Effects of regional sympathectomy on the cardiovascular responses and pulmonary changes induced by cerebral compression
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In anesthetized and vagotomized rats, mechanical compression was accomplished by impacting a space-occupying mass into the cranium. The procedure evoked tachycardia, pressor response and severe pulmonary venous hypertension (PVH) followed by fulminating pulmonary hemorrhagic edema (PHE). We studied the effects of selective interruption of regional sympathetic outflows, i.e., upper thoracic sympathectomy (UTS), splanchnic nerves and celiac plexus excision (SCE), and femoral and sciatic nerves section (FSS) on such changes. Cardiopulmonary denervation by UTS did not affect the pressor response, but significantly reduced the tachycardia, PVH and PHE. Such effects were not attributed to a cardiac denervation because propranolol abolished the tachycardia but did not alter the other changes. Splanchnic denervation by SCE greatly reduced the pressor response and prevented the PVH and PHE. Interruption of a large part of sympathetic outflows to the limbs by FSS did not affect the cardiovascular responses and pulmonary changes. The results indicate that the limb vessels contribute little to the overall cardiovascular responses to cerebral compression. Splanchnic vasomotor responses are essential for the production of the centrogenic PHE. Direct sympathetic impulses to the lungs play an auxiliary role in the genesis of hemodynamic PHE. They are not important in the absence of splanchnic vasomotor reaction, but tend to exacerbate the PHV and PHE when a systemic hemodynamic crisis is induced.