Decreased vascular marking

Glucocorticoids do not directly relax airway smooth muscle and thus have little effect on acute bronchoconstriction. Their anti-inflammatory effects in asthma include modulation of cytokine and chemokine production inhibition of eicosanoid synthesis marked inhibition of accumulation of basophils, eosinophils, and other leukocytes in lung tissue and decreased vascular permeability. Because of their profound and generalized anti-inflammatory actions, glucocorticoids are the most effective drugs used in the treatment of asthma. 

Peripheral vascular disease, often one of the sequelia of atherosclerosis, is characterized by markedly decreased circula-... 

The prevalence of CHE increases and prognosis worsens with age. Some studies demonstrate that age markedly influences all follow-up events, including total mortality, and mortality or hospitalisation related to CHE. Some studies suggest that physiological changes occur in CHE with ageing with an age-related increase in systemic vascular resistance and circulating noradrenaline (norepinephrine) concentrations and a decrease in renal function. 

Slow intravenous infusion of therapeutic doses of isoproterenol in humans produces a marked decrease in total peripheral resistance, owing to the predominance of vasodilation in skeletal muscle vascular beds. As a consequence, diastolic and mean blood pressures fall (Fig. 10.4). The depressor action of isoproterenol is more pronounced than that of epinephrine because isoproterenol causes no vasoconstriction, whereas epinephrine does in some vascular beds. Systolic blood pressure may remain unchanged or may increase. When an increase in systolic blood pressure is seen, it is due to the marked increase in cardiac output produced by isoproterenol. 

There is a dose-dependent decrease in systemic blood pressure during isoflurane anaesthesia. This is mainly the result of a marked reduction in peripheral vascular resistance. In contrast, the decrease in arterial blood pressure during halothane anaesthesia appears to be mainly the result of a reduction in myocardial contractility. Isoflurane, in common with other volatile agents, has little effect on pulmonary artery pressure or pulmonary vascular resistance. 

The net cardiovascular effects of moderate doses of cholinesterase inhibitors therefore consist of modest bradycardia, a fall in cardiac output, and an increased vascular resistance that result in a rise in blood pressure. (Thus, in patients with Alzheimer s disease who have hypertension, treatment with cholinesterase inhibitors requires that blood pressure be monitored to adjust antihypertensive therapy.) At high (toxic) doses of cholinesterase inhibitors, marked bradycardia occurs, cardiac output decreases significantly, and hypotension supervenes. 

Blood vessels receive chiefly vasoconstrictor fibers from the sympathetic nervous system therefore, ganglionic blockade causes a marked decrease in arteriolar and venomotor tone. The blood pressure may fall precipitously because both peripheral vascular resistance and venous return are decreased (see Figure 6-7). Hypotension is especially marked in the upright position (orthostatic or postural hypotension), because postural reflexes that normally prevent venous pooling are blocked. 

The primary direct result of an effective dose of nitroglycerin is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. Pulmonary vascular pressures and heart size are significantly reduced. In the absence of heart failure,... 

Mannitol Physical osmotic effect on tissue water distribution because it is retained in the vascular compartment Marked increase in urine flow, reduced brain volume, decreased intraocular pressure, initial hyponatremia, then hypernatremia Renal failure due to increased solute load (rhabdomyolysis, chemotherapy), increased intracranial pressure, glaucoma IV administration Toxicity Nausea, vomiting, headache... 

Flalothane, desflurane, enflurane, sevoflurane, and isoflurane all decrease mean arterial pressure in direct proportion to their alveolar concentration. With halothane and enflurane, the reduced arterial pressure appears to be caused by a reduction in cardiac output because there is little change in systemic vascular resistance despite marked changes in individual vascular beds (eg, an increase in cerebral blood flow). In contrast, isoflurane, desflurane, and sevoflurane have a depressant effect on arterial pressure as a result of a decrease in systemic vascular resistance with minimal effect on cardiac output. 

The hypotensive action of guanethidine early in the course of therapy is associated with reduced cardiac output, due to bradycardia and relaxation of capacitance vessels. With long-term therapy, peripheral vascular resistance decreases. Compensatory sodium and water retention may be marked... 

Diabetic patients are 3 4 times more susceptible to atherosclerosis and vascular insufficiency. The situation is similar for those suffering from renal insufficiency, independent of diabetes. Makita et al.5sl found that there was a direct correlation CP < 0.005) between serum AGE-peptide levels and renal function, as assessed by creatinine clearance. This led Bucala et a/.145 to consider that the modification of the plasma proteins, such as LDL, may arise due to the reaction with reactive, circulating AGE-peptides rather than glucose. AGE-LDL did form readily in vitro when native LDL was incubated with either synthesised AGE-peptides or AGE-peptides isolated directly from the plasma of patients. Such AGE-LDL exhibited markedly impaired clearance kinetics when injected into transgenic mice, expressing human LDL receptor. Their data indicate that AGE modification could contribute to elevated LDL levels in patients with diabetes or renal insufficiency. This hypothesis was further supported by the administration of AG to diabetic patients, when circulating levels of LDL decreased by almost 30%. Levels of Hb-AGE decreased too. 

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