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Biomedical subjects

B Biber

Publications and source records attributed to B Biber.

At least 37 records · Page 2Linked to original sources
PubMed1999

Continuous interscalene brachial plexus block for postoperative analgesia following shoulder surgery.

BACKGROUND: Severe postoperative pain is a well-known problem following shoulder surgery. This study evaluates the clinical efficacy of continuous interscalene brachial plexus block, patient-controlled analgesia, and morphine (i.v. and i.m.) for postoperative analgesia in this setting. METHODS: Thirty patients, scheduled for acromioplasty during general anesthesia, were randomly allocated to one of three different postoperative pain management groups. Group MO received morphine (5 mg i.m. and 2 mg i.v.) when visual analogue pain score (VAS) > 3, group PL received a continuous interscalene brachial plexus block with bupivacaine (1.25 mg kg-1 + 0.25 mg kg-1 h-1) and group PCA received patient-controlled analgesia with morphine (bolus 1 mg). Postoperative pain relief was assessed (24 h) by VAS, circulatory and respiratory stress parameters (heart rate, systemic arterial pressure and respiratory rate) and stress metabolites (glucose, lactate, glycerol by abdominal subcutaneous microdialysis). RESULTS: Pain relief in the PL group was effective (VAS < 3) and significantly more potent than in groups MO and PCA, except at 16 and 20 h. Lactate was significantly increased in the PL group, glucose was significantly increased in all groups, while glycerol showed a variable pattern. There were no significant stress metabolite differences among groups. VAS showed no statistical correlation with microdialysate, respiratory or circulatory data. CONCLUSION: Successful continuous interscalene brachial plexus block provides very good pain relief following shoulder surgery and is superior to the other methods studied. However, we were unable to demonstrate a correlation between VAS pain scores and stress indicators in metabolic, circulatory and respiratory parameters.

Adolescent↗
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↗
PubMed1999

Panic disorder subtypes: differential responses to CO2 challenge.

OBJECTIVE: The purpose of this study was to investigate the possibility of a differential sensitivity to CO2 in patients diagnosed with panic disorder subtypes that were defined by the presence of prominent respiratory symptoms. METHOD: The authors used a 35% CO2 and 65% O2 mixture as a challenge agent. Fifty-one unmedicated subjects with DSM-III-R panic disorder, who were divided into respiratory (N = 28) and nonrespiratory (N = 23) subtypes by their symptom profiles, underwent a CO2 challenge procedure. Patients in the two groups were compared with regard to physiological and psychological measures, pulmonary function tests, panic rates, and smoking habits. RESULTS: The patients in the respiratory group were significantly more sensitive to CO2 than were the patients in the nonrespiratory group. The respiratory group also had higher scores on the Panic and Agoraphobia Scale and had a longer duration of illness; both of these factors can be indicators of illness severity. In addition, the respiratory group's higher cigarette consumption (mean = 12.46 package-years, SD = 2.49) may have been a contributory factor not only for illness severity but also for the pathogenesis of panic disorder. CONCLUSIONS: The CO2 challenge procedure appears to be a good dissection tool in the understanding of different subtypes of panic disorder. Moreover, there may be a more specific association with prominent respiratory symptom subtype and CO2 hypersensitivity.

Administration, Inhalation↗
PubMed1999

Evaluation of dispatcher-assisted cardiopulmonary resuscitation.

The outcome of out-of-hospital cardiac arrest (CA) following cardiopulmonary resuscitation (CPR) initiated by dispatcher-provided telephone instructions (T-CPR) in the area of Gothenburg, Sweden was studied. During a period of 27 months, 475 cases categorized by the dispatchers at the Emergency Co-ordination and Dispatch Centre as being suspected CA were offered T-CPR and were included in one of the following groups: (1) T-CPR completed (caller without previous CPR training); (2) T-CPR completed (caller with previous CPR training); (3) T-CPR started, but not completed; (4) T-CPR declined by caller due to previous CPR training; (5) T-CPR declined by caller due to other reasons; or, (6) T-CPR not offered. Of the patients, 473 could be followed up and of them 427 fulfilled the criteria for CA on ambulance arrival. Among the latter cases, 10% were hospitalized alive, 4% could be discharged from hospital, and the distribution among groups was: (1) 7%; (2) 18%; (3) 5%; (4) 11%; (5) 3%; and (6) 1%. The study concludes that although more attention should be paid to the detection of CA patients by the dispatchers, when the dispatchers suspected CA, their accuracy was high. Half of the witnesses accepted the offer of T-CPR and one-third completed T-CPR. More efforts and research are needed, however, to increase the percentages of callers completing CPR. The impact of T-CPR on survival might be limited. Indeed, the comparison of 'resuscitable' patients in whom T-CPR played an important role in supporting bystanders (i.e. groups 1 and 2) with 'resuscitable' patients in whom T-CPR was not performed (i.e. groups 3, 5 and 6) suggests an increase in survival from 6% (groups 3, 5 and 6) to 9% (groups 1 and 2).

