Comment; Chronic Inflammatory Response Syndrome causes lethal pulmonary hypertension–which can fully resolve with VIP treatment–yet severe shortness of breath & exercise tolerance can persist due to mitochondrial dysfunction and a diminished VO2 Max. Mitochondrial support supplements are needed but VIP should also be continued.
Sami ISaidKathleen GDickmanShow morehttps://doi.org/10.1016/S0167-0115(00)00174-9Get rights and content
Abstract
The pathogenesis of tissue injury in disease is a complex process that is only partially understood. We have investigated different models of acute lung injury, representing the clinical entity known as the acute respiratory distress syndrome, and tested their possible modulation by the neuropeptide vasoactive intestinal peptide (VIP). Three major mechanisms of injury appear to be involved in many of these models as common denominators: (1) activation of nuclear transcriptions factor NFκB; (2) apoptotic cell death; and (3) excitotoxic phenomena, due to activation of N-methyl-d-aspartate glutamate receptors. These pathogenetic mechanisms and pathways are logical targets of therapeutic intervention. Protection by VIP against lung injury, and against related forms of injury/cell death of neuronal cells and heart muscle, is attributable, in large measure, to the ability of VIP to suppress these mechanisms, and to additional anti-inflammatory and anti-oxidant actions. Finally, a hypothesis is presented for survival-promoting pathways that can be augmented by VIP and the related pituitary adenylyl cyclase-activating peptide.
- COVID UPDATE: What is the truth? - 2022-11-08
- Pathologist Speaks Out About COVID Jab Effects - 2022-07-04
- A Massive Spike in Disability is Most Likely Due to a Wave of Vaccine Injuries - 2022-06-30
