Sudden infant death syndrome (SIDS) and disordered blood flow

Abstract

Naeye (1) has long linked SIDS with low utero-placental blood flow and foetal hypoxia. Gestational hypotension, maternal smoking and disorders of the foetal membranes are considered by Naeye to promote brainstem and neurological abnormalities. Naeye also found that SIDS' victims often showed a growth lag after birth and suggested a reduced oxygen environment after birth which pointed to chronic under-ventilation of the lungs. Another abnormality observed by Naeye was that brown fat was retained for an abnormally long time. Now Mitchell (New Zealand Herald, 27.11.90) has concluded a 3-year study of SIDS' victims in New Zealand and found a combination of stomach sleeping position, mothers' smoking and bottle feeding was implicated in 79% of SIDS' victims. (The sleeping position and maternal smoking may be additive in disordered blood flow). The effect of circulatory shock (cardiogenic) on skeletal muscle mitochondrial activity shows there is a large decrease in the activity of the mitochondrial enzyme cytochrome oxidase during circulatory shock. There is also a reduced capacity to oxidase succinate, pyruvate and palmitoyl carnitine (2). These authors discuss cellular oxidative damage due to severe hypoxia during circulatory shock and the effect on the skeletal muscle mitochondrial electron transport chain (ETC). The reasons for carnitine supplement to these patients are explained. It was concluded that during the course of circulatory shock in humans inactivation or damage to the mitochondrial ETC plays a crucial role in cellular oxidative damage. The activation of brown fat mitochondria via the ETC revolves around elevated blood flow, and the high content of cytochromes which give this tissue its characteristic brownish colour (3)). Other forms of interrupted blood flow, similar to cardiogenic shock disorders in skeletal muscle, will be discussed.