Anaesthetic techniques affect vascular responsiveness in experimental hemorrhagic shock

Clinical and experimental circulation was injected intravenously in both groups and then data collection was performed. In group R, hydroxyethyl-starch was continuously infused at a rate of 1 ml/kg/min for 25 min. Data were obtained at 5 and 60 min after fluid resuscitation in group R and at same timing in group N. Correlations between CBV and the parameters were analyzed using linear regression analysis. P ! 0.05 was considered statistically significant. Results and Discussions: The correlation between CBV and total power (R2 " 0.241, p " 0.0004) of PSSAPV was more significant as compared to high frequency (R2 " 0.172, p " 0.003), low frequency (R2 " 0.105, p " 0.025) of PSSAPV, and central venous pressure (R2 " 0.113, p " 0.020), while no correlations were noted between CBV and SPV (R2 " 0.065, p " 0.080), PPV (R2 " 0.025, p " 0.283), and mean arterial pressure (R2 " 0.003, p " 0.692). Conclusion(s): Total power of PSSAPV best reflected the changes of CBV even in endotoxin induced hypotension as compared to conventional circulatory parameters. Reference: 1

55

higher survival rate, smaller infarct size as compared to poor collaterals (2). We tested the hypothesis that diabetes inhibits the coronary collateral development in a canine model of repetitive coronary occlusion. Materials and Methods: Dogs were subjected to brief (2 min), repetitive coronary artery occlusions (1/h, 8/day, 21day duration) in the absence (control) or presence of diabetes (diabetes). A sham group was instrumented identically but received no occlusion. Myocardial blood flow was determined in the myocardium perfused by the LAD and the LCCA. Peak reactive hyperemia response (PRH) was recorded. Collateral blood flow was expressed as the percentage of normal zone blood flow. Results and Discussions: Coronary collateral blood flow was shown in the figure. PRH in the control group was significantly lower than that on day 1. PRH remained unchanged in the diabetes and the sham group. Conclusion(s): Diabetes inhibits the development of coronary collateral blood flow.

Lai HY, Yang CCH, Huang FY, et al. Clin. Sci. 2003; 105: 491–497.

100 Coronary collateral blood flow (% of normal zone)

4AP9-3 Anaesthetic techniques affect vascular responsiveness in experimental hemorrhagic shock I. Samarska, A.H. Epema, H. Buikema, L.P.H.J. Aarts, R.H. Henning Departments of Anesthesiology and Clinical Pharmacology, University Medical Center Groningen, Groningen, The Netherlands Background and Goal of Study: Altered vascular reactivity after severe hemorrhagic shock may be influenced by the choice of anaesthetic technique and interfere with the therapeutic effectiveness of vasoactive agents. The aim of the present study was to explore the changes in vascular reactivity following hemorrhagic shock using two types of general anaesthesia. Materials and Methods: After institutional approval, mice (n " 24) were randomized to undergo hemorrhagic shock (90 min, 30 mmHg) by withdrawal of blood, or a sham-procedure. Half of the animals were anaesthetized with isoflurane (ISO, 1.4%), the other half received additional nitrous oxide (N2O, 66%). Vasomotor responses were studied in 2-mm rings of aorta mounted in a wired myograph. Results and Discussions: Contraction to phenylephrine (PE) was increased in shock-mice anaesthetized with ISO compared to SHAM (P ! 0.05; fig). In contrast, addition of N2O to ISO resulted in similar PE-evoked contractions in mice with and without shock (fig). In SHAM, acetylcholine (ACh) caused a biphasic curve consisting of an initial relaxation followed by a contractile response sensitive to the COX-inhibitor indomethacin (1 #M). In contrast, in ISO animals undergoing shock, ACh evoked only relaxing responses. Isoflurane & N2O

Isoflurane

Contraction (mN)

5

Shock Sham

4

Shock Sham

3

*

2 1 0 '10 '9 '8 '7 '6 '5

'10 '9 '8 '7 '6 '5

'Log [PE]

'Log [PE]

Conclusion(s): Short-term hemorrhagic shock affects both contractile and relaxing vasomotor responses in aortic rings of mice anaesthetized with ISO. Addition of nitrous oxide attenuates shock-dependent changes. References: Savoye G. Shock 2005; 23 (5): 411–416. Baumert J.-H. BJA 2005; 94 (6): 727–32.

4AP9-4 Diabetes inhibits coronary collateral development in a canine model of repetitive coronary occlusion W. Gu, B. Yu, J. Tessmer, D. Warltier, J. Kersten Department of Anesthesiology, Ruijin Hospital, Shanghai, China Background and Goal: Diabetic individuals with acute coronary syndrome have an increased risk of adverse cardiovascular events (1). Recent studies demonstrated that a well-developed collateral circulation is associated with

Control Diabetes Sham

80

* *

60

*

40

& &

&

20

&

& &

0 1d

7d

14 d

21 d

Fig. *P ! 0.05 vs day 1; †P ! 0.05 vs the respective value in the control group.

References: 1 2

Fergus TS, Fazel R, Fang J, et al. Heart 2004; 90: 1051–1052. Perez-Castellano N, Garcia EJ, Abeytua M, et al. J Am Coll Cardiol 1998; 31: 512–518.

4AP9-5 Alterations of mitochondrial apoptotic pathways in loadinduced right ventricular failure C. Dewachter, B. Rondelet, L. Dewachter, S. Brimioulle, F. Kerbaul Service d’Anesthésiologie Réanimation, Hopital ERASME, Bruxelles, Belgium Background and Goals: We previously reported an experimental model of persistent right ventricular (RV) failure consecutive to a transient, 90-min increase in afterload induced by pulmonary arterial banding (1). We hypothesized that this particular type of ventricular stunning might be related to an early activation of apoptotic pathways. Material and Methods: Pulmonary arterial elastance (Ea) and RV end-systolic elastance (Ees) were determined by a single beat method (2) in 7 anaesthetized dogs before and 30 min after the release of a transient PA banding. The animals were killed by an anaesthetic overdose and RV and left ventricular (LV) myocardial tissue sampled for the measurements of mitochondrial mRNA of Bax (proapoptotic) and Bcl-2 (antiapoptotic) by real time polymerase chain reaction (RTQPCR). The Bax/Bcl-2 ratio was taken as an index of apoptototic activity. Results and Discussion: Values are reported as mean $ SEM. The transient increase in PA pressure persistently increased right atrial pressure from 8.0 $ 0.4 to 10.0 $ 0.8 mmHg (P ! 0.05), Ea from 0.99 $ 0.05 to 2.86 $ 0.15 mmHg/ml (P ! 0.05), and decreased Ees from 1.12 $ 0.05 to 0.55 $ 0.03 mmHg/ml (P ! 0.05), Ees/Ea from 1.14 $ 0.06 to 0.20 $ 0.02 (P ! 0.05), and cardiac output from 4.5 $ 0.1 to 2.3 $ 0.1 L/min (P ! 0.05), indicating RV failure with altered RV-arterial coupling. As compared to 8 normal control dogs, RV Bax/Bcl-2 mRNA was increased (1.86 $ 0.35 vs. 1.00 $ 0.30; P ! 0.05), while LV Bax/Bcl-2 mRNA was not different (1.61 $ 0.41 vs. 1.00 $ 0.30; P % 0.05). Conclusion: An early induction of apoptotic pathways may be involved in persistent RV failure induced by a transient increase in pulmonary artery pressure. References: 1 2

Kerbaul et al. Crit Care Med. 2004; 32: 1035–40. Brimioulle et al. Am J Physiol. 2003; 284: H1625–30.