Hypoxia and Medicine

What is called hypoxia ? How it affects male ? How to cure this ?

Public Comments

1. read the following link it will answer everything http://www.wisegeek.com/what-is-hypoxia.htm
2. Hi Firstname. Despite major advances in monitoring technology and knowledge of fetal and neonatal pathologies, perinatal asphyxia or, more appropriately, hypoxic-ischemic encephalopathy (HIE), remains a serious condition that causes significant mortality and long-term morbidity. Hypoxic-ischemic encephalopathy is characterized by clinical and laboratory evidence of acute or subacute brain injury due to asphyxia (ie, hypoxia, acidosis). Most often, the exact timing and underlying cause remain unknown. The American Academy of Pediatrics (AAP) and American College of Obstetrics and Gynecology (ACOG) published guidelines to assist in the diagnosis of severe hypoxic-ischemic encephalopathy. PATHOPHYSIOLOGY Brain hypoxia and ischemia due to systemic hypoxemia, reduced cerebral blood flow (CBF), or both are the primary physiological processes that lead to hypoxic-ischemic encephalopathy. The initial compensatory adjustment to an asphyxial event is an increase in CBF due to hypoxia and hypercapnia. This is accompanied by a redistribution of cardiac output to essential organs, including the brain, heart, and adrenal glands. A blood pressure (BP) increase due to increased release of epinephrine further enhances this compensatory response. In adults, CBF is maintained at a constant level despite a wide range in systemic BP. This phenomenon is known as the cerebral autoregulation, which helps maintain cerebral perfusion. The physiological aspects of CBF autoregulation has been well studied in perinatal and adult experimental animals. In human adults, the BP range at which CBF is maintained is 60-100 mm Hg. Limited data in the human fetus and the newborn infant suggest that CBF is stable over much narrower range of BPs.6,7 Some experts have postulated that, in the healthy term newborn, the BP range at which the CBF autoregulation is maintained may be only between 10-20 mm Hg (compared with the 40 mm Hg range in adults noted above). In addition, the autoregulatory zone may also be set at a lower level, about the midpoint of the normal BP range for the fetus and newborn. However, the precise upper and lower limits of the BP values above and below which the CBF autoregulation is lost remain unknown for the human newborn. In the fetus and newborn suffering from acute asphyxia, after the early compensatory adjustments fail, the CBF can become pressure-passive, at which time brain perfusion depends on systemic BP. As BP falls, CBF falls below critical levels, and the brain injury secondary to diminished blood supply and a lack of sufficient oxygen occurs. This leads to intracellular energy failure. During the early phases of brain injury, brain temperature drops, and local release of neurotransmitters, such as gamma-aminobutyric acid transaminase (GABA), increase. These changes reduce cerebral oxygen demand, transiently minimizing the impact of asphyxia. At the cellular level, neuronal injury in hypoxic-ischemic encephalopathy is an evolving process. The magnitude of the final neuronal damage depends on duration and severity of the initial insult combined to the effects of reperfusion injury, and apoptosis. At the biochemical level, a large cascade of events follow hypoxic-ischemic encephalopathy injury. Excitatory amino acid (EAA) receptor overactivation plays a critical role in the pathogenesis of neonatal hypoxia-ischemia. During cerebral hypoxia-ischemia, the uptake of glutamate the major excitatory neurotransmitter of the mammalian brain is impaired. This results in high synaptic levels of glutamate and EAA receptor overactivation, including N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methyl-4 isoxazole propionate (AMPA), and kainate receptors. NMDA receptors are permeable to Ca++ and Na+, whereas AMPA and kainate receptors are permeable to Na+. Accumulation of Na+ coupled with the failure of energy dependent enzymes such as Na+/ K+ -ATPase leads to rapid cytotoxic edema and necrotic cell death. Activation of NMDA receptor leads to intracellular Ca++ accumulation and further pathologic cascades activation. EAAs accumulation also contributes to increasing the pace and extent of programmed cell death through secondary Ca++ intake into the nucleus. The pattern of injury seen after hypoxia-ischemia demonstrate regional susceptibility that can be largely explained by the excitatory circuity at this age (putamen, thalamus, perirolandic cerebral cortex). Finally, developing oligodendroglia is uniquely susceptible to hypoxia-ischemia, specifically excitotoxicity and free radical damage. This white matter injury may be the basis for the disruption of long-term learning and memory faculties in infants with hypoxic-ischemic encephalopathy. Intracellular Ca++ concentration increases following hypoxia-ischemia as a result of (1) NMDA receptor activation, (2) release of Ca++ from intracellular stores (mitochondria and endoplasmic reticulum [ER]), and (3) failure of Ca++ efflux mechanisms. Cons