Adolescent↗
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

Hemodynamic, sympathetic and angiotensin II responses to PEEP ventilation before and during administration of isoflurane.

BACKGROUND: Positive end-expiratory pressure (PEEP) ventilation and isoflurane anesthesia may opposingly affect the sympathetic nervous and renin-angiotensin systems. This study was performed to elucidate the modulatory effects of isoflurane anesthesia on the neurohumoral and cardiovascular responses to PEEP. METHODS: Renin-angiotensin and sympathetic nervous activity were investigated in mechanically ventilated, normovolemic, chloralose anesthetized pigs before and during administration of 1.4% isoflurane. Arterial angiotensin II (AII) concentrations were measured and systemic, mesenteric, hepatic and renal spillover of norepinephrine (NE-SO) were calculated using isotope dilution. Regional hemodynamic variables were investigated in parallel. RESULTS: PEEP10 alone moderately elevated AII levels (+12.5 +/- 4.9 pg/ml, P < 0.05) and increased systemic (+22 +/- 2.9 pmol.min.100 g-1, P < 0.05) and notably mesenteric (+32 +/- 9.6 pmol.min.100 g-1, P < 0.05) NE-SO. Blood flow decreased in all vascular beds studied. Except for in the liver, isoflurane generally reduced NE-SO compared to baseline but did not change AII concentrations. Strikingly, the sympathoexcitatory response to PEEP10 was inhibited, whereas AII increased markedly (+284 +/- 64 pg/ml, P < 0.05) during PEEP10 and isoflurane. Renal blood flow was significantly more reduced during PEEP10 and isoflurane compared to PEEP10 alone, whereas the magnitude of reductions were similar in the other vascular beds. CONCLUSION: The data suggest that renin-angiotensin activation is important to attenuate the impact of PEEP ventilation on cardiovascular performance during administration of the sympathodepressant isoflurane. Interference with the renin-angiotensin system may cause cardiovascular decompensation in isoflurane anesthetized patients subjected to PEEP-ventilation.

Anesthesia, 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

Effects of fentanyl, nitrous oxide, or both, on baroreceptor reflex regulation in the cat.

We have investigated the effects of fentanyl, nitrous oxide, or both, on carotid sinus baroreceptor reflexes in cats during basal chloralose anaesthesia. The bilaterally isolated carotid sinuses were perfused at prevailing systemic arterial pressure or at predetermined levels of pump-controlled pulsatile pressures of 50-200 mm Hg in steps of 25 mm Hg. Other major baroreceptor sites were denervated by bilateral vagotomy. Fentanyl decreased arterial pressure dose-dependently when the carotid sinuses were perfused at prevailing systemic arterial pressure and when the perfusion pressure was controlled artificially. High-dose fentanyl reduced significantly baroreceptor reflex responses in the sinus perfusion pressure range 50-125 mm Hg. Nitrous oxide increased arterial pressure in the carotid sinus perfusion range 75-125 mm Hg. There was no interaction between nitrous oxide and fentanyl for baroreceptor reflex responses. Our results indicated that baroreceptor reflexes, with and without nitrous oxide, were well preserved by moderate doses of fentanyl while high doses of fentanyl depressed baroreceptor reflexes.

Analgesics, Opioid↗
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

Splanchnic and renal sympathetic activity in relation to hemodynamics during isoflurane administration in pigs.

The aim of the present study was to investigate the impact of isoflurane on regional neurogenic mechanisms in the control of vascular tone. Therefore, regional determinations of sympathetic activity and hemodynamics were made in chloralose-anesthetized swine before and during administration of 1.4% isoflurane. Sympathetic activity was examined from spillover of norepinephrine (NE) into the circulation using an isotope dilution technique. Administration of isoflurane caused a marked decrease in mesenteric (65 +/- 9 pmol.min-1.100 g-1; P < 0.05) NE spillover. Renal NE spillover was moderately decreased (25 +/- 6 pmol.min-1.100 g-1; P < 0.05), whereas liver NE spillover did not change significantly during isoflurane administration, suggesting that liver sympathetic activity is maintained at this level of isoflurane anesthesia. Total body NE spillover decreased (13 +/- 2 pmol.min-1.100 g-1, P < 0.05). Thus, isoflurane affected sympathetic outflow in a regionally differentiated pattern. Significant correlations were found between total body, mesenteric, and renal NE spillovers and vascular resistances, supporting the concept that the observed reductions in vascular resistances in these circulations during isoflurane administration were in part a consequence of reduced sympathetic outflow. In the liver circulation, no correlation was found between NE spillover and liver portal or liver arterial vascular resistances. Liver arterial resistance was significantly reduced during isoflurane administration while liver portal resistance was unchanged. Administration of isoflurane caused reductions in cardiac output, renal, portal, hepatic arterial, and total hepatic blood flows, whereas mesenteric blood flow was unchanged. To summarize, isoflurane decreased mesenteric and renal NE spillover with concomitant reductions in vascular resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