The SARS-CoV-2 enters the human airways and comes into contact with the mucous membranes lining the mouth, nose, and eyes. The virus enters the healthy cells and uses cell machinery to make several copies of the virus. Critically ill patients infected with SARS-CoV-2 may have damaged lungs, air sacs, lining, and walls. Since COVID-19 causes cytokine storm, it damages the alveolar cells of the lungs and fills them with fluid, making it harder to exchange oxygen and carbon dioxide. The SARS-CoV-2 infection causes a range of complications, including mild to critical breathing difficulties. It has been observed that older people suffering from health conditions like cardiomyopathies, nephropathies, metabolic syndrome, and diabetes instigate severe symptoms. Many people who died due to COVID-19 had impaired metabolic health [IMH], characterized by hypertension, dyslipidemia, and hyperglycemia, i.e., diabetes, cardiovascular system, and renal diseases making their retrieval challenging. Jeopardy stresses for increased mortality from COVID-19 include older age, COPD, ischemic heart disease, diabetes mellitus, and immunosuppression. However, no targeted therapies are available as of now. Almost two-thirds of diagnosed coronavirus patients had cardiovascular diseases and diabetes, out of which 37% were under 60. The NHS audit revealed that with a higher expression of ACE-2 receptors, viral particles could easily bind their protein spikes and get inside the cells, finally causing COVID-19 infection. Hence, people with IMH are more prone to COVID-19 and, ultimately, comorbidities. This review provides enormous information about tissue [lungs, heart and kidneys] damage, pathophysiological changes, and impaired metabolic health of SARS-CoV-2 infected patients. Moreover, it also designates the possible therapeutic targets of COVID-19 and drugs which can be used against these targets.
The role of cAMP and prostaglandins as specific intracellular effectors of gastrin action at the level of the parietal cells has not been sufficiently clarified. For this reason we studied the responses of the parietal cells to stimulation with pentagastrin (6 micrograms/kg i.m.) during theophylline infusion (which causes an increase in the intracellular cAMP) and during acetylsalicylic acid infusion (which inhibits the prostaglandin synthesis) in 28 healthy volunteers. Both theophylline and acetylsalicylic acid provoked a significant increase of gastric acid secretion after pentagastrin. Our results suggest that: 1. an increase in intracellular cAMP may be the basis of the stimulatory effect of gastrin on gastric acid secretion 2. a decrease in the synthesis of prostaglandins may lead to a greater gastric acid response after pentagastrin.
The effect of secretin on insulin release has been studied in normal subjects after prestimulation with arginine. In order to make a comparison a pulse of glucose with arginine prestimulation was given. A pulse of 1 U/kg b.w. of secretin provokes a secretion of insulin that is weak and brief compared to that provoked by glucose; thus secretin fails to potentiate arginine-induced insulin secretion. Such a result does not support the hypothesis of secretin as the central hormone in the enteroinsular axis.
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