Intrathecal midazolam reduces isoflurane MAC and increases the apnoeic threshold in rats

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - The purpose of this study was to examine the anaesthetic requirement of intrathecal midazolam in a dose-response fashion in...     

In vivo myocardial infarct area at risk assessment in the rat using manganese enhanced magnetic resonance imaging (MEMRI) at 1.5T.

The aim of this study was to measure the myocardial area at risk in rat, using MRI and manganese injection during a coronary occlusion/reperfusion model at 1.5T. A sequential protocol with occlusion and MnCl2 injection immediately followed by MRI was used with the assumption that MnCl2-induced contrast persistence is enough to accurately image the area at risk 90 min after occlusion. A total of 15 adult rats underwent a single 30-min episode of coronary occlusion followed by reperfusion. MnCl2 was injected (25 micromol/kg) at the beginning of the occlusion for 11 rats (group 1) and 6 h after reperfusion for four animals (group 2). A deficit of signal enhancement was observed in all rats. Hypoenhancement area in group 1 was correlated to the area at risk delineated by methylene blue (r=0.96, P<0.0001) whereas in group 2 it was correlated to the infarct area given by triphenyltetrazolium chloride (TTC) solution (r=0.98, P=0.003). The area at risk size was significantly correlated with left ventricle ejection fraction (LVEF), end-systolic volume and anterolateral wall thickening. This work demonstrates that hypoenhanced zone obtained after manganese injection during occlusion represents the area at risk and not only the infarct zone.     

Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction

Non-infarcted myocardium after coronary occlusion undergoes progressive morphological and functional changes. The purpose of this study was to determine whether non-infarcted myocardium exhibits (1) alteration of the substrate pattern of myocardial metabolism and (2) concomitant changes in the expression of regulatory proteins of glucose and fatty acid metabolism. Myocardial infarction was induced in rats by ligation of the left coronary artery. One day and eight weeks after coronary occlusion, glucose and palmitate oxidation were measured. Expression of selected proteins of metabolism were determined one day to 12 weeks after infarction. One day after coronary occlusion no difference of glucose and palmitate oxidation was detectable, whereas after eight weeks, glucose oxidation was increased (+84%, P<0.05) and palmitate oxidation did not change significantly (-19%, P=0.07) in infarct-containing hearts, compared with hearts from sham-operated rats. One day after coronary occlusion, myocardial mRNA expression of the glucose transporter GLUT-1 was increased (+86%, P<0.05) and the expression of GLUT-4 was decreased (-28%, P<0.05) in surviving myocardium of infarct-containing hearts. Protein level of GLUT-1 was increased (+81%, P<0.05) and that of GLUT-4 slightly, but not significantly, decreased (-16%, P=NS). mRNA expressions of heart fatty acid binding protein (H-FABP), and of medium chain acyl-CoA dehydrogenase (MCAD), were decreased by 36% (P<0.05) and 35% (P=0. 07), respectively. Eight weeks after acute infarction, the left ventricle was hypertrophied and, at this time-point, there was no difference in the expression of GLUT-1 and GLUT-4 between infarcted and sham-operated hearts. However, myocardial mRNA and protein content of MCAD were decreased by 30% (P<0.01) and 27% (P<0.05), respectively. In summary, in surviving myocardium, glucose oxidation was increased eight weeks after coronary occlusion. Concomitantly, mRNA and protein expression of MCAD were decreased, compatible with a role of altered expression of regulatory proteins of metabolism in post-infarction modification of myocardial metabolism.     

Noninvasive measurement of absolute renal perfusion by contrast medium-enhanced magnetic resonance imaging

OBJECTIVE: The aim of this study was to validate the quantification of absolute renal perfusion (RP) determined by dynamic magnetic resonance imaging (MRI) and contrast media using an experimental model in the rabbit and a transit-timed ultrasound flow probe around the left renal artery as comparison. MATERIAL AND METHODS: An MR-compatible ultrasonic time-of-flight flow-probe was placed around the left renal artery in 9 New Zealand white rabbits. Absolute RP in basal state, after mechanical renal artery stenosis, intravenous dopamine, angiotensin II, or colloid infusion was measured using dynamic MRI and intravenous injection of gadoteridol. The results were correlated to the renal artery flow measured inside the magnet with the transit-timed flow-probe. For the signal intensity concentration conversion, we applied different calibrations according to various velocities measured in the aorta by a phase contrast sequence to correct for inflow effect. MRI-derived RP (in mL/min) was calculated by the maximum upslope method, where RP/volume was defined as the ratio of the cortex contrast enhancement slope over the maximum of the arterial input function determined in the aorta. RESULTS: Reproducible arterial and renal transit curve with excellent contrast to noise ratio were obtained. The MRI derived perfusion was systematically underestimated by comparison to the ultrasonic transit-timed flow-probe but was linearly correlated with these measures (r = 0.80, P < 0.001). CONCLUSIONS: Using a flow-sensitive calibration, an accurate arterial input function can be measured from the blood MR signal and used in a realistic model to assess the RP. There was a good correlation between the MR-derived RP and the renal artery blood flow measured by the flow-meter. This experimental study validates absolute RP quantification by MRI and contrast media injection and justifies further clinical studies.