying the new vessel formation and participation
of endothelial cells, basement membrane, extracellular matrix
and perivascular cells as well fibrocytes and macrophages are
required [5].
In
our studies, morphological features underlying the formation
of new vessels and their maturation in cerebral cortex and neurohypophysis
induced by pathological conditions after traumatic injury of
brain cerebral cortex were investigated. The mechanical injuries
directly induced angiogenesis not only in cerebral cortex, but
also in neurohypophysis. Our studies currently being conducted
to determine if this mechanism of angiogenesis is the same as
observed in neurohypophysis after focal fotochemically-induced
cerebral ischemia [6].
