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O Winsö

Publications and source records attributed to O Winsö.

At least 19 recordsLinked to original sources
PubMed2003

Do lung recruitment maneuvers decrease gastric mucosal perfusion?

OBJECTIVE: To evaluate effects of lung recruitment maneuvers on gastric mucosal perfusion, systemic circulation, and lung mechanics in patients with acute lung injury. DESIGN: Prospective observational clinical study. SETTING. General intensive care unit of university hospital. PATIENTS AND PARTICIPANTS: Fourteen patients with acute lung injury (ten in the main study group and four in a validation group). INTERVENTIONS. Three 2-min-long recruitment maneuvers (RM) with transient increases in mean airway pressure to 35 cmH(2)O (RM1 and RM2) and 44 cmH(2)O (RM3). MEASUREMENTS AND RESULTS: Measurements of systemic hemodynamics, gastric mucosal perfusion (laser Doppler flowmetry), and lung mechanics were performed immediately before, at the end of, and 3 min after each RM. Cardiac index decreased during all RMs while mean arterial pressure decreased only during RM3. Gastric mucosal perfusion was not significantly changed during any of the RMs. When comparing values obtained before the first RM with values after the third RM there was a significant decrease in cardiac index ( P=0.043) and a non-significant ( P=0.051) decrease in gastric mucosal perfusion. There were no significant changes in systemic oxygenation or lung mechanics after three RMs, even though four patients showed marked transient increases in systemic oxygenation during RMs. CONCLUSIONS: In this study of ten patients there were no significant changes in gastric mucosal perfusion during lung recruitment maneuvers. There was, however, a trend towards gradual decreases in gastric mucosal perfusion.

Adult↗
PubMed2002

Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent.

BACKGROUND: Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model. METHODS: Ang II was infused in incremental doses (0-200 microg x h-1) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (PSMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (PtiO2) and lactate fluxes. RESULTS: Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (RSMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased RSMA only minimally when PSMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased PtiO2 at a PSMA of 50 mmHg, splanchnic lactate production was not observed. CONCLUSION: We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure.

Angiotensin II↗
PubMed2002

Does dopexamine influence regional vascular tone and oxygenation during intestinal hypotension?

BACKGROUND: Local effects of dopexamine on intestinal vascular tone and oxygenation were investigated during intestinal hypotension. To this end, we employed an experimental model, in which the superior mesenteric arterial pressure (PSMA) was controlled by an adjustable perivascular clamp. This approach enabled us to keep the intestinal perfusion pressure (IPP) constant in the face of any systemic circulatory alterations. METHODS: In 11 barbiturate-anesthetized pigs, we instrumented the superior mesenteric circulation for assessments of vascular resistance (RMES), IPP, jejunal mucosal perfusion (Laser Doppler) and intestinal tissue oxygenation (microoximetry). Measurements were carried out before and during dopexamine infusions (0.5 and 1.0 micro g.kg-1.min-1) at a freely variable PSMA (i.e. the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. RESULTS: At a constant PSMA of 50 mmHg, dopexamine had no significant intestinal vascular effects. However, at a constant PSMA of 30 mmHg, both doses of dopexamine were associated with decreases in RMES. Effects of dopexamine on intestinal oxygen delivery and extraction were minimal during these procedures, while a minor decrease in intestinal tissue oxygen tension was observed during dopexamine administration at the lowest IPP level. CONCLUSION: At very low intestinal perfusion pressures (approximately 30 mmHg) dopexamine produces intestinal vasodilation in excess of what is produced by intrinsic autoregulation. This suggests that there is a vasodilatory reserve in the intestine under such conditions and that a pharmacological vasodilator like dopexamine may improve intestinal circulation during regional severe hypotension.

Animals↗
PubMed2001

Effects of positive end-expiratory pressure on intestinal circulation during graded mesenteric artery occlusion.

