Pierre Marie L Robitaille

Cognitive, cardiac, and physiological safety studies in ultra high field magnetic resonance imaging.

A systematic analysis of the effect of an 8.0 tesla static magnetic field on physiological and/or cognitive function is presented in the normal volunteer and in the swine. A study of ten human subjects revealed no evidence of detectable changes in body temperature, heart rate, respiratory rate, systolic pressure, and diastolic blood pressure after 1 hour of exposure. In addition, no cognitive changes were detected. Important ECG changes were noted which were related both to the position of the subject in the magnet and to the absolute strength of the magnetic field. As such, the ECG tracing at 8 tesla was not diagnostically useful. Nonetheless, all subjects exhibited normal ECG readings both before and following exposure to the 8 tesla field. Cardiac function was also examined in detail in the swine. No significant changes in body temperature, heart rate, left ventricular pressure, left ventricular end diastollic pressure, time rate of change of left ventricular pressure, myocardial stiffness index, cardiac output, systolic volume, troponin, and potassium levels could be detected following 3 h of exposure to a field strength of 8.0 tesla. It is concluded that no short term cardiac or cognitive effects are observed following significant exposure to a magnetic field of up to 8.0 tesla.

Myocardial high energy phosphate metabolism during ventricular fibrillation with total circulatory arrest

The study of high energy phosphates in myocardial energy metabolism has provided important insights into the factors that affect cellular injury during ischemia and metabolic and mechanical recovery with reperfusion. The term high energy phosphates (HEP) in the context of this paper includes adenine nucleotides (ATP and ADP) and creatine phosphate (CP). ATP directly provides the energy for mechanical, homeostatic, and synthetic myocardial functions. CP is postulated to function as an energy reservoir, transferring high energy bonds in the cytosol for the regeneration ATP from ADP. During severe or complete ischemia, myocytes become oxygen deficient and oxidative phosphorylation in the mitochondria ceases. As a result energy utilization exceeds production and myocardial HEP are depleted. Although no causal relationship has been demonstrated, under physiologic conditions there is a strong association between the depletion of myocardial HEP during ischemia, and the onset of myocardial injury. During reperfusion, the regeneration of HEP may also provide an indication of cell viability and adequacy of reperfusion. The focus of this paper is on myocardial HEP metabolism during cardiac arrest due to ventricular fibrillation (VF), which will be referred to as ventricular fibrillation with total circulatory arrest (VF-TCA). This is to be distinguished from cardiopulmonary bypass studies in which circulation to extra-cardiac organs can be maintained during VF. Since few studies to date have investigated HEP metabolism during in vivo VF-TCA, most of the information presented here is derived from other models of ischemia. Considerable variation exists among these experimental models of myocardial ischemia and the methods used to quantify myocardial HEP. These factors make comparison of studies difficult. For the most part, however, HEP depletion and associated myocardial injury during ischemia

31P-NMR analysis of lethal and sublethal lesions produced by KCl-intoxication in the zebra mussel, Dreissena polymorpha

Noninvasive phosphorus-31 nuclear magnetic resonance spectroscopy (31P-NMR) was utilized to investigate the mechanism of potassium chloride (KCl) toxicity in zebra mussels. 31P-NMR spectra showed several bioenergetically important high energy phosphates, including ATP, ADP, phosphoarginine, and inorganic phosphate. Exposure of mussels to 8.6 mM KCl caused changes in these metabolites and proved lethal to the mussels when exposed over a 24 h period. This result matched that of the molluscicide Bayluscide. Here, losses in phosphoarginine and ATP were accompanied by a rise in inorganic phosphate and a shift toward intracellular acidosis. KCl levels below 8.6 mM caused marked changes in mussel high energy phosphates and pH1. However, these changes were reversible once mussels were returned to fresh standard reference water (SRW). In contrast, mussels exposed to 8.6 mM KCl under hyperbaric conditions (20 mg/L O2) survived during the 24 h KCl exposure and showed normal ATP peaks and pH1. The latter mussels, however, died when O2 supplementation was removed and mussels were transferred to SRW. Exposure to hypoxic conditions (<1.5 mg/LO2) resulted in loss of ATP and reduction in pH1 similar to that produced to exposure to 8.6 mM KCl. The effect of KCl on ciliary beating within the zebra mussel gills was also examined. Ciliary beating stopped in all mussels receiving treatment with KCl including those jointly exposed to 8.6 mM KCl and elevated O2 (20 mg/L). However, ciliary beating resumed in mussels exposed to KCl concentrations less than 4.3 mM when the mussels were transferred to clean SRW. Ciliary beating was not affected by exposure to hypoxic conditions or to elevated O2 alone. These data suggest: (1) cessation of ciliary beat is a specific response to potassium intoxication but is insufficient to cause mussel death; (2) two levels of potassium-induced injury were observed and were dependent upon the concentration of potassium to which mussels were exposed. Exposure to KCl below, 4.3 mM resulted in reversible alterations of gill physiology while exposure to concentrations above 4.3 mM resulted in permanent lesions from which recovery was not possible.

