Hyperaemia

Abstract: Intermittent claudication has been studied in cardiovascular surveys but limited information is available on asymptomatic peripheral arterial disease. The purpose of this paper is to describe the prevalence of both asymptomatic and symptomatic disease and relation to ischaemic heart disease in the Edinburgh Artery Study. A cross-sectional survey was conducted on an age-stratified sample of men and women aged 55 to 74 years selected from age-sex registers in ten general practices in the city. Arterial disease was assessed in 1592 participants by means of the WHO questionnaire on intermittent claudication and measurement of the ankle brachial systolic pressure index (ABPI) and change in ankle systolic pressure during reactive hyperaemia. The prevalence of intermittent claudication was 4.5% (95% confidence interval (CI): 3.5%-5.5%). Major asymptomatic disease causing a significant impairment of blood flow occurred in 8.0% (95% CI: 6.6%-9.4%). A further 16.6% (95% CI: 14.6%-18.5%) had criteria considered abnormal in clinical practice: 9.0% had ABPI less than 0.9 and 7.6% had reactive hyperaemia pressure reduction greater than 20%. Intermittent claudication was equally common in both sexes. The ABPI and reactive hyperaemia results suggested a slight preponderance of asymptomatic disease in males and were consistent with an increasing prevalence with age and lower social class. Mean ABPI was higher in normal men than women, and was lower in the left leg than the right suggesting a unilateral predisposition to disease. Subjects with major asymptomatic disease had more evidence of ischaemic heart disease than in the normal population (relative risk (RR) 1.6; 95% CI: 1.3-1.9).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract: The cerebral hyperaemia is one of the fundamental mechanisms for the central nervous system homeostasis. Due also to this mechanism, oxygen and nutrients are maintained in satisfactory levels, through vasodilation and vasoconstriction. The brain hyperaemia, or coupling, is accomplished by a group of cells, closely related to each other; called neurovascular unit (NVU). The neurovascular unit is composed by neurones, astrocytes, endothelial cells of blood-brain barrier (BBB), myocytes, pericytes and extracellular matrix components. These cells, through their intimate anatomical and chemical relationship, detect the needs of neuronal supply and trigger necessary responses (vasodilation or vasoconstriction) for such demands. Here, we review the concepts of NVU, the coupling mechanisms and research strategies.

Abstract: Understanding the pathophysiology of a burn injury is important for effective management. In addition, different causes lead to different injury patterns, which require different management. It is therefore important to understand how a burn was caused and what kind of physiological response it will induce. Burn injuries result in both local and systemic responses. ![][1] Clinical image of burn zones. There is central necrosis, surrounded by the zones of stasis and of hyperaemia ### Local response The three zones of a burn were described by Jackson in 1947. Zone of coagulation —This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins. Zone of stasis —The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults—such as prolonged hypotension, infection, or oedema—can convert this zone into an area of complete tissue loss. Zone of hyperaemia —In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion. These three zones of a burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening. ![][2] ackson's burns zones and the effects of adequate and inadequate resuscitation ### Systemic response The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area. Cardiovascular changes —Capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of tumour necrosis factor α. These changes, coupled with fluid … [1]: /embed/graphic-1.gif [2]: /embed/graphic-2.gif

Abstract: Local cerebral blood flow has been measured by quantitative autoradiography, employing (14C)iodoantipyrine as tracer, in rats killed half an hour after occlusion of the middle cerebral artery. The results were compared with pattern of local cerebral blood flow (CBF) in sham-operated rats and with neuropathological findings. In every animal there was a profound reduction (to 13% of control levels)in blood flow in the neocortex previously by the occluded artery. The level of blood flow in the areas in which ischaemic brain damage occurred was 0.24 +/- 0.03 ml g-1 min-1 (mean +/- SEM). this level of CBF is considerably greater than that reported following a similar surgical procedure in cats and primates. Moderate reductions in blood flow were also seen outside the territory of the occluded artery and in parts of the opposite hemisphere. Absolute increases in blood flow (hyperaemia) were seen only in the substantia nigra and globus pallidus ipsilateral to the occlusion. It is of the middle cerebral artery are reflections of alterations in neuronal function and metabolic activity secondary to the ischaemic lesion.