BACKGROUND: Reduced gut perfusion is associated with multiple organ failure. Positive end-expiratory pressure (PEEP) reduces cardiac output (CO) and portal blood flow, and might be detrimental in a situation of already compromised intestinal circulation. The aim of this study was to investigate regional circulatory and metabolic effects of PEEP during graded regional hypoperfusion. METHODS: In 12 barbiturate-anesthetized pigs, we measured systemic and regional blood flows (superior mesenteric arterial, QSMA and portal venous, QPORT), jejunal mucosal perfusion (LDF), tissue oxygenation (PO2TISSUE) and metabolic parameters at PEEP (0, 4, 8 and 12 cm H2O) in a randomized order. Measurements were performed at unrestricted intestinal perfusion pressures (IPP) and at IPP levels of 50 and 30 mmHg. RESULTS: During unrestricted IPP, PEEP decreased MAP, CO, QSMA and QPORT, while systemic, and preportal (RPORT) vascular resistances and jejunal mucosal perfusion were not significantly changed. Preportal tissue oxygen delivery and PO2TISSUE decreased, while preportal tissue oxygen uptake was unaltered. During restricted IPP, PEEP produced the same pattern of hemodynamic alterations as when IPP was not restricted. QPORT and QSMA were lowered by the reductions in IPP, and QPORT was further reduced during PEEP. At an IPP of 30 mmHg, this reduction in QPORT decreased preportal tissue oxygen uptake. Consequently, intestinal ischemia, as indicated by increased net lactate production, occurred. Simultaneously, jejunal mucosal perfusion and PO2TISSUE declined. CONCLUSION: At IPP levels below 50 mmHg, even moderate levels of PEEP impaired local blood flow enough to cause intestinal ischemia. Our data underscore the importance of considering regional circulatory adaptations during PEEP ventilation.

Anesthesia↗
PubMed2000

Cutaneous sympathetic vasoconstrictor reflexes for the evaluation of interscalene brachial plexus block.

BACKGROUND: Although signs of sympathetic blockade following interscalene brachial plexus block include Horner's syndrome, increased skin temperature and vasodilatation, the degree of sympathetic blockade is not easily determined. The aim of this study was, therefore, to use activation of cutaneous finger pad vasoconstrictor reflexes for description and quantification of the degree of sympathetic blockade following unilateral interscalene brachial plexus block. METHODS: Eight patients scheduled for acromioplasty under general anesthesia were studied. An interscalene plexus catheter was inserted preoperatively on the side to be operated upon and used postoperatively for administration of bupivacaine, given as a bolus (1.25 mg kg(-1)) followed by a continuous infusion (0.25 mg kg(-1) h(-1)). Skin blood flow (SBF) in the pad of the index finger was assessed by the laser Doppler technique, and regional skin vascular resistance (RVR) was calculated. The inspiratory gasp test (apnea at end-inspiration) or a local heat provocation were used as provocations of the cutaneous microcirculation. RESULTS: Interscalene brachial plexus block increased SBF and decreased RVR at rest, and produced satisfactory sensory and motor block. The inspiratory gasp test decreased SBF and increased RVR in the unblocked arm, while the opposite, increased SBF and decreased RVR, were observed during local heat provocation. In the blocked arm, these gasp-induced cutaneous vasoconstrictor and heat-induced vasodilator responses were attenuated. CONCLUSIONS: Interscalene brachial plexus block reduces regional sympathetic nervous activity, illustrated by increases in skin blood flow, skin temperature and attenuated vasoconstrictor responses to an inspiratory gasp. The inspiratory gasp vasoconstrictive response is a powerful and sensitive indicator for monitoring the sympathetic blockade following interscalene brachial plexus block.

Adult↗
PubMed1999

Systemic levels and preportal organ release of tissue-type plasminogen activator are enhanced by PEEP in the pig.

