View clinical trials related to Autoregulation.
Filter by:The purpose of this research, which has been determined as non-significant risk by the central IRB overseeing the study, is to obtain information to help further develop a machine (a medical device) to measure the pressure around the brain from the outside (this pressure is called intracranial pressure or ICP). Monitoring and managing ICP is an important part of care for patients with conditions such as Traumatic Brain Injury (TBI). However, the current way of measuring ICP requires surgery to drill a hole into the skull, and therefore can introduce additional risks such as infections and pain. Recent research has shown it may be possible to measure ICP without needing surgery. This technology is in development, but large amounts of data is required to build these new devices. Through collecting a large database of information from patients who have both the routine surgical device and the research device applied to their head, the research team will work to develop and test an effective and potentially safer way of monitoring patient ICP.
Blood flow autoregulation is defined as the ability of a tissue to maintain a relatively constant flow, despite moderate alterations in perfusion pressure. Similar to the cerebral, renal, coronary and skeletal muscle circulations, the ocular vascular bed shows the property of flow autoregulation. This homeostatic mechanism allows blood supply to the eye to match metabolic demand during daily activities, such as changes in posture, or in more critical conditions. Autoregulation has been found to be a complex phenomenon, showing heterogeneity in its site and time course of action. Since metabolic, myogenic, neurogenic and possibly endothelium-related mechanisms may be involved, several factors may vary depending on the challenging stimulus, the vessel tone, or the degree of impairment of autoregulation. To study the dynamics of ocular autoregulation, it is necessary to introduce a step disturbance (stimulus) in ocular perfusion pressure and to record the responses of ocular blood flow continuously before and after this step disturbance. The investigators have employed a mechanical noninvasive technique to induce an ocular perfusion pressure step disturbance without drugs or changes in the concentration of vasoactive substances in the blood by using the thigh cuff technique inducing a small step decrease in ocular perfusion pressure. With this technique the investigators could show significant differences in the time response of blood velocities in the ophthalmic and middle cerebral artery. This clearly indicates different mechanisms to be responsible for autoregulatory mechanisms distal to the vessels. Interestingly our results indicate that in the ophthalmic artery a late vasoconstriction occurs. Many previous investigations have demonstrated that sympathetic nerve stimulation causes vasoconstriction in the ocular circulation. Accordingly, the present study tests the hypothesis that α2-adrenoceptors are involved in the dynamic regulation of blood flow in the ophthalmic and middle cerebral artery after a step decrease in perfusion pressure.
Autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. For a long time it had been assumed that the choroid is a strictly passive vascular bed, which shows no autoregulation. However, recently several groups have identified some autoregulatory capacity of the choroid. Choroidal autoregulation was first shown in a rabbit model where intraocular pressure (IOP) and arterial blood pressure could be varied independently. In these experiments regulation of choroidal blood flow was not only dependent on ocular perfusion pressure, but was also dependent on the value of IOP. This indicates that a myogenic mechanism contributes to choroidal autoregulation, because the regulatory capacity is dependent on the transmural pressure. In the model of myogenic autoregulation arterioles change their vascular tone depending on the pressure inside the vessel and outside the vessel. The present experiments are designed to test whether a myogenic mechanism may also be involved in choroidal autoregulation in humans. For this purpose the investigators perform experiments during which the IOP and the arterial blood pressure is increased. According to the myogenic theory of autoregulation one would expect stronger vasoconstriction at lower IOPs for the same increase in ocular perfusion pressure.
Autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. For a long time it had been assumed that the choroid is a strictly passive vascular bed, which shows no autoregulation. However, recently several groups have identified some autoregulatory capacity of the human choroid. In the brain and the retina the mechanism behind autoregulation is most likely linked to changes in transmural pressure. In this model arterioles change their vascular tone depending on the pressure inside the vessel and outside the vessel. In the choroid, several observations argue against a direct involvement of arterioles. However, the mechanism behind choroidal autoregulation remains unclear. In the present study autoregulation of the choroid will be investigated during a decrease in ocular perfusion pressure, which will be achieved by an increase in intraocular pressure. Pressure/flow relationships will be investigated in the absence or presence of a NO synthase inhibitor. As a control substance the alpha-receptor agonist phenylephrine will be used.
Annually, almost 5,000 extremely low birth weight (9 ounces to about 2 lbs) infants born in the US survive with severe bleeding in the brain (intraventricular hemorrhage); this devastating complication of prematurity is associated with many problems, including mental retardation, cerebral palsy, and learning disabilities, that result in profound individual and familial consequences. In addition, lifetime care costs for these severely affected infants born in a single year exceed $3 billion. The huge individual and societal costs underscore the need for developing care strategies that may limit severe bleeding in the brain of these tiny infants. The overall goal of our research is to evaluate disturbances of brain blood flow in these tiny infants in order to predict which of them are at highest risk and to develop better intensive care techniques that will limit severe brain injury. 1. Since most of these infants require ventilators (respirators) to survive, we will investigate how 2 different methods of ventilation affect brain injury. We believe that a new method of ventilation, allowing normal carbon dioxide levels, will normalize brain blood flow and lead to less bleeding in the brain. 2. We will also examine how treatment for low blood pressure in these infants may be associated with brain injury. We believe that most very premature infants with low blood pressure actually do worse if they are treated. We think that by allowing the infants to normalize blood pressure on their own will allow them to stabilize blood flow to the brain leading to less intraventricular hemorrhage. 3. In 10 premature infants with severe brain bleeding, we have developed a simple technique to identify intraventricular hemorrhage before it happens. Apparently, the heart rate of infants who eventually develop severe intraventricular hemorrhage is less variable than infants who do not develop this. We plan to test this method in a large group of infants, to be able to predict which infants are at highest risk of developing intraventricular hemorrhage and who could most benefit from interventions that would reduce disturbances of brain blood flow.