Effects of desflurane on the pig intestinal circulation during hypotension.

BACKGROUND: The aim of the present study was to analyze the perfusion pressure dependency for the splanchnic vascular effects of desflurane (DES). METHODS: We measured portal blood flow (QPORT, perivascular ultrasound) and jejunal mucosal perfusion (JMP; laser Doppler) in pentobarbital-anesthetized pigs (n=10). Experimentally, decreases in mean arterial pressure (MAP) were produced by pericardial infusions of dextran. The protocol included sets of measurements at incremental doses of DES (1, 2, 4 and 6%) prior to and during pericardial infusions. RESULTS: Although QPORT and JMP decreased significantly during pericardial infusions, DES, irrespective of dose, did not reduce QPORT until MAP had decreased below 65-70 mm Hg. In higher MAP ranges, vasodilation in pre-portal tissues was powerful enough to maintain QPORT in spite of concurrent decreases in driving arterial pressure, as produced by either DES or pericardial infusion, or by a combination of both. We found no effects of DES on JMP even at very low MAP (about 40 mm Hg during pericardial infusion), indicating that the normal physiological response of the small intestine to redistribute blood flow from deeper to more superficial layers during hypotension was unimpaired by DES. CONCLUSIONS: Our data suggest a wide dose-tolerability of DES as regards the splanchnic circulation during hypotensive states.

The effects of desflurane on cardiac function as measured by conductance volumetry in swine.

UNLABELLED: The purpose of the investigation was to assess the effects of desflurane (DES) on left ventricular heart function during basal barbiturate anesthesia in a closed-pericardium, closed-chest acute swine model. The study was performed in 11 normoventilated adult pigs. Hemodynamic measurements were obtained using arterial, central venous, and pulmonary artery catheters, as well as a conductance volumetry and tip manometry catheter placed in the left ventricle. Hemodynamic measurements were recorded during basal pentobarbital anesthesia and with the addition of 1%, 2%, 4%, and 6% DES. DES dose-dependently decreased mean arterial pressure, systemic vascular resistance, left ventricular end-systolic pressure, dP/dtMAX and dP/dtMIN. At doses >1%, decreases in CO, stroke volume, ejection fraction, end-systolic elastance, preload recruitable stroke work, preload adjusted maximal power, and peak filling rate were observed. Heart rate decreased at 4% and 6% DES. Isovolumetric relaxation time increased only at 6% DES. We conclude that smaller doses of DES have a significant cardiodepressive effect in the setting of barbiturate infusion, as measured by conductance volumetry. IMPLICATIONS: Desflurane, in very small doses, depressed cardiac function during pentobarbital anesthesia with ketamine and benzodiazepine premedication in swine, as assessed by conductance volumetry and left ventricular pressure and volume relationship analysis. These results suggest that desflurane, in combination with certain anesthetics, can be cardiodepressive even in very small doses.

Autoregulation and vasodilator responses by isoflurane and desflurane in the feline renal vascular bed.

BACKGROUND: Inhalational anesthetics have agent-specific effects on the renal circulation. This study investigated renal vasodilator responses produced by either autoregulation, 0.8% isoflurane (ISO) or 3.5% desflurane (DES). METHODS: We measured systemic mean arterial pressure (MAP-SYST; axillary artery), renal blood flow (QREN; perivascular ultrasound) and central venous pressure (CVP) in normoventilated cats (n = 8) during basal chloralose anesthesia (control) and after the addition of ISO and DES. Renal mean arterial pressure (MAPREN) was controlled by an aortic clamp. QREN was measured at pre-set-MAPREN levels of 50, 70 and 90 mmHg. Renal vascular resistance (RREN) was derived. RESULTS: When MAPREN was artificially restrained from 133 +/- 5 mmHg to 90 mmHg during control, RREN decreased by 35% and no significant change in QREN was observed, reflecting an intact autoregulation. RREN levels during ISO or DES at stages with unrestrained MAPREN (95 +/- 6 and 102 +/- 9 mmHg, respectively), were not significantly different from RREN at 90 mmHg during control. When MAPREN was artificially decreased below 90 mmHg, QREN decreased in a similar fashion among control and ISO/DES sequences. The autoregulatory capacity was not significantly different among these sequences. Between 90-70 mmHg, the autoregulatory capacity was reduced and not demonstrable below 70 mmHg. CONCLUSION: The renal autoregulatory capacity was not attenuated by either ISO or DES. These agents produced equipotent renal vasodilation, which was not more powerful than that produced by autoregulation alone. The renal vasorelaxant effects of ISO and DES may therefore to a substantial extent be attributable to autoregulation.

Low cardiac output abolishes cardiovascular responses to infra-renal aortic cross-clamping in the pig.

