الفهرس 
NEUROLOGICAL SEQUELAE
Apoptosis and Delayed Cell DeathOnly 14 pages are availabe for public view
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Abstract
Introduction
Perinatal asphyxia is an insult to the fetus or newborn due to lack of oxygen (hypoxia) and/or a lack of perfusion (ischemia) to various organs. It is associated with tissue lactic acidosis .It may be associated by hypercapnia. The effects of hypoxia and ischemia may not be identical, but they are difficult to separate clinically. Both factors probably contribute to asphyxial injury (Snyder and Cloherty, 1998).
Perinatal asphyxia is caused by a decreased supply of oxygen to the fetus or newborn. It can happen in the antepartum period, during labor, or at the time of birth. When it occurs, it results in an inadequate exchange of respiratory gases and impaired tissue perfusion. Various systemic functions of the newborn suffering from birth asphyxia have been evaluated and have been found to be deranged (Marcio, 2002).
Biochemical and molecular biological evidence indicates that endothelin-1 and its receptors are selectively up regulated in the lung during exposure to hypoxia, while functional evidence indicates that endothelin-1 is a major mediator of hypoxia-induced pulmonary vasoconstriction and vascular remodeling (Jain et al., 2002).
Furchott and Zawadzki in 1980 demonstrated that vascular endothelial cells release a highly unstable vasodilator substance which they named endothelium-derived relaxing factor. This was later identified as nitric oxide subsequently shown to be generated from L-arginine (Billiar, 1995).
Plasma NO levels after perinatal asphyxia are related to the severity of neonatal hypoxic ischemic encephalopathy outcome (Yuan et al.,2000).
Nako et al., (1997) concluded that hypoxia would injury vascular endothelial cells and consequently raised plasma thrombomodulin levels in asphyxiated infants. They studied the plasma thrombomodulin concentration at birth in 11 asphyxiated infants was significantly elevated compared with that in 48 infants without asphyxia.
We studied the possibility of using nitric oxide, endothelin-1 and thrombomodulin as complementary parameters for early and sensitive diagnosis of perinatal asphyxia. Through comparing the levels of the three studied parameters in healthy neonates with the levels in neonates with different grades of perinatal asphyxia, we could prove statistically that each of the three studied parameters can be used as a marker for the occurrence of perinatal asphyxia, and hence, using them in a complementary way would add positively on their diagnostic value.
This study was conducted on 65 neonates from the neonatal intensive care unit in obestetric and gynaecology hospital of Ein Shams university as well as Mubarak hospital of police authority in Nasr City. They were divided into tow groups:-
Control group: - They are 22 neonates, 11 males (50%) and 11 females (50 %). The control group was divided into, 16 full term (72.75 %) with the gestational age ranges from 37-40 weeks, 4 near term subjects (18.15 %) with the gestational age 36 weeks, and 2 preterm subjects (9.1 %) with the gestational age ranging from 34-35 weeks. The entire control group didn’t have perinatal asphyxia as proven by clinical examination at birth, after birth, and laboratory results of blood gases of cord blood.
Patient group:- They are 43 cases of perinatal asphyxia as proven by clinical examination during resuscitation and Apgar scoring at one and five minutes , as well as by the laboratory findings of umbilical cord blood gases . They were then divided according to the severity of perinatal asphyxia into three subgroups based on the clinical grading of Sarnat and Sarnat’s 3 clinical stages of perinatal hypoxic ischemic brain injury.
1 Subgroup (A), showing mild perinatal asphyxia, is composed of 13 subjects (30.23 %), 7 of them are males (53.84 %) and 6 are females (46.16 %). The subjects of subgroup (A) compromised 6 full term (46.16 %) , 5 near term (38.46%) , and 2 preterm subjects (15.38 %) with the gestational age of the subjects in this subgroup ranging from 34 : 38 weeks .
2 Subgroup (B), showing moderate perinatal asphyxia, is composed of 11 subjects (25.58 %), 6 of them are males (54.54 %) and 5 are females (45.46 %). The subjects of subgroup (B) compromised 8 full term (72.72 %) , 2 near term (18.18%) , and 1 preterm subjects (9.1 % ) with the gestational age of the subjects in this subgroup ranging from 35 : 39 weeks .
3 Subgroup (C), showing severe perinatal asphyxia, is composed of 19 subjects (44.18 %), 11 of them are males (57.89 %) and 8 are females (42.1 %). The subjects of subgroup (A) compromised 6 full term (31.58 %) , 1 near term (5.26 %) , and 12 preterm subjects (63.16%) with the gestational age of the subjects in this subgroup ranging from 27 : 39 weeks .
It was shown in our study that all the studied parameters namely endothelin-1, thrombomodulin and nitric oxide, could be used in perinatal asphyxia as indicators for the occurrence of perinatal asphyxia and moreover they could differentiate significantly between the different grades of perinatal asphyxia.