Lower Limit Of Cerebral Autoregulation Research Articles

Increase in transcranial Doppler pulsatility index does not indicate the lower limit of cerebral autoregulation.

Transcranial Doppler pulsatility index was reported clinically to increase when cerebral perfusion pressure decreased, hypothetically marking the lower limit of cerebral autoregulation. We sought to investigate the relationship between pulsatility index, cerenbrovascular resistance, and cerebral perfusion pressure in various states of autoregulation in an animal model of moderate intracranial hypertension. Eight New-Zealand White Rabbits were studied with basilar artery blood flow velocity (ultrasound Doppler) and cortical blood flow (laser Doppler) monitored continuously during subarachnoid saline infusion to increase intracranial pressure (< 55 mm Hg). Four animals demonstrated a stable cortical blood flow, and four demonstrated decreasing blood flow when cerebral perfusion pressure decreased. Pulsatility index showed the same pattern of increase when cerebral perfusion pressure decreased, independent on whether cortical blood flow was stable or falling. The percentage rate of increase in the pulsatility index was not different in autoregulating and non autoregulating animals. The rate of decrease in cerebrovascular resistance was significantly lower (p < 0.05) in non-autoregulating than in autoregulating animals. The increase in transcranial Doppler pulsatility index when cerebral perfusion pressure falls cannot be interpreted as a phenomenon able to mark the lower limit of cerebral autoregulation.

Effect of indomethacin on cerebral blood flow and oxygenation in the normal and ventilated fetal lamb.

Indomethacin lowers fetal and neonatal brain blood flow and may reduce the risk of periventricular-intraventricular hemorrhage. However, concerns have been raised that cerebral O2 metabolism may be compromised at lower cerebral perfusion pressures. In 17 near-term lamb fetuses, changes in brain blood flow and cerebral O2 metabolism (CMRO2) were measured at mean carotid arterial pressures (MCBP) ranging from 8 to 70 mm Hg. MCBP was adjusted by inflating balloon occluders around the aortic isthmus and brachiocephalic trunk. This was done before and during intrauterine pulmonary ventilation and oxygenation. Nine fetuses were pretreated with indomethacin (1 mg/kg i.v.); eight served as control. Changes in brain blood flow were assessed from carotid arterial blood flow (Qcar, mL/min) measured with flow transducers. In 15 animals, brain blood flow was also measured intermittently by radionuclide-labeled microspheres (Qbrain). Qcar correlated closely with Qbrain (r = 0.94, p < 0.0001); this relationship was not altered by indomethacin or by ventilation with oxygen. In the nonventilated fetuses, indomethacin decreased Qcar at pressures above the lower limit of cerebral autoregulation (43 mm Hg). However, at MCBP below 44 mm Hg, Qcar with indomethacin was not significantly different from controls. CMRo2 fell when MCBP was decreased below 30 mm Hg (range 8-29 mm Hg), but there was no significant difference between control and indomethacin-pretreated fetuses. In the ventilated fetuses, indomethacin reduced the slope of the pressure-flow relationship above the lower limit of cerebral autoregulation (43 mm Hg), suggesting improved cerebral autoregulation. When MCBP was decreased below 44 mm Hg (range 10-43 mm Hg), indomethacin did not lower Qcar or CMRO2 as compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of cerebrovascular parasympathetic nerves on resting cerebral blood flow, spontaneous vasomotion, autoregulation, hypercapnic vasodilation and sympathetic vasoconstriction

Activation of perivascular parasympathetic nerves enhances cerebral blood flow. In the present experiments, functional aspects of this flow regulating capacity were investigated. It was found that parasympathetic nerve stimulation does not facilitate the normalization of the cerebral blood flow reduced by sympathetic stimulation. In contrast, activation of sympathetic nerves may contribute to a rapid normalization of the cerebral blood flow increased by parasympathetic stimulation. The lower limit of cerebral autoregulation is shifted towards higher blood pressures in parasympathetically denervated rats. Parasympathetic nerves do not influence hypercapnic cerebral vasodilatation, but CO 2 influence the effect of parasympathetic stimulation on cerebral blood flow. We conclude that activity in parasympathetic nerves does not contribute to cerebral vasomotion.

