pH-stat strategy and hypothermia of 25[deg ]C alone should protect the central nervous system consistently from 75 minutes of circulatory arrest

2001 ◽  
Vol 121 (3) ◽  
pp. 597-597
Author(s):  
Tadaomi-Alfonso Miyamoto ◽  
Koho-Julio Miyamoto
1993 ◽  
Vol 3 (3) ◽  
pp. 308-316 ◽  
Author(s):  
Gil Wernovsky ◽  
Richard A. Jonas ◽  
Paul R. Hickey ◽  
Adré J. du Plessis ◽  
Jane W. Newburger

The dramatic reduction in surgical mortality associated with repair of congenital heart anomalies in recent decades has been accompanied by a growing recognition of adverse neurologic sequels in some of the survivors. Abnormalities of the central nervous system may be a function of coexisting cerebral abnormalities or acquired events unrelated to surgical management (such as paradoxical embolus, cerebral infection, or effects of chronic cyanosis), but insults to the central nervous system appear to occur most frequently during or immediately after surgery. In particular, techniques of support used during neonatal and infant cardiac surgery—cardiopulmonary bypass, profound hypothermia and circulatory arrest—have been implicated as important causes of cerebral injury. This paper will review the effects of bypass and deep hypothermic circulatory arrest on neurodevelopmental outcome.


Author(s):  
Gladys Harrison

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.


Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.


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