BACKGROUND: Endothelium-derived tissue-type plasminogen activator, t-PA, is the key enzyme in the initiation of endogenous thrombolysis. Plasma levels of t-PA increase in response to sympatho-adrenergic activation. In the mesenteric vascular bed an increased norepinephrine spillover has been observed during positive end-expiratory pressure ventilation, PEEP. This experimental study examines the effects of PEEP-induced alterations on regional release rates and systemic levels of t-PA in vivo. METHODS: The protocol included measurements of arterio-venous concentration gradients of t-PA and the respective plasma flow across the pulmonary, coronary, hepatic and preportal vascular beds, in pigs, during zero-PEEP and at 2, 4 and 10 min after the application of a PEEP of 10 cm H2O. Both total plasma t-PA antigen (ELISA with a porcine t-PA standard) and active t-PA (spectrophotometric functional assay) were determined. RESULTS: During zero-PEEP, a high preportal basal net release and hepatic net uptake of total t-PA was observed. With PEEP, the magnitude of the preportal net release of t-PA was markedly enhanced (+24+/-5%), as was hepatic net uptake (+21+/-8%), simultaneously to a significant decrease in liver plasma flow (-30+/-2%). PEEP-induced alterations in active t-PA mirrored those observed in total t-PA. No significant net fluxes of total or active t-PA were observed across the coronary or the pulmonary vascular beds. CONCLUSIONS: Clinically used levels of PEEP induce increases in net release of endothelially derived t-PA within preportal organs. The application of PEEP is associated with increased systemic levels of total and active t-PA, in spite of a simultaneous increase in hepatic net uptake, indicating that the preportal vascular bed can not account for the systemic t-PA response.

Animals↗
PubMed1999

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.

Anesthetics, Inhalation↗
PubMed1998

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.

Anesthetics, Inhalation↗
PubMed1997

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.

Animals↗
PubMed1997

Aortic cross-clamping influences regional net release and uptake rates of tissue-type plasminogen activator in pigs.

BACKGROUND: The key regulator of intravascular fibrinolysis, tissue-type plasminogen activator (t-PA), is released from a dynamic endothelial storage pool. The aim of the study was to investigate regional t-PA net release and uptake rates in response to infra-renal aortic cross-clamping (AXC) and declamping (DC). METHODS: Anesthetized pigs were studied during 5 min of AXC, followed by a 35-min declamping (DC) period. Arterio-venous concentration gradients of total and active t-PA, as well as respective plasma flows, were simultaneously obtained across the preportal, hepatic, coronary and pulmonary vascular beds. Plasma levels of total t-PA (ELISA with purified porcine t-PA as standard), and active t-PA (spectrophotometric functional assay) were determined. RESULTS: Prior to AXC, we found a high net release rate of total t-PA across the preportal vascular bed (1700 ng.min-1 P < 0.001), and a high hepatic net uptake (4900 ng.min-1, P < 0.001), while coronary and pulmonary t-PA net fluxes were small and variable. AXC per se did not induce significant alterations in net fluxes of t-PA. Following DC, preportal and coronary net releases of total t-PA increased (to 2900 ng.min-1 and 60 ng.min-1, respectively). Despite an increase in hepatic net uptake of total t-PA (to 6100 ng.min-1) after DC, a significant increase in hepatic venous total t-PA occurred. CONCLUSIONS: The release and uptake of t-PA is indicated to be dynamic and organ-specific. DC induces an acute profibrinolytic reaction in preportal organs. The high hepatic t-PA uptake capacity restricts preportal profibrinolytic events to affect the systemic circulation.

Anesthesia↗
PubMed1997

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.

Anesthetics, Inhalation↗
PubMed1997

An experimental multiple-organ model for the study of regional net release/uptake rates of tissue-type plasminogen activator in the intact pig.

Experimental data indicate large between-organs variations in rates of synthesis of tissue-type plasminogen activator (t-PA), which may reflect important differences in the capacity for constitutive and stimulated t-PA release from the vascular endothelium. In this report we describe a new multiple-organ experimental in vivo model for simultaneous determinations of net release/uptake rates of t-PA across the coronary, splanchnic, pulmonary, and hepatic vascular beds. In eleven intact anesthetized pigs, blood samples were obtained simultaneously from the proximal aorta, coronary sinus, pulmonary artery, and portal and hepatic veins. Plasma flows were monitored separately for each vascular region. Total plasma t-PA was determined by ELISA with a porcine t-PA standard. Regional net release/uptake rates were defined as the product of arteriovenous concentration gradients and local plasma flows. The net release of t-PA across the splanchnic vascular bed was very high, with a mean output of 1,919 ng total t-PA x min(-1) (corresponding to 90 ng per min and 100 g tissue). The net coronary t-PA release was 68 ng x min(-1) (30 ng x min(-1) X 100 g(-1)). Pulmonary net fluxes of t-PA were variable without any significant net t-PA release. The net hepatic uptake rate was 4,855 ng x min(-1) (436 ng x min(-1) x 100 g(-1)). Net trans-organ changes of active t-PA mirrored those of total t-PA. The results demonstrate marked regional differences in net release rates of t-PA in vivo. The experimental model we present offers new possibilities for evaluation of regional secretion patterns in the intact animal.

