Description

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This book describes a totally new observation/hypothesis which details how nitrogen gas can become an opportunistic poison. The hypothesis is that the function of the long studied mitochondrial permeability transition pore (pore) acts as an oxygen pump transferring angstrom size bubbles of oxygen from the cell cytosol to the interior of the mitochondrion where it is used to synthesize adenosine triphosphate (ATP. This oxygen pump is controlled by a feedback pump wherein low cytosolic levels of ATP trigger the pump to deliver more oxygen. When oxygen becomes unavailable, e.g. following a heart attack, the pump is signaled, and lacking oxygen, pumps nitrogen gas instead. This results in massive swelling of mitochondria and leads to apoptosis and death. This hypothesis fits with published literature, and explains the phenomenon of reperfusion injury following stroke and heart attack. Whereas these are acute events, a slow failure of the pump in chronic central nervous system diseases (Alzheimer's, Parkinson's, ALS, Huntingtons, dementia and even Autism) can lead to a slowly developing filling and failure of mitochondria. The book develops the reasoning for decreased oxygen availability in chronic disease states as resulting from impaired blood flow based on several related factors. These include blood vessels which are at the lower end of lumen diameters and have very little flow redundancy with respect to downstream tissue requirements, and pathological changes which further impede flow such as atherosclerosis and arteriosclerosis. Further, decreased cardiac output, increased pulse pressure and decreased diastolic blood flow will add to inadequate oxygen delivery problems. Another. potentially major issue, is intracranial pressure. In the skull there is a finite volume which must be shared by the brain, cerebrospinal fluid (CSF), and blood. When the intracranial pressure (ICP) becomes elevated, cerebral blood flow is depressed, and the only way to decrease ICP is to reduce the intracranial volume of CSF. Since these diseases are largely characterized by slowly dying brain tissue, it is critical to initiate therapy as early as possible. There are now sensitive non-invasive methods for measuring ICP, such that early diagnosis of elevated ICP could trigger the administration of carbonic anhydrase inhibitors to effect a decrease in the production of CSF as a means to keep ICP values at normal 10mmHg levels. In addition to the above, there is another treatment, acute and chronic, for controlling the poisoning effects of nitrogen gas. That is Total Body Nitrogen Washout (TBNW). TBNW could be instituted in the ambulance and continued for 60-90 minutes following cath-lab reflow procedures. Simply put one implements the breathing of heliox. nominally 30% oxygen/ 70% helium, with exhalation shunted to ambient atmosphere. This will effect a TBNW in about 30-45 minutes. In the chronic use of TBNW, one could envision 'heliox houses' wherein patients with chronic CNS diseases could come in periodically for 2 hours and breath the heliox atmosphere, which would be recycled continuously and nitrogen-scrubbed. Other topics, not covered here, including the Fog, are addressed in the 19 chapters and 40 pages that follow----