Influence of desflurane on regional distribution of coronary blood flow in a chronically instrumented canine model of multivessel coronary artery obstruction

The influence of desflurane on myocardial perfusion measured by a microsphere technique during a total occlusion of the left anterior descending coronary artery and concomitant moderate or severe stenosis of the left circumflex coronary artery was evaluated in chronically instrumented dogs. Hemodynamics, regional contractile function, and myocardial blood flow were measured during the conscious state and after anesthesia with desflurane (8.2%-9.2% and 12.5%-12.7%) with and without control of arterial pressure. Total left anterior descending occlusion produced in combination with a left circumflex coronary artery stenosis significantly (P less than 0.05) increased heart rate and left ventricular end diastolic pressure in the absence of desflurane anesthesia. Desflurane, administered only in the presence of left anterior descending occlusion and left circumflex stenosis, significantly (P less than 0.05) decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular positive dP/dt50 without change in heart rate. Blood flow to the subendocardium of normal myocardium was reduced during the high concentration of desflurane (P less than 0.05), but perfusion of the subepicardium and midmyocardium was maintained at conscious levels. When the left circumflex stenosis was of moderate severity, only blood flow to the subendocardium distal to the stenosis was reduced by desflurane (P less than 0.05). In the presence of a severe stenosis, perfusion was decreased in the subepicardium, midmyocardium, and subendocardium of the stenotic zone (P less than 0.05). During the reduction in arterial pressure produced by desflurane, collateral blood flow in the left anterior descending region was reduced in dogs with either a moderate or severe left circumflex stenosis (P less than 0.05). When arterial pressure and heart rate conditions observed in the postocclusion conscious state were restored during the high concentration of desflurane, myocardial blood flow in all regions returned to those levels present in the conscious state (P less than 0.05). Ratios of flow between occluded and normal zones were decreased when hypotension produced by desflurane was uncontrolled, but when arterial pressure and heart rate were adjusted to conscious postocclusion levels using partial thoracic aorta occlusion and atrial pacing, the ratio remained at conscious control levels regardless of the degree of left circumflex stenosis severity (P less than 0.05). Results of this investigation indicate that desflurane does not redistribute blood flow away from collateral-dependent myocardium to other regions via a "coronary steal" mechanism in a chronically instrumented canine model of multivessel coronary artery disease.     

Recovery of contractile function of stunned myocardium in chronically instrumented dogs is enhanced by halothane or isoflurane

Following brief periods (5-15 min) of total coronary artery occlusion and subsequent reperfusion, despite an absence of tissue necrosis, a decrement in contractile function of the postischemic myocardium may nevertheless be present for prolonged periods. This has been termed "stunned" myocardium to differentiate the condition from ischemia or infarction. Because the influence of volatile anesthetics on the recovery of postischemic, reperfused myocardium has yet to be studied, the purpose of this investigation was to compare the effects of halothane and isoflurane on systemic and regional hemodynamics following a brief coronary artery occlusion and reperfusion. Nine groups comprising 79 experiments were completed in 42 chronically instrumented dogs. In awake, unsedated dogs a 15-min coronary artery occlusion resulted in paradoxical systolic lengthening in the ischemic zone. Following reperfusion active systolic shortening slowly returned toward control levels but remained approximately 50% depressed from control at 5 h. In contrast, dogs anesthetized with halothane or isoflurane (2% inspired concentration) demonstrated complete recovery of function 3-5 h following reperfusion. Because the anesthetics directly depressed contractile function, additional experiments were conducted in which a 15-minute coronary artery occlusion was produced during volatile anesthesia; however, each animal was allowed to emerge from the anesthetized state at the onset of reperfusion. Similar results were obtained in these experiments, demonstrating total recovery of contractile function within 3-5 h following reperfusion. Thus, despite comparable degrees of contractile dysfunction during coronary artery occlusion in awake and anesthetized dogs, the present results demonstrate that halothane and isoflurane produce marked improvement in the recovery of segment function following a transient ischemic episode. Therefore, volatile anesthetics may attenuate postischemic left ventricular dysfunction occurring intraoperatively and enhance recovery of regional wall motion abnormalities during reperfusion.     

