Middle cerebral artery (MCA) flow velocity was continuously monitored during smoking in an observational study (n = 14) using transcranial Doppler (TCD) ultrasonography. Cerebral autoregulatory vasodilator capacitance under inspired CO2 challenge was also measured before smoking and at peak smoking effect. Several puffs on a single lighted cigarette over a period of five minutes acutely increased MCA mean flow velocity in every subject (group mean increase: 19%, individual increases ranged 2-64%) with a response onset and offset detectable within several seconds of beginning and ending smoking. The mechanism for the increase in MCA flow velocities appeared to be independent of the CO2 autoregulatory mechanism. Gender subgroup analysis showed smoking acutely suppressed the CO2 vasodilator capacitance by 56% in men but only by 5% in women (p = 0.05). The magnitude of the acute smoking-induced increases in MCA flow velocities appeared to be independent of the estimated cigarette yields for nicotine, carbon monoxide, and "tar." Smoking in healthy subjects acutely increased MCA mean flow velocity, which may reflect a global increase in cerebral blood flow via complex influences on the cerebral autoregulation.

Ultrasound-derived volumetric flow analysis may be useful in answering questions of basic physiological interest in the cerebrovascular circulation. Using this technique, the authors have sought to describe quantitatively the complete concurrent flow relations among all four arteries supplying the brain. The aim of this study of normal subjects was to determine the relative flow contributions of the anterior (internal carotid arteries) and posterior (vertebral arteries) cerebral circulation. Comparisons between the observed and theoretically expected anterior and posterior flow distribution would provide an opportunity to assess traditional rheological conceptions in vivo. Pulsed color Doppler ultrasonography was used to measure mean flow rates in the internal carotid and vertebral arteries in 21 normal adults. The anterior circulation (internal carotid arteries bilaterally) carried 82% of the brain's blood supply and comprised 67% of the total vascular cross-sectional area. These values demonstrate precise concordance between observations in vivo and the theoretically derived (Hagen-Poiseuille) expected flow distribution. These cerebrovascular findings support the traditional conception of macroscopic blood flow. Further studies using ultrasound-derived volumetric analysis of the brain's arterial flow relations may illuminate the vascular pathophysiology underlying aging, cerebral ischemia, and dementias.

Tha pathophysiology of brain injury in patients undergoing cardiopulmonary bypass remains unclear despite several decades of inquiry. The advent of noninvasive high-resolution brain and cerebrovascular imaging by magnetic resonance, computed tomography, and pulsed Doppler ultrasonography now permits in vivo assessment of pathophysiological mechanisms. Neuroradiographic and carotid duplex studies were performed in patients who developed neurological deficits following cardiopulmonary bypass. Among 30 symptomatic patients undergoing magnetic resonance or computed tomography brain scans, 18 (60%) had findings of acute ischemic injury. Embolic infarction was evident in 14 (78%) of these 18 patients. Watershed injury was the predominant finding in a single patient, while findings consistent with global anoxia were present in another patient. Carotid atheroemboli were excluded as a possible source of embolism in 11 patients whose carotid duplex studies were unremarkable preoperatively as well as in 3 further patients whose neuroradiographic findings did not correspond with their moderate carotid disease. It is concluded that infarction due to noncarotid embolism is the primary pathophysiology of neurological deterioration following cardiopulmonary bypass.