急性等容血液稀释及联合降压对犬胃肠灌注的影响

目的 观察急性等容血液稀释联合硝普钠控制性降压对犬胃肠灌注的影响。方法 健康杂种犬16只,随机分为血液稀释组和联合组。以6％羟乙基淀粉等量置换全血实施急性等容血液稀释(ANH),分别使Het降至20％～25％(HD1)、10％～15％(HD2);控制性降压期间,0．02％硝普钠溶液泵人,使MAP降至50mmHg维持30min。监测各稀释水平以及稀释联合降压时的血液动力学和胃粘膜二氧化碳分压(PgCO2)的变化。结果 (1)血液稀释组HD1及HD2时CO、SI显著增高,SVRI、PVRI显著降低(P＜0．01),MAP、HR、CVP、PAP、PCWP不变;(2)血液稀释组HDl及HD2时Hb、CaO2、CvO2、DO2显著降低(P＜0．01),而ERO2增高,VO2不变;(3)与基础值比,联合组CO、SI、MAP、SVRI、PVRI显著降低(P＜0．01);(4)血液稀释组PgCO2、胃粘膜与呼气末二氧化碳分压差(KETCO2)无显著变化;联合组PgCO2、Pg-ET CO2分别由48．6mmHg、9．8mmHg增高至70．7mmHg、29．3mmHg。结论 血液稀释联合硝普钠降压时,因静脉回心血量下降,心输出量因而降低,内脏灌注受损。     

Sildenafil (Viagra) augments sodium nitroprusside-induced but not nitroglycerin-induced hypotension in dogs

We investigated whether sildenafil citrate (Viagra) may reduce the dose of nitrovasodilators to induce deliberate hypotension. Ten mongrel dogs were acutely instrumented with a femoral artery catheter and a pulmonary artery catheter. Sodium nitroprusside (SNP; 1-16 microg. kg(-1). min(-1)) or nitroglycerin (NTG; 2-32 microg. kg(-1). min(-1)) was IV given to induce hypotension. The study consisted of two occasions, in a random order, in each animal: one with sildenafil pretreatment (1 mg/kg IV followed by 0.3 mg. kg(-1). h(-1)) and the other without to serve as a control. Hemodynamic variables were continuously monitored. Plasma cyclic guanosine monophosphate (cGMP) concentrations were measured by radioimmunoassay. Both SNP and NTG produced dose-dependent decreases in mean arterial blood pressure without affecting the heart rate in the presence as well as in the absence of sildenafil. Systemic vascular resistance index and mean pulmonary arterial pressure were also decreased. The magnitude of mean arterial blood pressure and systemic vascular resistance index reductions caused by SNP was augmented by sildenafil, whereas that caused by NTG was not affected. Neither SNP nor NTG alone altered the plasma cGMP concentrations. Sildenafil increased the plasma cGMP concentration, which was further increased by SNP but not affected by NTG. These results indicate that sildenafil may reduce the dose of SNP in producing deliberate hypotension in the dog. The potentiation of SNP-induced hypotension by sildenafil may be related to an augmented accumulation of cGMP. IMPLICATIONS: Sildenafil may reduce the dose of sodium nitroprusside required to induce deliberate hypotension and hence the potential for cyanide toxicity.     

硝普钠控制性低血压对犬胃粘膜灌注的影响

目的　观察硝普钠控制性低血压对犬胃粘膜灌注的影响。方法　 1 6只健康杂种犬 ,随机分为对照组和控制性低血压组。基础麻醉后气管插管 ,经口置入胃张力计导管 ,股动、静脉置管 ,右颈内静脉放置Swan Ganz四腔漂浮导管。控制性低血压组静脉泵注 0 0 2 %硝普钠溶液进行控制性低血压 ,将MAP维持在 6 0mmHg 30min。监测降压期间血液动力学参数MAP、HR、CVP、肺动脉压 (MPAP)、肺毛细血管楔压 (PCWP)、心输出量 (CO)、每搏指数 (SVI)、体循环阻力指数 (SVRI)、肺循环阻力指数 (PVRI)、左室搏功指数 (LVSWI)、右室搏功指数 (RVSWI)、胃粘膜二氧化碳分压 (Pg CO2 )及胃粘膜与呼气末二氧化碳分压差 (Pg etCO2 )的变化。结果　与对照组相比 ,低血压组SVRI、PVRI显著下降 (P <0 0 5 ) ,LVSWI亦显著下降 (P <0 0 5 ) ;而CO、SVI、CVP、PCWP、RVSWI不变。在MAP 6 0mmHg的低血压水平 ,PgCO2 、Pg etCO2 分别由 4 7.4 5、9 0 7mmHg显著升高至 6 0 5 4、2 1 2 1mmHg(P <0 0 5 ) ,血压回升后上述指标均恢复正常。 结论　在保持充足血管内容量的条件下 ,硝普钠控制性低血压期间全身血管阻力显著下降 ,而心输出量不变。低血压期间胃粘膜灌注短暂受损 ,与血流重分布有关     

