Mechanisms of flow-induced responses in piglet isolated cerebral arteries
Abstract
We examined the effect of changing both steady and pulsatile flow on piglet cerebral artery diameter. Cerebral arteries were mounted on glass cannulas and bathed in and perfused with heated physiologic saline solution (PSS). An electronic system controlled pressure and a syringe pump provided constant flows. To produce pulsatile flow a solenoid occluded the inflow tubing. Vessel diameter was measured with a video system. Flow was increased from 0 to 1.6 ml/min at 20 mm Hg and vessel diameter measured (F/D curves). Increasing flow at constant pressure resulted in constriction at low flows and dilation at higher ones. The F/D curves were repeated in the presence of nitro-L-arginine (NLA), nitro-L-arginine methyl ester (L-NAME), indomethacin (IND), 6-hydroxydopamine (6-OHDA), ryanodine (RYN), after perfusion with glutaraldehyde (GLU) and in PSS with Na$\sp+$ reduced or Ca$\sp{2+}$ removed. In the presence of NLA, L-NAME, and RYN dilation was abolished; constriction was abolished when Na$\sp+$ was reduced or Ca$\sp{2+}$ removed. IND and 6-OHDA had no effect while perfusion with GLU abolished all response to flow. These data indicate that while neither prostaglandins nor adrenergic innervation play a role in either response, nitric oxide (NO) mediates flow-induced dilation through intracellular Ca$\sp{2+},$ constriction is modulated by extracellular Na$\sp+$ and Ca$\sp{2+}$ and both responses are due to deformation of endothelial cells. The effect of pulsatile flow was determined by increasing mean flow under pulsatile conditions and by changing from steady to pulsatile flow at each mean flow. Pulses were $\pm$4 mm Hg, frequency was 2 Hz. Next, either frequency or amplitude was increased (2 Hz to 4 Hz; $\pm$4 to $\pm$8 mm Hg). Each protocol was repeated in the presence of NLA and after GLU perfusion. Arteries dilated upon initiation of pulses but diameter did not change with increased mean flow. Arteries also dilated when both pulse amplitude and frequency increased. NLA diminished and GLU abolished dilation to pulsatile flow, increased frequency and increased amplitude, suggesting that dilation was due to changes in shear stress and was mediated by NO.
Recommended Citation
Shimoda, Larissa Akimi, "Mechanisms of flow-induced responses in piglet isolated cerebral arteries" (1995). Dissertations (1962 - 2010) Access via Proquest Digital Dissertations. AAI9626942.
https://epublications.marquette.edu/dissertations/AAI9626942