Peripheral contribution

Reduction of oxygen is one of the predominant cathodic reactions contributing to corrosion. Awareness of the importance of the role of oxygen was developed in the 1920s (19). In classical drop experiments, the corrosion of iron or steel by drops of electrolytes was shown to depend on electrochemical action between the central relatively unaerated area, which becomes anodic and suffers attack, and the peripheral aerated portion, which becomes cathodic and remains unattacked. In 1945 the linear relationship between rate of iron corrosion and oxygen pressure from 0—2.5 MPa (0—25 atm) was shown (20). 

From these facts, we concluded that the cytokines from peripheral whole blood cells were induced by the action of the synthetic polycarboxylic polymer itself. Hydrophobization may contribute to the higher affinity... 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Cytotoxics also cause cellular damage and the release of serotonin and other mediators from enterochromaffin cells. There is conflicting evidence regarding whether 5-HT3 receptors in the medulla are activated also during chemotherapy and contribute to production of emesis. Currently, the weight of evidence favours peripheral 5-HT3 receptors, with minor involvement of central receptors. 

It is easy to speculate that in an active neuron with a rapid firing pattern, the continued release of a peptide may eventually lead to depletion of the peptide occurring. This has been shown in the peripheral nervous system. If this also happens in the CNS it would provide a mechanism whereby the release and resultant receptor effects of a transmitter no longer match the firing pattern and demands of the neuron and so could contribute to long-term adaptations of neurons by a reduction in the time over which a peptide is effective. 

There are a number of side-effects of opiates that are due to their actions on opiate receptors outside the central nervous system. Opiates constrict the pupils by acting on the oculomotor nucleus and cause constipation by activating a maintained contraction of the smooth muscle of the gut which reduces motility. This diminished propulsion coupled with opiates reducing secretion in the gut underlie the anti-diarrhoeal effect. Opiates contract sphincters throughout the gastrointestinal tract. Although these effects are predominantly peripheral in origin there are central contributions as well. Morphine can also release histamine from mast cells and this can produce irritation and broncho-spasm in extreme cases. Opiates have minimal cardiovascular effects at therapeutic doses. 

Activation of both the RAAS and the SNS also contribute to vasoconstriction in an attempt to redistribute blood flow from peripheral organs such as the kidneys to coronary and cerebral circulation.7 However, arterial vasoconstriction leads to impaired forward ejection of blood from the heart due to an increase in afterload. This results in a decrease in CO and continued stimulation of compensatory responses, creating a vicious cycle of neurohormonal activation. 

---