Cerebrovascular reactivity to carbon dioxide is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane

PURPOSE: Maintenance of cerebrovascular reactivity to CO(2) (CCO(2)R) is important during neurosurgical anesthesia. This study was designed to determine the effect of different desflurane concentrations on CCO(2)R in children. METHODS: Children undergoing urological surgery were enrolled. Anesthesia was induced with sevoflurane in air/oxygen. After intubation, sevoflurane was switched to desflurane. Analgesia was provided with an epidural neuraxial block. Mechanical ventilation was adjusted to an initial EtCO(2) of 30 mmHg. Exogenous CO(2) was used to achieve an EtCO(2) of 40 and 50 mmHg. Patients were randomized to the sequence of desflurane concentration (1.0 and 1.5 MAC) and the EtCO(2). Transcranial Doppler was used to measure middle cerebral artery blood flow velocity (Vmca). Five minutes were allowed to reach steady state after each change in EtCO(2) and 15 min after changing the desflurane concentration. RESULTS: Sixteen patients were studied. The mean age and weight were 3.5 +/- 1.5 yr and 14.4 +/- 3.1 kg, respectively. Mean arterial pressure remained stable throughout the study, while at an EtCO(2) of 50 mmHg, heart rate decreased at both desflurane concentrations (P < 0.05). At 1.0 MAC, Vmca increased from 30 to 40 mmHg (P < 0.05), but not from 40 to 50 mmHg EtCO(2). At 1.5 MAC, Vmca increased between 30 and 50 mmHg (P < 0.05). CONCLUSION: CCO(2)R is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane. The lack of further increase in Vmca at higher EtCO(2) concentrations implies that desflurane may cause significant cerebral vasodilatation in children. This may have important implications in children with reduced intracranial compliance.     

Comparison of adenosine,isoflurane, and desflurane on myocardial tissue oxygen pressure during coronary artery constriction in dogs

OBJECTIVE: To compare adenosine-, isoflurane-, or desflurane-induced hypotension with and without left anterior descending (LAD) coronary artery constriction for the effects on myocardial tissue oxygen pressure (PmO(2)) in dogs. DESIGN: Prospective, randomized, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred dogs (n = 18). INTERVENTIONS: Dogs were anesthetized with 1.5% isoflurane (n = 12) or 8% desflurane (n = 6). A flow probe and balloon occluder were placed on the LAD artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial minus coronary sinus oxygen content. MEASURES AND MAIN RESULTS: Measures were made during hypotension produced by adenosine infusion, 2.8% isoflurane, or 14% desflurane with and without LAD constriction to decrease blood flow 30%. Without LAD artery constriction, adenosine infusion increased LAD flow 90% and MVO(2) 70%, 2.8% isoflurane produced no change in MVO(2), and 14% desflurane decreased MVO(2) 25%, but no treatment changed PmO(2). LAD artery constriction decreased PmO(2) 50% by itself. Adenosine infusion during LAD constriction decreased tissue oxygen pressure an additional 60%, 2.8% isoflurane produced no change, and 14% desflurane increased PmO(2) 100%. CONCLUSION: There was an inverse relationship between the effect of adenosine, 2.8% isoflurane, and 14% desflurane on MVO(2) and PmO(2) during ischemia. This is consistent with reports that increasing oxygen demand worsens myocardial ischemia.     

Acetate fails to reverse myocardial depression in dogs anesthetized with halothane

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.     

Epidural clonidine produces antinociception, but not hypotension, in sheep

Intrathecally administered clonidine produces analgesia, but also produces hypotension. To assess the effects of epidural administration, the authors inserted lumbar epidural catheters in seven nonpregnant ewes, and injected, on separate days, clonidine (50-750 mcg), morphine (5-10 mg), and a clonidine-morphine combination (clonidine 150 mcg + morphine 5 mg). Clonidine produced dose-dependent antinociception and sedation, with the lowest maximally effective antinociceptive dose being 300 mcg. Morphine produced less intense antinociception than clonidine, and did not potentiate clonidine's effect. Antinociception, but not sedation, following clonidine injection was reversed by epidural injection of the alpha 2-adrenergic antagonist, idazoxan. Epidurally administered naloxone and prazosin did not reverse clonidine's antinociceptive effect, nor did intravenously administered idazoxan. Epidurally administered clonidine did not decrease blood pressure or heart rate or affect arterial blood gas tensions or spinal cord histology. These data suggest that epidurally administered clonidine produces analgesia by a local, alpha 2-adrenergic mechanism. In sheep, epidurally administered clonidine does not produce hypotension.     

