Pulmonary vascular response to increase in intracranial pressure: role of sympathetic mechanisms.
The pulmonary vascular response to intracranial hypertension was studied in anesthetized controlled ventilated dogs in which intracranial pressure (ICP) was elevated to 20 Torr below the mean arterial pressure for a 20-min period, and regulated at this level. Pulmonary vascular resistance (PVR) increased from control value of 2.7 +/- 0.30 to 8.3 +/- 0.51 Torr-l-1-min at the end of 20-min increase in ICP. The increase in PVR was associated with marked increase (P less than 0.001) in pulmonary arterial pressure from 14.4 +/- 1.3 to 35.4 +/- 4.0 Torr, small increase in left atrial pressure from 5.4 +/- 1.2 to 7.9 +/- 1.9 Torr, and no significant change in pulmonary blood flow. The increase in PVR occurred independently of changes in the arterial pressure. The increase in PVR induced by elevated ICP was correlated with increases in lung water, physiological shunt (Qs/Qt), alveolar dead space (VD), and with hypoxemia. Pretreatment with propranolol (1.5 mg-kg-1) attenuated the increase in PVR during elevation in ICP; the smaller increase in PVR was associated with a marked increase in left atrial pressure and a smaller increase in pulmonary perfusion pressure than in the control group. The propranolol-treated dogs also developed increases in lung water, Qs/Qt, VD, and hypoxemia. In contrast, pretreatment with phenoxybenzamine (1.5 mg-kg-1) inhibited the increases in pulmonary perfusion pressure and PVR induced by ICP elevation as well as the associated increases in lung water, Qs/Qt, VD, and hypoxemia. Therefore, a sustained elevation in ICP at a level below the mean arterial pressure in the intact dog evokes pulmonary vasoconstriction which is mediated by alpha-adrenergic mechanisms. The neurogenic pulmonary vasoconstriction results in the increases in lung water, Qs/Qt, VD, and in the hypoxemia.
Pulmonary vascular response to increase in intracranial pressure: role of sympathetic mechanisms. The pulmonary vascular response to intracranial hypertension was studied in anesthetized controlled ventilated dogs in which intracranial pressure (ICP) was elevated to 20 Torr below the mean arterial pressure for a 20-min period, and regulated at this level. Pulmonary vascular resistance (PVR) increased from control value of 2.7 +/- 0.30 to 8.3 +/- 0.51 Torr-l-1-min at the end of 20-min increase in ICP. The increase in PVR was associated with marked increase (P less than 0.001) in pulmonary arterial pressure from 14.4 +/- 1.3 to 35.4 +/- 4.0 Torr, small increase in left atrial pressure from 5.4 +/- 1.2 to 7.9 +/- 1.9 Torr, and no significant change in pulmonary blood flow. The increase in PVR occurred independently of changes in the arterial pressure. The increase in PVR induced by elevated ICP was correlated with increases in lung water, physiological shunt (Qs/Qt), alveolar dead space (VD), and with hypoxemia. Pretreatment with propranolol (1.5 mg-kg-1) attenuated the increase in PVR during elevation in ICP; the smaller increase in PVR was associated with a marked increase in left atrial pressure and a smaller increase in pulmonary perfusion pressure than in the control group. The propranolol-treated dogs also developed increases in lung water, Qs/Qt, VD, and hypoxemia. In contrast, pretreatment with phenoxybenzamine (1.5 mg-kg-1) inhibited the increases in pulmonary perfusion pressure and PVR induced by ICP elevation as well as the associated increases in lung water, Qs/Qt, VD, and hypoxemia. Therefore, a sustained elevation in ICP at a level below the mean arterial pressure in the intact dog evokes pulmonary vasoconstriction which is mediated by alpha-adrenergic mechanisms. The neurogenic pulmonary vasoconstriction results in the increases in lung water, Qs/Qt, VD, and in the hypoxemia.