Human rapid acquisition with relaxation enhancement imaging at 8 T without specific absorption rate violation

A standard fast imaging sequence, rapid acquisition with relaxation enhancement (RARE), has been applied to human magnetic resonance at 8 T. RARE is known for its speed, good contrast and high RF power content. HighlyT2 weighted images, the hallmark of RARE imaging, were acquired from the human brain. It is demonstrated that whileT2 values may be reduced at 8 T, high quality RARE images could still be acquired at this field strength. Most importantly however, it is demonstrated that RARE images could be acquired without violating specific absorption rate (SAR) guidelines. Since it is well known thatT2 weighted images are of significant value in clinical diagnosis, the implementation of RARE at this field strength will provide ultra high field MRI (UHFMRI) with a valuable imaging protocol at this field strength without exceeding SAR limitations.

MDEFT imaging of the human brain at 8 T

T1-weighted images of the human brain obtained with the MDEFT sequence at 8 T are presented. These images are characterized by an excellent contrast and good signal to noise ratio. Importantly, results were obtained with adiabatic spin inversion and demonstrate that such pulses can be used event in the ultra high frequency (>300 MHz) range. It is thus possible to obtain high quality results at this field strength without violating SAR guidelines.

Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine.

Objective: To determine whether epinephrine in combination with high flow worsens left ventricular (LV) myocardial high‐energy phosphate stores during reperfusion of ischemic ventricular fibrillation (VF). Design: Blinded, prospective block randomized, placebo controlled study. Setting: University medical center research laboratory. Subjects: A total of 22 mixed breed swine weighing 22.0 ± 3.3 kg (SD). Interventions: Open‐chest swine, anesthetized with α‐chloralose, underwent 10 mins of nonperfused VF followed by reperfusion with cardiopulmonary bypass for 90 mins and then defibrillation. Animals were block randomized to four groups for reperfusion: Group 1 (n = 5), high flow (100 mL/kg/min) and epinephrine (2.5 μg/kg/min); Group 2 (n = 5), high flow and placebo; Group 3 (n = 6), low flow (30 mL/kg/min) and epinephrine; and Group 4 (n = 6), low flow and placebo. Measurements and Main Results: In vivo LV creatine phosphate (CP) and adenosine triphosphate (ATP) were determined using whole wall and spatially localized 31P NMR spectroscopy at 4.7 Tesla. During perfusion of the fibrillating myocardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation rates (p < .01). ATP levels during reperfusion were significantly decreased within all groups compared with baseline. There were no differences in ATP levels between groups. High flow, independent of epinephrine, was associated with increased preservation of ATP (p < .05), increased CP/ATP ratios (p < .02) in all layers of the LV wall, and decreased aortic and cardiac vein lactates (p < .001). Conclusions: Epinephrine, in combination with flow higher than standard cardiopulmonary resuscitation flows, increased perfusion pressure and defibrillation rates, but did not significantly alter myocardial ATP during VF reperfusion in the in vivo heart. Reperfusion flow, independent of epinephrine, is a critical determinant of myocardial ATP preservation.