Influence of desflurane,isoflurane and halothane on regional tissue perfusion in dogs

The actions of desflurane, isoflurane and halothane on regional tissue perfusion were studied using radioactive microspheres in dogs chronically instrumented for measurement of arterial and left ventricular pressure, global (left ventricular dP/dtmax) and regional (percent segment shortening) contractile function, and diastolic coronary blood flow velocity. Systemic and coronary haemodynamics and regional tissue perfusion were measured in the conscious state and during anaesthesia with equihypotensive concentrations of desflurane, isoflurane, and halothane. All three volatile anaesthetics (P < 0.05) increased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dtmax Myocardial perfusion was unchanged in subendocardial midmyocardial, and subepicardial regions by the administration of either dose of desflurane. No redistribution of intramyocardial blood flow (endo/epi ratio) was observed during desflurane anaesthesia. Although regional myocardial perfusion was reduced (P < 0.05) in a dose-related fashion by halothane and by isoflurane at high concentrations, redistribution of intramyocardial blood flow was not observed during halothane or isoflurane anaesthesia. All three volatile anaesthetics reduced blood flow to the renal cortex, but only desflurane produced a decrease in renal cortical vascular resistance. Hepatic blood flow decreased in response to halothane but not desflurane or isoflurane. Concomitant decreases in hepatic resistance were observed during administration of desflurane and isoflurane. Dose-related decreases in intestinal and skeletal muscle blood flow were observed during halothane and isoflurane but not desflurane anaesthesia. The results suggest that desflurane maintains myocardial, hepatic, intestinal, and skeletal muscle blood flow while halothane and isoflurane decrease regional tissue perfusion in these vascular beds to varying degrees during systemic hypotension in the chronically instrumented dog.     

Phenylephrine does not limit myocardial blood flow or oxygen delivery during isoflurane-induced hypotension in dogs.

Experiments were performed on seven fentanyl-pentobarbital-anesthetized, open-chest dogs to determine whether stimulation of coronary alpha 1-adrenergic receptors by phenylephrine causes coronary vasoconstriction and impaired myocardial oxygen delivery when phenylephrine is infused to correct isoflurane-induced hypotension. Myocardial blood flow was measured with radioactive microspheres, and myocardial oxygen and lactate extraction were determined. The Fick equation was used to calculate myocardial oxygen consumption. Measurements were obtained (a) under control conditions, (b) after a 30-min inhalation of isoflurane sufficient to decrease mean aortic pressure by 30%, and (c) while maintaining administration of isoflurane, 5-10 min after restoration of mean aortic pressure by intravenous infusion of phenylephrine. Isoflurane-induced hypotension was accompanied by a baroreceptor-mediated increase in heart rate and by a decrease in myocardial oxygen consumption; however, myocardial blood flow was maintained, resulting in decreased oxygen extraction and increased coronary sinus PO2, thus implying a direct coronary vasodilating effect for isoflurane. Lactate extraction was unaffected. Phenylephrine infusion during inhalation of isoflurane returned mean aortic pressure and heart rate to their respective control values, and it did not change myocardial oxygen consumption, myocardial blood flow, myocardial oxygen extraction, coronary sinus PO2, or lactate extraction from values obtained during isoflurane alone. These latter findings are consistent with undiminished coronary vasodilation by isoflurane in the presence of phenylephrine. In conclusion, infused phenylephrine to restore aortic pressure during isoflurane administration had no vasoconstrictor effect in the coronary circulation and did not impair myocardial oxygen delivery. Apparently, the direct coronary vasodilating action of isoflurane completely nullified phenylephrine-induced vasoconstriction via local alpha 1-adrenergic receptors.     

Administration of epinephrine does not increase learning of fear to tone in rats anesthetized with isoflurane or desflurane

Previous reports suggest that the administration of epinephrine increases learning during deep barbiturate-chloral hydrate anesthesia in rats but not during anesthesia with 0.4% isoflurane in rabbits. We revisited this issue, using fear conditioning to a tone in rats as our experimental model for learning and memory and isoflurane and desflurane as our anesthetics. Expressed as a fraction of the minimum alveolar anesthetic concentration (MAC) preventing movement in 50% of rats, the amnestic 50% effective dose (ED(50)) for fear to tone in control rats inhaling isoflurane and injected with saline intraperitoneally (i.p.) was 0.32 +/- 0.03 MAC (mean +/- se) compared with 0.37 +/- 0.06 MAC in rats injected with 0.01 mg/kg of epinephrine i.p. and 0.38 +/- 0.03 MAC in rats injected with 0.1 mg/kg of epinephrine i.p. For desflurane, the amnestic ED(50) were 0.32 +/- 0.05 MAC in control rats receiving a saline injection i.p. versus 0.36 +/- 0.04 MAC in rats injected with 0.1 mg/kg of epinephrine i.p. We conclude that exogenous epinephrine does not decrease amnesia produced by inhaled isoflurane or desflurane, as assessed by fear conditioning to a tone in rats.     