From Deutsche Zeitschrift to International Journal of Legal Medicine—100 years of legal medicine through the lens of journal articles

From its launc h in 1922 to the end of the Second World War, the Deutsche Zeitschrift für die gesamte gerichtliche Medizin spanned 38 volumes. The 1762 papers contained in those volumes reflect contemporary interests and include many papers from peripheral fields and non-medico-legal disciplines. Publications concerned with issues outside core legal medicine fields in particular allow two distinct tendencies in the development of German institutes of legal medicine to be discerned. Firstly, there is a focus on the psychological and psychiatric aspects of the discipline. Secondly, there is tendency towards a scientific-criminalistic outlook. The fatal consequences of the Nazi seizure of power in 1933 did not spare the sciences. For legal medicine, a discipline with close links to the state, it is unsurprising that fundamental changes to the political system had a significant impact on subject matter. Leaving aside articles notable principally for their ideological content, our analysis of the 38 volumes shows that the papers examined contain new insights into many subjects, some of which are still valid today.

     

Editorial

International Journal of Legal Medicine -     

Anatomical reconstruction of the medial patellofemoral ligament using a free gracilis autograft

Since biomechanical studies have shown that the medial patellofemoral ligament (MPFL) is the main restraint against lateral patella displacement, reconstruction of the MPFL has become an accepted surgical technique to restore patellofemoral stability. Recently, various procedures have been described that address reconstruction of the medial patellofemoral complex. We present a technique, where the MPFL is reconstructed anatomically to restore physiological kinematics and stability, using a free gracilis tendon autograft.     

Electron microscopic stereology of capillary endothelial cells and cardiomyocytes in artificially arrested canine hearts

In open heart surgery and transplantation, sufficient structural preservation of the myocardium immediately following cardioplegic arrest is a precondition for overcoming ischemia and for resumption of postischemic function. Therefore, we compared the protective effect of three clinically applied cardioplegic solutions with fibrillating and beating hearts using structural criteria. Left ventricular samples were taken from (1) beating, or (2) fibrillating or arrested hearts following coronary perfu-sion with (3) St. Thomas' Hospital solution, (4) histidine tryptophane ketoglutalate (HTK) (Custodiol), or (5) University of Wisconsin (UW) solution and fixed by immersion. Ultrastructural differences in the swelling of capillary endothelial cells and myocytes were quantitatively evaluated using stereological methods. Endothelial cells were somewhat more swollen after St. Thomas perfusion than those in beating and fibrillating hearts. HTK-arrested hearts showed significantly lower values for cellular edema than beating hearts. UW perfusion resulted in the (significantly) lowest degree of endothelial cell edema. Edematous changes in myocytes were significantly greater in St. Thomas-arrested hearts than in UW- or HTK-arrested hearts. Cardiomyocyte edema in beating and fibrillating hearts was comparable to that in St. Thomas-perfused hearts. Thus, the stereol-ogical analysis revealed significant differences between cardioplegic solutions in structural preservation of myocardial ultrastructure.     

Dexmedetomidine modulates cardiovascular responses to stimulation of central nervous system pressor sites

Halothane attenuates the alterations in arterial pressure (BP) and heart rate (HR) produced by central nervous svstem (CNS) stimulation. We examined the effects of the alpha2-adrenergic agonist dexmedetomidine, with and without halothane, on cardiovascular regulation during CNS pressor site stimulation in chronically instrumented cats. Stimuli trains via bipolar stimulating electrodes in the hypothalamus and reticular formation elicited pressor responses. Dexmedetomidine-induced (15 microg/kg PO) bradycardia was greater in the presence of halothane. CNS stimulation increased BP and HR, which were dose-dependently attenuated by halothane (hypothalamic stimulation 71 +/- 9 mm Hg at control, 25 +/- 5 and 15 +/- 3 mm Hg at 1.0% and 1.5% halothane, respectively). Although dexmedetomidine alone did not alter pressor responses, halothane plus dexmedetomidine attenuated pressor responses in a potentially synergistic fashion (hypothalamic stimulation 67 +/- 8 mm Hg at control, 2 +/- 1 and 1 +/- 0.4 mm Hg at 1.0% and 1.5% halothane, respectively). These results suggest differences in the disruptive effects of CNS-mediated cardiovascular responses by halothane and dexmedetomidine, and that dexmedetomidine has an anesthetic-sparing effect on these CNS-mediated cardiovascular control mechanisms, potentiating the depressant effect of halothane. IMPLICATIONS: A new potential anesthetic adjunct, dexmedetomidine, does not attenuate brain-mediated increases in blood pressure, but the combination of dexmedetomidine and the anesthetic halothane acts to modulate central cardiovascular responses.