The<unk>  is rapid delivery of blood to active neuronal tissue. Complications in this response arise in acute coronary syndromes and pulmonary arterial hypertension. These complications lead to a change in the regulation of blood flow to the brain, and in turn the amount of glucose and oxygen that is supplied to neurons, which may have serious effects not only on the functioning of the nervous system, but functioning of all bodily systems. Acute coronary syndrome Acute infections, such as community-acquired pneumonia (CAP), act as a trigger for acute coronary syndromes (ACS). ACS deals with symptoms that result from the obstruction of coronary arteries. Due to this obstruction there are thrombotic complications at the sites of atherosclerotic plaques. The most common symptom that prompts diagnosis is chest pain, associated with nausea and sweating. Treatment usually includes aspirin, Clopidogrel, nitroglycerin, and if chest pain persists morphine. Recent study suggests that acute respiratory tract infection can act as a trigger for ACS. This in turn has major prothrombotic and<unk>  effects. These effects result from coagulation, which is normally prevented in the vascular endothelium by expression of antithrombotic factors on its surface. Sepsis, which causes disruption and apoptosis of endothelial cells results in the endothelium switching to a procoagulant phenotype. This promotes platelet adhesion and aggregation. Moreover, only once disruption of the plaque surface has occurred are these prothrombotic effects likely to be significant in the pathogenesis of ACS. Sepsis is also largely associated with<unk>  changes. Coronary artery perfusion pressure is reduced in peripheral vasodilation, which results in reduced blood pressure and reduced myocardial contractility. Endothelial dysfunction induces coronary vasoconstriction. This is caused by catecholamine release and by infections. Severe infections lead to increase myocardial metabolic demands and hypoxia. When neuronal tissue is deprived of adequate oxygen, the<unk>  has less of an effect at active neuronal tissue. All of these disturbances increase the likelihood of ACS, due to coronary plaque rupture and thrombosis. Overall, ACS results from the damage of coronaries by atherosclerosis, so primary prevention of ACS is to prevent atherosclerosis by controlling risk factors. This includes eating healthy, exercising regularly, and controlling cholesterol levels. Pulmonary arterial hypertension Pulmonary hypertension (PAH) is disease of small pulmonary arteries that is usually caused by more than one mechanism. This includes pneumonia, parasitic infections, street drugs, such as cocaine and methamphetamines that cause constriction of blood vessels, and many more. Vasoactive mediators, such as nitric oxide and prostacyclin, along with overexpression of vasoconstrictors not only affect vascular tone but also promote vascular remodeling. PAH deals with increase blood pressure in pulmonary arteries, which leads to shortness of breath, dizziness, fainting, rarely hemoptysis, and many other symptoms. PAH can be a severe disease, which may lead to decreased exercise tolerance, and ultimately heart failure. It involves vasoconstrictions of blood vessels connected to and within the lungs. As a result, the heart has a hard time pumping blood through the lungs, and the blood vessels eventually undergoes fibrosis. The increased workload on the heart causes hypertrophy of the right ventricle, which leads less blood being pump through the lungs and decreased blood to the left side of the heart. As a result of all of this, the left side of the heart has a hard time pumping a sufficient supply of oxygen to the rest of the body, which deteriorates the effect of the<unk> . Impaired<unk> s in turn diminish exercise capacity in patients with PAH. The severity of<unk>  dysfunction during progressive exercise in PAH can be recorded using cardiopulmonary exercise testing (CPET), and/or impedance cardiography (ICG). Furthermore, there are no current cures for pulmonary arterial hypertension, but there are treatment options for patients with the disease to help prolong their survival and quality of life. A few of these treatments include basic therapy, calcium-channel blockers, and prostacyclin therapy. Basic therapy can lead to dramatic clinical improvements in patients with right heart failure by instituting diuretic therapy. This reduces the right ventricular preload. Moreover, high-dose calcium-channel blockers among patients who have a response to this treatment can prolong survival and improve pulmonary<unk> s. Calcium channel blocking drugs results in regression of right ventricular hypertrophy. On the other hand, prostacyclin therapy prolongs survival by inducing relaxation of vascular smooth muscles. This stimulates the production of cyclic AMP (cAMP), which inhibits the growth of smooth-muscle cells. Overall, pulmonary arterial tension and acute coronary syndromes are few of the many diseases that lead to hypoxia of neuronal tissue, which in turns deteriorates the<unk>  and leads to neuronal death. Prolonged hypoxia induces neuronal death via apoptosis. With a dysfunctional<unk> , active neuronal tissue due to membrane depolarization lacks the necessary energy to propagate signals, as a result of blood flow hindrance. This affects many functions in the body, and may lead to severe symptoms. Reduced<unk>  diseases Alzheimer's disease In this disease, there is a build of the amyloid beta protein in the brain. This ultimately leads to a reduction in the<unk>  and less blood flow in the brain. This reduced cerebral blood flow not only kills neuronal cells because of shortages in oxygen and glucose but it also reduces the brain's ability to remove amyloid beta. In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques which reduce blood flow. Two proteins are involved in this accumulation of amyloid beta: serum response factor or SRF and myocardin. Together, these 2 proteins determine whether smooth muscle of blood vessels contract. SRF and myocardin are more active in the brains of people with Alzheimer's disease. When these proteins are active, they turn on SREBP2 which inhibits LRP-1. LRP-1 helps the brain remove amyloid beta. Therefore, when SRF and myocardin are active, there is a buildup in amyloid beta protein which ultimately leads to less blood flow in the brain because of contracted blood vessels. Ischemia A decrease in circulation in the brain vasculature due to stroke or injury can lead to a condition known as ischemia. In general, decrease in blood flow to the brain can be a result of thrombosis causing a partial or full blockage of blood vessels, hypotension in systemic circulation (and consequently the brain), or cardiac arrest. This decrease in blood flow in the cerebral vascular system can result in a buildup of metabolic wastes generated by neurons and glial cells and a decrease in oxygen and glucose delivery to them. As a result, cellular energy failure, depolarization of neuronal and glial membranes, edema, and excess neurotransmitter and calcium ion release can occur. This ultimately ends with cell death, as cells succumb to a lack of nutrients to power their metabolism and to a toxic brain environment, full of free radicals and excess ions that damage normal cell organelle function.
Haemodynamic response
Optokinetic response
Electrodermal activity
Muscle tone
Cardiovascular physiology
Vagovagal reflex
Respiratory adaptation
Seizure threshold