Animals↗
PubMed1996

Cardiovascular responses to experimental infra-renal aortic cross-clamping. Modulating effects of isoflurane, sodium nitroprusside and milrinone.

BACKGROUND: Pharmacological control of blood pressure is usually indicated during aortic cross-clamping (AXC). The aim of this study was to analyze the modulation by isoflurane (ISO), sodium nitroprusside (SNP) and milrinone (MIL) of the systemic circulatory responses to a standardized infra-renal AXC. METHODS: Chloralose-anaesthetized pigs were exposed to AXC at control (no vasoactive drugs) and during the administration of each of the drugs. RESULTS: During control, AXC increased mean arterial pressure (MAP, 17 +/- 4%) and systemic vascular resistance (SVR, 27 +/- 7%), but induced no significant changes in cardiac output (CO), heart rate (HR), pulmonary arterial pressures, pulmonary vascular resistance or central venous pressure. Low-dose ISO (0.7%) and investigated doses of SNP and MIL did not significantly alter this response. High-dose ISO (1.4%, attenuated the AXC-induced increase in SVR, but not in MAP. All drugs decreased non-clamp MAP levels. Therefore, with low-dose ISO and with SNP or MIL, peak MAP during AXC was not significantly different from control non-clamp levels (i.e. prior to pharmacological or surgical interventions). High-dose ISO was associated with a MAP during AXC that was below control non-clamp levels. CONCLUSIONS: The objective that during AXC MAP should not exceed control non-clamp levels was achieveable by ISO, SNP or MIL. The modulating actions of the drugs on MAP during AXC were exerted mainly through reductions in non-clamp levels. This systemic hypotension was associated with decreased CO and SVR during ISO, and with decreased SVR and increased HR during SNP and MIL. Attenuation of the AXC-induced increase in SVR was produced only by 1.4% ISO.

Anesthetics, Inhalation↗
PubMed1996

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.

Anesthetics, Inhalation↗
PubMed1995

Are the cardiovascular actions of dopamine altered by isoflurane?

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 micrograms.kg-1.min-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 micrograms.kg-1.min-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Inhalation↗
PubMed1995

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.

Anesthetics, Inhalation↗
PubMed1994

Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine.

Interactive effects between exogenous dopamine (DA) and isoflurane (I) combined with thoracic epidural blockade (TEA) were studied in dogs during chloralose anesthesia. The I-TEA intervention per se decreased heart rate (HR; 28%), mean arterial pressure (MAP; 63%), cardiac output (CO; 54%), left ventricular dP/dt (LVdP/dt; 75%) and LVdP/dt/systolic arterial pressure (SAP; 42%). Prior to the I-TEA intervention, dopamine increased MAP, CO, LVdP/dt, LVdP/dt/SAP and stroke volume (SV) already at the dose 10 micrograms.kg-1.min-1 and, additionally, increased mean pulmonary artery pressure (MPAP) at the dose 20 micrograms.kg-1.min-1. During the I-TEA intervention, the DA-induced increases in MAP and systemic vascular resistance (SVR) were significantly higher than prior to I-TEA, as indicated by significant ANOVA interactive effects. At the dose 10 micrograms.kg-1.min-1, DA restored MAP, CO, LVdP/dt, LVdP/dt/SAP and SV to levels found before the I-TEA intervention, while HR was restored first at the dose 20 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1, DA also increased MAP (39%), LVdP/dt (119%), LVdP/dt/SAP (73%), SVR (28%) and MPAP (70%) above levels prior to I-TEA. To conclude, exogenous dopamine effectively and dose-dependently counters cardiovascular depression induced by the anesthetic technique of combining I and TEA. The pressor and systemic vasoconstrictor actions of dopamine are potentiated by conjoint administration of I and TEA.

Anesthesia, Epidural↗