title: The postpartum period of pregnancy worsens brain injury and functional outcome after cerebellar hemorrhage in rats.
abstract: BACKGROUND
  Intracerebral hemorrhage (ICH) is one of the most common causes of maternal deaths related to the postpartum period. This is a devastating form of stroke for which there is no available treatment. Although premenopausal females tend to have better outcomes after most forms of brain injury, the effects of pregnancy and child birth lead to wide maternal physiological changes that may predispose the mother to an increased risk for stroke and greater initial injury.
  
  
  METHODS
  Three different doses of collagenase were used to generate models of mild, moderate and severe cerebellar hemorrhage in postpartum female and male control rats. Brain water, blood-brain barrier rupture, hematoma size and neurological evaluations were performed 24 h later.
  
  
  RESULTS
  Postpartum female rats had worsened brain water, blood-brain barrier rupture, hematoma size and neurological evaluations compared to their male counterparts.
  
  
  CONCLUSIONS
  The postpartum state reverses the cytoprotective effects commonly associated with the hormonal neuroprotection of (premenopausal) female gender, and leads to greater initial injury and worsened neurological function after cerebellar hemorrhage. This experimental model can be used for the study of future treatment strategies after postpartum brain hemorrhage, to gain a better understanding of the mechanistic basis for stroke in this important patient subpopulation.
authors: Department of Physiology, Loma Linda University, School of Medicine, Loma Linda, CA 92354, USA.
authors: Tim
authors: T
authors: Lekic
authors: Robert P
authors: RP
authors: Ostrowski
authors: Hidenori
authors: H
authors: Suzuki
authors: Anatol
authors: A
authors: Manaenko
authors: William
authors: W
authors: Rolland
authors: Nancy
authors: N
authors: Fathali
authors: Jiping
authors: J
authors: Tang
authors: John H
authors: JH
authors: Zhang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D051401:Aquaporin 4 / Q000378:metabolism; D001324:Autoantigens / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000503:physiopathology; D001929:Brain Edema / Q000209:etiology; D002531:Cerebellum / Q000503:physiopathology*; D002543:Cerebral Hemorrhage / Q000139:chemically induced* / Q000150:complications / Q000401:mortality / Q000473:pathology*; D024141:Collagen Type IV / Q000378:metabolism; D017364:Collagenases / Q000009:adverse effects*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D005786:Gene Expression Regulation; D006406:Hematoma / Q000209:etiology / Q000473:pathology; D053208:Kaplan-Meier Estimate; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009460:Neurologic Examination; D010750:Phosphoproteins / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D062826:Zonula Occludens-1 Protein
chemical_list: D051401:Aquaporin 4; D001324:Autoantigens; D024141:Collagen Type IV; D008565:Membrane Proteins; D010750:Phosphoproteins; C569044:Tjp1 protein, rat; D062826:Zonula Occludens-1 Protein; C057112:type IV collagen alpha3 chain; D017364:Collagenases