Lecture 2 Flashcards
Ovulation?
Ovulation 2?
Block the neurogene passageways
Atropin, clorpromazin, pentobarbital, morfin
Stimulate: Histamin, oestrogens low doses
Ovulation phases?
Ovulation theories
- The endosmosis Theory
- The enzyme theory
- The hormonal Theory
- Fibrilar system on the ovary surface
The Endosmosis Theory
- Dehiscence and expulsion of the egg by increased follicular fluid pressure
- The space between the basal membrane and the internal theca, is invaded by capillaries
- Ovulation is preceded by a physiological ovarian congestion 9h before ovulation, 4 h after LH surge
- Increases the permeability of the vascular wall in the follicle
- Follicular edema occurs, diapedesis of red blood cells
The enzyme theory
- Depolymerisation of mucopolysaccharids by hyaluronidase,(more active arround stygma);
- The mature ovarian follicle contains proteolytic enzymes
- Cyclic AMP and prostagladin E 1 şi E 2 are also capable to stimulate the internal theca cells to be able to produce a
- plasmogen activator which leads to the plasmin’s activation;
- Fibroblasts from albuginea and external theca digest the follicular walls;
- It is suggested that the oocytes release a deutoplasmatic material, which reacts towards the follicles wall;
Hormonal theory
- The modifications of the follicular wall are due to the gonadotropic hormones;
- FSH⇒follicular growth⇒oestradiol⇒Gn Rh⇒ LH ⇒ ovulation;
- The preovulatory growth of prostaglandins is necessary forovulation;
- P4 (progesterone) induce PGF synthesis(vasoconstriction,
reduced blood flow at the stigma level) şi PGE synthesis
(hyperemia, increase blood flow in the follicle) produced by granulosa cells; - PGE stimulate cAMP, syntesis, colagenase activation;
- Antiprostaglandins drugs and gestagen (stimulate the
collagease ativity) secretion can supress ovulation(AINS
flunixin)
Fibrilar system
The ovarian stroma and the walls of
preovulatory follicles contain smooth
muscle cells innervated by autonomic nerve
terminals.
Laparoscopic investigation of ovulation and
ultrasonographic studies in mares show
contractions of the follicle during ovulation
especially at the base of the follicle
In vitro studies show a pharmacological
respons (ovarian contraction) after α-
adrenergic receptor activation (vasopresin,
acetilcolin, adrenalin, prostaglandin F2α
In vitro, ovarian contractions due to
chemical stimuli.
Catecolamins, activate by LH play a major
rol.
Adrenergic neurons from the follicle wall
may be activated by LH. They secrete
norepinephrine, ⇒ stimulate histamine
release from mast cells.
Mechanical changes ⇒ Follicular rupture
Corpus luteum Formation
- CL is an engocrine gland, secrete progesteron
- originate from the maturefollicular structures.
- Generate the luteal phase of the cycle Under LH, LTH influence the P4 (progesterone) secretion increase
- 3 stages:
1. Organisation
2.Eflorescence (activity)
3.Regression
Organization stage of formation of Corpus lutem 1
Organization stage of formation of Corpus lutem 2
Organization stage of formation of Corpus lutem 3
Eflorescence (activity) stage
Lysis of Crpous Lutem
Lutheolysis
Luteothrop factors
Luteothrop factors:
LH-Gonadotrop hormone;
Placentary luteothrphin(trophoblastina), secretet by
placenta, passing the uteroovarin blood vessels to the
ovary;
Supress the synthesis and releasing of PgF2α
Luteolitic factors
PgF2α; from the uterus is transported to the ipsilateral
ovary through the vascular coutercurrent exchange
mechanism without dilution in the sistemic
circulation (cow, ewe, goat).
Not in the mare where enter the genaral circulation
and 90% denatuate in the pulmonary circulation.
The mare CL is more sensitve to PgF2α
Prostaglandin receptors (day 5-6 in cow, 7-8 in mare, 12-14 in sow
Luteothrop and luteolitic
factors
Luteal oxytocin:
Large luteal cells sythesize and secrete oxytocin, stores in
secretory granules
Work together with PgF2α
Stimulate each other in a positive feedback manner