Hypoglycemia and cerebral autoregulation in anesthetized dogs

We examined the effects of moderate hypoglycemia with near-normal cerebral glucose consumption on cerebral autoregulation during graded hemorrhagic hypotension in anesthetized dogs. Four groups of animals (n = 8 each) were studied: normoglycemia, insulin-induced hypoglycemia (1.1 mM), normoglycemia plus alpha- and beta-adrenergic blockade [propranolol (1 mg/kg loading dose + 1 mg.kg-1.h-1 infusion) plus phentolamine (2 mg/kg loading dose + 2 mg/min infusion)], and hypoglycemia plus alpha- and beta-adrenergic blockade. As cerebral perfusion pressure was reduced to 40-50 mmHg, cerebral blood flow and O2 consumption increased in the hypoglycemic group. These increases were not observed after adrenergic blockade or in the normoglycemic groups. The perfusion pressure at which cerebrovascular resistance was minimal was higher during hypoglycemia (40 mmHg) and hypoglycemia plus blockade (50 mmHg) than in either of the normoglycemic groups (30 mmHg). This study demonstrates that hypoglycemia increases the lower limit of cerebral autoregulation during hypotension. Furthermore, adrenergic mechanisms acting during combined hypoglycemia and hemorrhagic hypotension increase cerebral blood flow and O2 consumption and attenuate the hypoglycemia-induced increase in the lower limit of autoregulation.

Some Observations on Cerebral Perfusion During Cardiopulmonary Bypass

Blood flow was recorded with an electromagnetic flow probe on one internal carotid artery (ICA) during cardiopulmonary bypass (CPB) in 5 patients. The ICA flow was monitored continuously along with arterial blood pressure, epidural intracranial pressure, and cerebral electrical activity using a cerebral function monitor (3 patients). The ICA flow increased by 50 to 100% at the inception of extracorporeal circulation. This rapid enhancement of flow occurred within a thirty-second period and was due to rapid arterial hemodilution caused by introduction of the priming solution. A transitory fall in ICA flow was observed during subsequent minutes when the well-recognized drop in blood pressure took place and the cerebral perfusion pressure (CPP = blood pressure - epidural intracranial pressure) was reduced to less than 30 mm Hg. In only one instance, however, when CPP fell to 15 mm Hg, was the fall in flow lower than the prebypass level. Throughout the rest of CPB, with steady-state hemodilution and CPP levels in the range of 30 to 50 mm Hg, ICA flow was markedly enhanced (50 to 100% above the prebypass level). The flow pattern, however, disclosed a pressure-passive system, indicating that cerebral autoregulation was impaired or that the CPP levels were lower than the individual lower limit of cerebral autoregulation during the period of steady-state hemodilution on CPB. A transient depression of cerebral electrical activity was seen in 2 patients shortly after the introduction of CPB. This phenomenon is suggestive of qualitatively insufficient perfusion and was observed even when ICA bulk flow was increased (hematocrit values, 13 to 17%).

Some Observations on Cerebral Perfusion during Cardiopulmonary Bypass

Blood flow was recorded with an electromagnetic flow probe on one internal carotid artery (ICA) during cardiopulmonary bypass (CPB) in 5 patients. The ICA flow was monitored continuously along with arterial blood pressure, epidural intracranial pressure, and cerebral electrical activity using a cerebral function monitor (3 patients). The ICA flow increased by 50 to 100% at the inception of extracorporeal circulation. This rapid enhancement of flow occurred within a thirty-second period and was due to rapid arterial hemodilution caused by introduction of the priming solution. A transitory fall in ICA flow was observed during subsequent minutes when the well-recognized drop in blood pressure took place and the cerebral perfusion pressure (CPP = blood pressure – epidural intracranial pressure) was reduced to less than 30 mm Hg. In only one instance, however, when CPP fell to 15 mm Hg, was the fall in flow lower than the prebypass level. Throughout the rest of CPB, with steady-state hemodilution and CPP levels in the range of 30 to 50 mm Hg, ICA flow was markedly enhanced (50 to 100% above the prebypass level). The flow pattern, however, disclosed a pressure-passive system, indicating that cerebral autoregulation was impaired or that the CPP levels were lower than the individual lower limit of cerebral autoregulation during the period of steady-state hemodilution on CPB. A transient depression of cerebral electrical activity was seen in 2 patients shortly after the introduction of CPB. This phenomenon is suggestive of qualitatively insufficient perfusion and was observed even when ICA bulk flow was increased (hematocrit values, 13 to 17%).

Lower limit of cerebral autoregulation in normotensive and spontaneously hypertensive rats

Cerebral autoregulation was examined in NTR and SHR. The lower blood pressure limit of autoregulation being 95 mm Hg in SHR was shifted upwards from 62 mm Hg in NTR.

Proceedings: Effects of bilateral carotid artery ligation on brain metabolism in spontaneously hypertensive and normotensive rats.

Bilateral carotid artery ligation may cause the more severe hemodynamic changes in SHR than in NR, resulting in cerebral ischemic damage to be pronounced in the former rats. The lower limit of cerebral autoregulation shifted to the higher level is necessary to explain the mechanism of hemodynamic crisis following carotid occlusion in SHR.

Cerebral blood flow and oxygen consumption in man.

Cerebral blood flow and oxygen consumption in man.