If both the carotids are occluded proximal to the carotid bifurcation, it would cause

Baroreceptors are located above the carotid bifurcation. When carotid aeries are occluded below the bifurcation, there would be a fall of pressure in the carotid sinus. This will reduce the stretch on its wall and the baroreceptors, being stretch receptors, decrease their discharge. The normal tonic effect of this discharge on the medullary VMC is inhibitory; the medullary vasoconstrictor area now escapes from that tonic inhibitory discharge. Carotid aeries supply blood to the brain; their occlusion may result in cerebral ischemia. However, increased BP and hea rate seen after their occlusion is NOT a result of VMC ischemia or CNS ischemic response. This may be concluded from two observations: If the carotid sinus nerves (IX N.) have been previously cut, abolishing the discharge of baroreceptors to VMC, rise in BP is not seen after carotid occlusion although there is cerebral ischemia. If the carotids are clamped beyond the carotid sinus baroreceptors, it produces cerebral ischemia but no rise in BP. Sectioning the carotid sinus nerves will produce the same effect as that of carotid clamping. decreased discharge to the VMC and a resultant increase in BP and hea rate. Carotid occlusion will also lead to reduced blood flow to the carotid body chemoreceptors; it will increase their discharge, resulting in an increased ventilatory drive and vasoconstriction as well.