Cardiopulmonary and arterial baroreflex-mediated control of forearm vasomotor tone is impaired after acute stroke.

Abstract

Elevated blood pressure (BP) levels are well recognized after acute stroke and are associated with increased BP variability. The underlying mechanisms producing such changes are unclear but may include abnormalities of baroreceptor-mediated control of heart rate and vasomotor tone. Lower body negative pressure (LBNP) can be used to assess the integrity of "low-pressure" cardiopulmonary and "high-pressure" arterial baroreceptor-derived responses by inducing nonhypotensive and hypotensive stimuli. Cardiovascular responses, including BP, heart rate, forearm blood flow, and forearm vascular resistance, to nonhypotensive and hypotensive LBNP were assessed in 13 consecutive stroke patients. Patients were studied within 72 hours of stroke (acute) and again at 10 to 14 days (subacute) and were compared with 13 control subjects individually matched for age, sex, and BP. At an LBNP of -10 mm Hg, BP was unchanged in all groups, but a significant increase in forearm vascular resistance occurred only in the control group (11 U [interquartile range, 7 to 15]; P < .05) compared with stroke patients in the acute (9 U [3 to 14]; P = NS) or subacute phases (7 U [2 to 12]; P = NS). After LBNP at -40 mm Hg, the reductions in systolic BP levels were similar in all groups (control: -9 mm Hg [-16 to -3]; acute stroke: -9 mm Hg [-22 to 3]; subacute stroke: -7 mm Hg [-35 to 20]), as was the associated increase in heart rate (control: 8 bpm ([4 to 11]; acute stroke: 6 bpm ([1 to 12]; subacute stroke: 9 bpm [2 to 19]). However, forearm vascular resistance increased significantly only in control subjects (20 U [9 to 30]; P < .01). The present study has identified abnormal vasomotor responses to LBNP after acute stroke, with an increase in FVR only being observed in control subjects in response to nonhypotensive and similar hypotensive levels of LBNP. In acute stroke patients, the stimulus of hypotensive LBNP appears to be compensated by an increase in cardiac output since there appears to be no increase in peripheral vascular resistance, unlike the changes seen in control subjects. However, the exact mechanisms for these changes are still unclear and are the subject of further study.