Vitas Zemgulis

Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study.

Background: Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. Methods: Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation‐perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double‐indicator distribution technique, and atelectasis was analyzed by computed tomography. Results: Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/‐ 6.2% vs. 3.5 +/‐ 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/‐ 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/‐ 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/‐ 1.9%) but still more (P < 0.05) than the controls (1.1 +/‐ 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). Conclusions: Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post‐CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.

Use of a Vital Capacity Maneuver to Prevent Atelectasis after Cardiopulmonary Bypass An Experimental Study

Background Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors previously found that the increase in intrapulmonary shunt was well correlated with the amount of atelectasis. They tested the hypothesis that post‐CPB atelectasis can be prevented by a vital capacity maneuver (VCM) performed before termination of the bypass. Methods Eighteen pigs received standard hypothermic CPB (no ventilation during bypass). The VCM was performed in two groups and consisted of inflating the lungs during 15 s to 40 cmH2 O at the end of the bypass. In one group, the inspired oxygen fraction (FIO2) was then increased to 1.0. In the second group, the FIO2 was left at 0.4. In the third group, no VCM was performed (control group). Ventilation‐perfusion distribution was measured with the inert gas technique and atelectasis by computed tomographic scanning. Results Intrapulmonary shunt increased after bypass in the control group (from 4.9 +/‐ 4% to 20.8 +/‐ 11.7%; P < 0.05) and was also increased in the vital capacity group ventilated with 100% oxygen (from 2.2 +/‐ 1.3% to 6.9 +/‐ 2.9%; P < 0.01) but was unaffected in the vital capacity group ventilated with 40% oxygen. The control pigs showed extensive atelectasis (21.3 +/‐ 15.8% of total lung area), which was significantly larger (P < 0.01) than the proportion of atelectasis found in the two vital capacity groups (5.7 +/‐ 5.7% for the vital capacity group ventilated with 100% oxygen and 2.3 +/‐ 2.1% for the vital capacity group ventilated with 40% oxygen. Conclusion In this pig model, postcardiopulmonary bypass atelectasis was effectively prevented by a VCM.

Nucleoside transport inhibition in ischemic myocardium results in enhanced taurine efflux.

We measured with the microdialysis technique energy-related metabolites in ischemic myocardium over time in an experimental pig model. Emphasis was put on the dipyridamole effect when administered in the microdialysis probe inserted in ischemic myocardium. Not only adenosine but also taurine and pyruvate concentrations were significantly higher in the microdialysate during the periods of ischemia and extracorporeal circulation with cardioplegia. The enhanced efflux of taurine in ischemic myocardium induced by dipyridamole is a new finding. A mechanistic role of taurine in the prevention of Ca(2+) overload in ischemic myocytes is discussed. Also, taurine may have stimulatory effects on glycolysis in ischemic heart.

Influence of blood/tissue differences in contrast agent relaxivity on tracer-based MR perfusion measurements

AbstractPurposenPerfusion assessment by monitoring the transport of a tracer bolus depends critically on conversion of signal intensity into tracer concentration. Two main assumptions are generally applied for this conversion; (1) contrast agent relaxivity is identical in blood and tissue, (2) change in signal intensity depends only on the primary relaxation effect. The purpose of the study was to assess the validity and influence of these assumptions.Materials and methodsBlood and cerebral tissue relaxivities r1, r2, and r2* for gadodiamide were measured in four pigs at 1.5xa0T. Gadolinium concentration was determined by inductively coupled plasma atomic emission spectroscopy. Influence of the relaxivities, secondary relaxation effects and choice of singular value decomposition (SVD) regularization threshold was studied by simulations.ResultsIn vivo relaxivities relative to blood concentration [in s−1xa0mM−1 for blood, gray matter (GM), white matter (WM)] were for r1 (2.614xa0±xa01.061, 0.010xa0±xa00.001, 0.004xa0±xa00.002), r2 (5.088xa0±xa00.952, 0.091xa0±xa00.008, 0.059xa0±xa00.014), and r2* (13.292xa0±xa03.928, 1.696xa0±xa00.157, 0.910xa0±xa00.139). Although substantial, by a nonparametric test for paired samples, the differences were not statistically significant. The GM to WM blood volume ratio was estimated to 2.6xa0±xa00.9 by r1, 1.6xa0±xa00.3 by r2, and 1.9xa0±xa00.2 by r2*. Secondary relaxation was found to reduce the tissue blood flow, as did the SVD regularization threshold.ConclusionContrast agent relaxivity is not identical in blood and tissue leading to substantial errors. Further errors are introduced by secondary relaxation effects and the SVD regularization.

Discrepant outcome between myocardial energy-related metabolites and infarct size limitation during retroperfusion of the coronary sinus.

The basic idea of retroperfusion of the coronary sinus (RCS) is to ameliorate detrimental consequences of myocardial ischaemia. Several experimental models of RCS have been introduced, most with an emphasis on functional myocardial status. Since only few studies have been devoted to energy metabolic considerations and none to continuous monitoring of energy-related metabolites of myocardium during RCS, we here present such a study using microdialysis. This study comprised the following components: Coronary occlusion and drainage on the beating heart with RCS-assist (60 min), hypothermic (30°C) extracorporeal circulation (ECC) and cardioplegia (45 min), reperfusion and rewarming to 38°C on ECC (30 min). The microdialysis analytical outcome mainly reflected anaerobic energy metabolism in potentially ischaemic myocardium. Additionally, a pronounced increase of microdialysate content of lactate, pyruvate and guanosine was observed in non-ischaemic myocardium especially during the reperfusion phase. The planimetric calculation revealed an infarct size reduction from 69% to 19% and was not correlated to clear-cut improvements of potentially ischaemic myocardial energy metabolism. We conclude that prolonged (60 min) anaerobic energy metabolism does not pose an immediate threat to cell viability but could even sustain myocyte survival.