BACKGROUND: Previous data suggest that preoperative myocardial dysfunction is associated with an altered cardiac response to infra-renal aortic cross-clamping (AXC). This study was designed to further explore how acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC. METHODS: In chloralose-anesthetized normoventilated pigs, graded increases in pericardial pressure (PPERICARD) were obtained by local infusions of dextran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAPPROX) and ultrasonic flowmetry for portal (QPORT) and renal (QREN) blood flows. In all animals, measurements were made a) prior to AXC, b) at the end of a 5 min AXC period and, c) 5 min following declamping. These recordings were repeated during control (PPERICARD 0 cmH2O) and during stages with increased PPERICARD (4 and 8 cmH2O, respectively). RESULTS: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to PPERICARD levels. Stroke volume, CO and mean arterial pressure decreased, while systemic vascular resistance (SVR) increased. In the preportal tissues, vascular resistance increased and QPORT decreased. Similarly, in the kidney, vascular resistance and QREN decreased, but only at a PPERICARD of 8 cmH2O. At control, AXC increased SVR, MAPPROX, QPORT and both renal and preportal vascular resistances. When PPERICARD was increased to 4 cm H2O, the responses to AXC concerning SVR and MAPPROX were not significantly altered, while renal and preportal circulatory responses were blunted. At stages with a PPERICARD of 8 cmH2O, we could not demonstrate any circulatory responses to AXC. CONCLUSIONS: AXC-induced systemic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output.

Effects of desflurane on systemic, preportal and renal circulatory responses to infra-renal aortic cross-clamping in the pig.

BACKGROUND: Different pharmacological approaches have been used in the control of cardiovascular responses to surgical infra-renal aortic occlusion (AXC). The aim of the present study was to explore the modulatory effects of desflurane (DES) on these responses. METHODS: The study was performed in normoventilated chloralose-anesthetized pigs (n = 14). Measurements included cardiac output (CO), pulmonary vascular pressures, heart rate (HR) and mean arterial pressure proximal to the AXC site (MAPPROX). Renal arterial (QREN) and portal venous (QPORT) blood flows were measured ultrasonically. Systemic (SVR), preportal (RPORT) and renal (RREN) vascular resistances were derived. Sets of measurements were done a) prior to, b) during and c) 5 min after AXC. This was repeated, in a randomized fashion, at control (no DES) and with 4.9% and 9.8% DES, respectively. RESULTS: DES decreased MAPPROX, CO, HR, SVR, RREN and RPORT. At control, AXC increased MAPPROX (+27%), SVR (+27%), QPORT (+14%), RPORT (+12%) and RREN (+43%). DES 4.9% did not change this response pattern. With 9.8% DES, the AXC-induced increases in MAPPROX (+17%) and SVR (+21%) were attenuated. At this stage, AXC caused no demonstrable changes in RREN or RPORT, while both QREN (+16%) and QPORT increased (+9%). CONCLUSIONS: DES effectively controlled increases in proximal blood pressure during AXC. The increases in RREN and RPORT that were seen during AXC at control were inhibited by 9.8% DES. Consequently, at this DES dose, both QREN and QPORT increased during AXC.

Vasodilator effects of desflurane and isoflurane in the feline small intestine.

The influence of desflurane (DES) and isoflurane (ISO) on the intestinal vasculature was investigated in normoventilated cats (n = 10) during basal chloralose anesthesia (control). We measured heart rate, mean arterial pressure (MAP), and intestinal blood flow (optical drop flowmetry). Intestinal vascular resistance (IVR) was derived. To avoid changes in local vascular tone related to alterations in transmural pressure gradients, intestinal arterial pressure was controlled and kept constant by a variable aortic clamp. Measurements were performed during control and during the administration of DES (3.5% and 7.0% end-tidal) or ISO (0.8% and 1.6% end-tidal). Each animal was exposed to both agents, prior to and after intestinal postganglionic denervation. In the innervated intestine, both DES and ISO dose-dependently decreased IVR. At the high dose, DES (50 +/- 10% decrease in IVR) was a significantly more powerful vasodilator than ISO (37 +/- 12% decrease in IVR). In the denervated intestine, less pronounced vasodilations were produced by both DES and ISO, as compared to the innervated state, and there were, in this situation, no significant differences between agents concerning the magnitude of the vasodilation. As indicated by comparisons between the innervated versus the denervated state, both neurogenic and non-neurogenic mechanisms contributed to the vasodilator responses. The vascular relaxation at the high dose was for ISO associated with a significantly more powerful non-neurogenic vasodilation, and for DES associated with a significantly more powerful neurogenic vasodilation. This suggests that withdrawal of sympathetic neurogenic vasoconstrictor tone is more important for the vasodilation produced by DES than it is for ISO.