Inflammation that occurs after acute myocardial infarction plays a pivotal role in healing by facilitating the creation of a supportive scar. (18)F-FDG, which is taken up avidly by macrophages, has been proposed as a marker of cell-based inflammation. However, its reliability as an accurate indicator of inflammation has not been established, particularly in the early postinfarction period when regional myocardial perfusion is often severely compromised.Nine adult dogs underwent left anterior descending coronary occlusion with or without reperfusion. Animals were imaged between 7 and 21 d after infarction with PET/MR imaging after bolus injection of gadolinium-diethylenetriaminepentaacetic acid (DTPA), bolus injection of (18)F-FDG, bolus injection of (99)Tc-DTPA to simulate the distribution of gadolinium-DTPA (which represents its partition coefficient in well-perfused tissue), and injection of (111)In-labeled white blood cells 24 h earlier. After sacrifice, myocardial tissue concentrations of (18)F, (111)In, and (99)Tc were determined in a well counter. Linear regression analysis evaluated the relationships between the concentrations of (111)In and (18)F and the dependence of the ratio of (111)In/(18)F to the apparent distribution volume of (99m)Tc-DTPA.In 7 of 9 animals, (111)In increased as (18)F increased with the other 2 animals, showing weak negative slopes. With respect to the dependence of (111)In/(18)F with partition coefficient, 4 animals showed no dependence and 4 showed a weak positive slope, with 1 animal showing a negative slope. Further, in regions of extensive microvascular obstruction, (18)F significantly underestimated the extent of the presence of (111)In.In the early post-myocardial infarction period, (18)F-FDG PET imaging after a single bolus administration may underestimate the extent and degree of inflammation within regions of microvascular obstruction.
Introduction: Selective brain cooling can minimize systemic complications associated with whole body cooling but maximize neuroprotection. Recently, we developed a non-invasive, portable and inexpensive system for selectively cooling the brain rapidly and demonstrated its safety and efficacy in porcine models. However, the widespread application of this technique in the clinical setting requires a reliable, non-invasive and accurate method for measuring local brain temperature so that cooling and rewarming rates can be controlled during targeted temperature management. In this study, we evaluate the ability of a zero-heat-flux SpotOn sensor, mounted on three different locations, to measure brain temperature during selective brain cooling in a pig model. Computed Tomography (CT) was used to determine the position of the SpotOn patches relative to the brain at different placement locations.Methods and Results: Experiments were conducted on two juvenile pigs. Body temperature was measured using a rectal temperature probe while brain temperature with an intraparenchymal thermocouple probe. A SpotOn patch was taped to the pig’s head at three different locations: 1-2 cm posterior (Location #1, n=1), central forehead (Location #2, n=1); and 1-2 cm anterior and lateral to the bregma i.e., above the eye on the forehead (Location #3, n=1). This cooling system was able to rapidly cool the brain temperature to 33.7 ± 0.2°C within 15 minutes, and maintain the brain temperature within 33-34°C for 4-6 hours before slowly rewarming to 34.8 ± 1.1°C from 33.7 ± 0.2°C, while maintaining the core body temperature (as per rectal temperature probe) above 36°C. We measured a mean bias of -1.1°C, -0.2°C and 0.7°C during rapid cooling in induction phase, maintenance and rewarming phase, respectively. Amongst the three locations, location #2 had the highest correlation (R2 = 0.8) between the SpotOn sensor and the thermocouple probe.Conclusions: This SBC method is able to tightly control the rewarming rate within 0.52 ± 0.20°C/h. The SpotOn sensor placed on the center of the forehead provides a good measurement of brain temperature in comparison to the invasive needle probe.
Hypothermia (brain temperature < 35°C) shows great promise to minimize neural damage in patients with cardiopulmonary arrest and traumatic head injuries.[1, 2] However, cooling the whole body below 33–34°C can induce severe complications.[3] Arrhythmia, infection and primary coagulopathy are the most commonly noted complications.[3] We have developed a Selective Brain Cooling (SBC) approach which can be initiated early after injury, induces rapid cooling and maintains the target brain temperature over an extended period of time before slowly rewarming without significantly affecting the core body temperature.[4] In our experiments, brain temperature was measured invasively by inserting a thermocouple probe into the brain parenchyma, which measured brain temperature accurately but is invasive, making it unsuitable for most patients. Invasive intracranial probe also can have complications such as intracranial hemorrhage or hematoma and infection.[5] Accordingly, the clinical adaptation of our SBC technique requires a reliable, non-invasive and accurate method for measuring local brain temperature so that cooling and rewarming rate can be controlled during targeted temperature management.
Mild hypothermia has become an effective neuroprotective strategy following head trauma, cardiac arrest and neonatal asphyxia. However, cooling the whole body below 33-34°C can induce severe complications; therefore, selective brain cooling (SBC) could minimize adverse effects by maintaining core body temperature at normal values over an extended period of time. Recently, we developed a novel method of SBC and demonstrated its safety and efficacy in a piglet model. the method was based on spraying room temperature or cold air into the nostrils at different flow rates. Pigs possess a carotid rete (a set of small parallel arteries) which is surrounded by the cavernous sinus; together these serve as an effective heat exchanger for the brain. However, in mammals in which the carotid rete is missing such as rabbits and humans, some suggest that there is no effective heat exchange in the cavernous sinus and, consequently, SBC is not efficient in these species.
OBJECTIVE
To evaluate the effectiveness of this approach on rabbits and compare it with previous finding on newborn piglets.
Photoacoustic imaging (PAI) has the potential to acquire 3-D optical images at high speed. Attempts at 3-D photoacoustic imaging have used a dense 2-D array of ultrasound detectors or have densely scanned a single detector on a 2-D surface. The former approach is costly and complicated to realize, while the latter is inherently slow. We present a different approach based on a sparse 2-D array of detector elements and an iterative reconstruction algorithm. This approach has the potential for fast image acquisition, since no mechanical scanning is required, and for simple and compact construction due to the smaller number of detector elements. We obtained spatial sensitivity maps of the sparse array and used them to optimize the image reconstruction algorithm. We then validated the method on phantoms containing 3-D distributions of optically absorbing point sources. Reconstruction of the point sources from the time-domain signals resulted in images with good contrast and accurate localization (1 mm error). Image acquisition time was 1 s. The results suggest that 3-D PAI with a sparse array of detector elements is a viable approach. Furthermore, the rapid acquisition speed indicates the possibility of high frame rate 3-D PAI.
