Vascular dilation

The dorsal skin fold window model allows direct observation of tumor microvasculature (11). This model also permits longitudinal assessment of the tumor vascular response to therapy. An accurate systematic measurement of tumor blood vessels in the window model is the linear summation of blood vessels using Optimas software. This approach corrects for vascular dilation and hemorrhage. Quantification of red... 

This xanthine derivative is an only a modest bron-chodilator in COPD, and because of its narrow therapeutic range, frequently seen adverse effect and drug interactions, it is becoming less frequently used, some patients experience side effects even within the therapeutic range. The non-bronchodilator effects of theophylline such as systemic and pulmonary vascular dilatation, central nervous system stimulation, improvement of the strength and effectiveness of respiratory muscles and possibly anti-inflammatory effects are of disputed clinical significance at usual therapeutic levels. 

Vasodilatation/vascular dilatation Dilation of blood vessels. 

Bikunin (Bik), a peptide excreted in the urine, is one of the primary inhibitors of the trypsin family of serine proteases. This peptide plays a key role in inflammation and innate immunity because of its two Kunitz-type binding domains [1, 2], Bik suppresses proteolytic activity in a variety of tissues and can also exert localized anti-inflammatory effect [3-5], Inflammation is an important indicator of infection, cancer, and tissue injury in acute and chronic states. In acute inflammation, fluids and plasma components accumulate in the affected tissues due to vascular dilation. Subsequent activation of platelets and increased presence of immune cells occur during repair. Long-standing inflammation may be present before the disorder is identified. Due to its inhibitory role and potential use as an early marker of inflammation, we will review the synthesis, structure, pathophysiology of Bik as well as the various approaches for its measurement in this chapter. 

Muscle cells release kallikrein during inflammation causing formation of active kinin peptides (bradykinin and kallidin) from kininogen [65, 66]. Kinins are peptide hormones that produce vasodilation, increase capillary permeability, and cause pain and infiltration of neutrophils. There is a direct correlation between the amount of kinin in plasma or tissues and the degree of inflammation. Vascular dilation causes increased blood flow to infection [67, 68], Bik inhibits formation of kinins and vascular dilation by kallikrein, thereby inhibiting smooth muscle contraction [69-71],... 

Endothelial cells Chronic proinflammatory response Leukocyte infiltration (rolling and adhesion), vascular dilation, inflammation mediator release (e.g., histamine, cytokines, eicosanoids)... 

Nitric oxide and NOS can be constitutive or inducible. Constitutive nNOS and eNOS occur in neuronal and endothelial cells, respectively, and are activated by CaM. In endothelial cells acetylcholine, bradykinin or blood flow derived shear stress elevate cytosolic Ca2+ with the successive consequences of eNOS activation by CaM, NO production, GC activation by NO, elevation of cGMP, PKG activation, specific protein phosphorylation, vascular smooth muscle relaxation and vascular dilation. 

Phosphorylation of specific protein substrates results in a conformational change of the phosphoproteins associated with a change in ligand binding and/or catalytic properties. Thus PKG has an important role in regulation of vascular smooth muscle, PKG-catalysed phosphorylation of specific proteins resulting in smooth muscle relaxation, vascular dilation and increased blood flow (see Chapter 7). 

This is the presence of excess fluid in the peritoneal cavity, leading to a swollen abdomen (Figure 4.3). The accumulation of ascitic fluid represents a state of sodimn excess in the body. Patients often present with hyponatraemia, but this is thought to be due to the dilutional effect of excess water rather than to low sodium. There are three theories of the cause of ascites formation. The underfill theory suggests that there is a reduction in circulating plasma volume as a result of accumulation in the splanchnic area due to vascular dilatation in portal hypertension. This activates the plasma renin, aldosterone and sympathetic nervous systems, which leads to sodium and water retention by the kidneys. 

The effect of a local anaesthetic is terminated by its removal from the site of application. Anything that delays its absorption into the circulation will prolong its local action and can reduce its systemic toxicity where large doses are used. Most local anaesthetics, with the exception of cocaine, cause vascular dilation. The addition of a vasoconstrictor such as adrenaline (epinephrine) reduces local blood flow, slows the rate of absorption of the local anaesthetic, and prolongs its effect the duration of action of lidocaine is doubled from one to two hours. Normally, the final concentration of adrenaline (epinephrine) should be 1 in 200 000, although dentists use up to 1 in 80 000. 

The type of peel must be carefully chosen. These vascular dilations must be treated preventively as indicated above (see Figure 37.20). 

Nitric oxide (NO) is a natural endothehum-derived relaxing factor that is important in regulating vascnlar tone, especially the pulmonary vasculature. Under normal physiologic conditions, NO is synthesized in endothebal cells and released into the vascular smooth muscle, where it stimulates cyclic GMP for vascular dilatation. At birth, NO helps in the transition from the markedly elevated pulmonary pres-snres in ntero to normal pulmonary pressnres and respiratory function. 

The physiological mechanism is by direct vascular dilation, both arterial and venous. The mechanism is not at all clear at the molecular level. The hypotension has been attributed to the thiocyanate ion, SCN, which is produced metabolically by rhodanese in the liver. The sulfur atom is supplied by thiosulfate ... 

Explain the actions of amiodarone on peripheral vascular dilatation. 

Thus, not all NO donors produce the same profile of vascular dilatation or therapeutic outcome. 

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