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WEEK 21:
Control of Blood Vessels: Blood Flow Regulation:
| Question | Answer |
|---|---|
| cerebral receives | 14% cardiac output at rest (50ml/100g/min) |
| endothelin | vasoconstrictor in pathological states |
| explain metabolic (local) control in cerebral to control blood flow | eg increasing blood flow/vasodilation when there is more H+, K+, adenosine, hypercapnia (high CO2), and hypoxia |
| explain neural and hormonal control in cerebral to control blood flow | minor importance compared to other organs |
| explain how mechanical factors can affect cerebral control of blood flow | brain is in rigid cranium influenced by CSF pressure so space occupying lesions increase intracranial pressure (ICP) and reduce cerebral blood flow (CBF) |
| explain how special features can affect cerebral control of blood flow | medullary ischaemic reflex (Cushing) eg tumour induced reduction in CBF causes medullary ischaemia which stimulates an increase in BP in an attempt to restore CBF (tunour reduces BF so try increase BF to normal by increasing BP) |
| coronary receives | 4% cardiac output |
| describe neural control in coronary | minor direct influence but secondary effect due to changes in cardiac function and thus metabolism |
| sympathetic stimulation in coronary causes | B-mediated adrenoreceptors increasing HR and supraventricular tachycardia (contraction) increasing oxygen consumption (more blood flow = more O2 consumption) |
| describe local factors in coronary | metabolites are major drivers for increasing BF -> hypoxia, hypercapnia, adenosine, causing vasodilation |
| hormonal factors in coronary | adrenaline - a vasodilator and stimulates metabolism (as increases HR) |
| mechanical influences in coronary | movement in cardiac cycle (diastole and systole) influence blood flow with peak flow in diastole and zero/negative flow in systole |
| skin receives | 4% cardiac output at rest in a thermoneutral environment (eg if hot blood flow low to disperse heat) varying between 1-200ml/100g/min |
| neural influences in skin to control blood flow | arterioles with weak innervation (A-V-A) anastomoses with a dense innervation to vary blood flow eg in high temperature AVAs dilate to promote heat loss |
| local influences in skin to control blood flow | arterioles show some degree of myogenic autoregulation (high BP-> stretch receptors -> vasoconstriction) where AVAs show no autoregulation and no reactive hyperaemia where Endothelin may be involved in pathological states (Raynauds) |
| hormonal influences | angiotensin, vasopressin, noradrenaline, and adrenaline which all cause vasoconstriction |
| mechanical influences in skin | minimal influence |
| special features in skin | thermoregulation = primary function so sweat glands have sympathetic cholinergic innervation (sudomotor) which can cause vasodilation via release of bradykinin |
| skeletal muscle receives | 15% cardiac output at rest (3-60ml/100g/min) |
| neural influences in skeletal muscles | important a-vasoconstriction, some b-vasoconstriction and maybe sympathetic cholinergic vasodilation |
| exercise influence on skeletal muscles | very little neural influence, some b-vasodilation but local metabolites have a major influence (K+, adenosine, lactate etc) |
| local influences in skeletal muscles | neural control (baroreflexes) override autoregulatory mechanisms |
| hormonal influences in skeletal muscle | adrenaline at low concentrations will vasodilate |
| mechanical influences in skeletal muscle | muscle pumping |
| special features in skeletal muscles | capacity to increase flow in exercise (20 fold) - active hyperaemia and large increase in flow post-occlusion - reactive hyperaemia |
| reactive hyperaemia | transient increase in organ blood flow that occurs following a brief period of ischaemia (artieral occlusion) |
| splanchnic (superior mesenteric) CO | 10% cardiac output |
| splanchnic (hepatic) CO | 25% cardiac output |
| cardiac output via HPV | 70-75% (low O2 pressure) |
| cardiac output via HPA | 23-30% (high O2 pressure) |
| neural influences on splachnic | intestinal (moderate vasoconstriction) and hepatic (important a-venoconstriction) |
| liver stores | 15% blood volume and hepatic venoconstriction can expel 50% hepatic blood volume into circulation |
| local influences on splanchnic | intestinal has poor autoregulation but influenced by local peptides whereas hepatic has portal vein with no autoregulation, hepatic artery has good autoregulation |
| hormones in splanchnic | G- hormones (gastrin, cholecystokinin) vasodilate, vasopressin, angiotensin, constrict potently |
| intestinal splanchnic local influences | poor autoregulation influenced by local peptides |
| portal vein local has | no autoregulation |
| hepatic artery local has | good autoregulation |
| special features in splanchnic | intestinal circulation exhibits functional hyperaemia following feeding where intense vasoconstriction can lead to damage and release of toxins |
| vasoconstriction (neurohumeral) beneficial in | baroreflex but can be detrimental in haemorrhage/ septic shock |
| renal receives | 25% cardiac output |
| neural influences in renal | important a-vasoconstriction, some b-vasoconstriction and renin secreting cells have a sympathetic innervation (B-adrenoreceptors) |
| local influences in renal | good autoregulation of flow over a WIDE PRESSURE RANGE \ |
| hormonal influences in renal | noradrenaline, adrenaline, and angiotensin can cause constriction where vasopressin may cause vasodilation via prostaglandin/ NO release and dopamine causes vasodilation |
| dopamine in renal causes | vasodilation |
| vasopressin in renal causes | vasodilation VIA prostaglandin/ NO release |
| mechanical influences in renal | renal capsule may restrict flow in pathological states |
| special features in renal** | excretory function of kidney depends on well-maintained flow (autoregulation), vascular connections provide for capacity to regulate afferent/ efferent resistances |
| pulmonary receives | 100% cardiac output |
| neural influences of pulmonary | relatively minor neural influence (a-vasoconstriction) |
| local influences in pulmonary | hypoxia causes vasoconstriction which is augmented by hypercapnia (mediated by endothelin) and NO causes dilation (used therapeutically) |
| pulmonary hypertension | possible therapeutic strategies including endothelin antagonism and NO inhalation |
| mechanical influences in pulmonary | flow is affected by changes in alveolar pressure and lung volume - increase in flow (CO) associated with recruitment and distension of micrvessels and decrease in vascular resistance |
| if alveolar pressure is more than intravascular pressure | pressure is reduced |
| lung inflation reduces resistance where | in extra-alveolar vessels (traction) and increases resistance in intra-alveolar vessels (compression) |
Created by:
kablooey
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