Chronic cocaine exposure alters carbon dioxide reactivity but does not affect cerebral blood flow autoregulation in anesthetized dogs

BACKGROUND: Cocaine use is common in trauma victims. Consequently, understanding how cocaine alters normal physiology is important to providing appropriate medical care for these patients. This study was designed to identify how chronic cocaine exposure alters cerebrovascular physiology. METHODS: Ten dogs (seven experimental, three control) were studied. Transcranial Doppler was used to measure CO2 reactivity and autoregulation of cerebral blood flow velocity (CBFvel). Measurements were made in anesthetized animals (0.6% or 1.8% isoflurane in oxygen and intravenous fentanyl) at baseline before cocaine exposure and then at weekly intervals for 4 weeks. During the 4-week study period, cocaine was administered intravenously four times per day. RESULTS: Cocaine did not alter autoregulation of CBFvel in response to changes in mean arterial pressure. However, cocaine markedly impaired CO2 reactivity in three of the seven animals. In this subset of animals, increasing Paco2 decreased CBFvel, which is consistent with vasoconstriction rather than vasodilation. CONCLUSION: Chronic cocaine exposure does not alter autoregulation of CBFvel but does alter CO2 reactivity in a subset of susceptible animals. If confirmed in humans, these findings have implications for traumatic brain injury patients who are chronic cocaine users. Specifically, the findings suggest that hyperventilation could exacerbate intracranial hypertension in a subset of these patients.     

Ropivacaine 0.25% and 0.5%, but not 0.125%, provide effective wound infiltration analgesia after outpatient hernia repair, but with sustained plasma drug levels

BACKGROUND AND OBJECTIVES: Ropivacaine is a long-acting local anesthetic similar to bupivacaine, but with lower cardiac toxicity and intrinsic vasoconstrictive properties that may reduce the risk and extent of systemic plasma absorption. Plasma levels and risks are associated with the total dose used and the extent of absorption, with lower doses potentially representing less risk. Although both 0.5% and 0.75% ropivacaine provide adequate analgesia for wound infiltration after hernia repair, the efficacy of lower doses and the early systemic absorption have not been reported. METHODS: We studied postoperative pain and systemic plasma levels following either the injection of 30 mL of saline or 0.125%, 0.25%, or 0.5% ropivacaine into the wounds in 110 healthy patients following hernia repair under spinal anesthesia. Pain was assessed using visual analog scale (VAS) scores and algometer readings at rest and after coughing, and oral analgesic requirements were assessed in the first 5 hours after surgery and for the week after discharge. RESULTS: Both 0.25% and 0.5% ropivacaine provided pain relief following surgery when compared with saline or 0.125%. No adverse reactions to the drug were reported in any group. Plasma levels of ropivacaine peaked between 30 and 60 minutes, at 0.109, 0.249, and 0.399 mg/L for 0.125%, 0.25%, and 0.5% concentrations, respectively. Although the levels were below those producing clinical symptoms, they remained elevated for the entire 2-hour sampling period. This implies an absorption-dependent elimination which is substantially longer than reported with other routes of injection. CONCLUSIONS: Ropivacaine 0.25% and 0.5% is adequate for pain relief after outpatient hernia repair, whereas the 0.125% solution is no more effective than saline. Prolonged systemic absorption from peripheral injection may be associated with prolonged elevations of plasma concentrations, which potentially could be associated with unexpectedly high plasma levels if repeated injections are performed in the perioperative period with higher concentrations or doses.     

Cerebral blood flow velocity increases when propofol is changed to desflurane, but not when isoflurane is changed to desflurane in children

BACKGROUND: Children may exhibit delayed emergence following maintenance of anesthesia with propofol or isoflurane. Desflurane is often used towards the end of procedures to facilitate emergence. This study evaluated the effect on middle cerebral artery blood flow velocity (Vmca) in anesthetized children when propofol or isoflurane was substituted with desflurane. METHODS: Forty-two healthy children aged 1-6 years were enrolled. A standardized anesthetic induction was used. Anesthesia was maintained with remifentanil (0.5 microg.kg(-1) bolus followed by an infusion of 0.2 microg.kg(-1).min(-1)) and a randomly selected sequence of propofol/desflurane/propofol, desflurane/propofol/desflurane, isoflurane/desflurane/isoflurane or desflurane/isoflurane/desflurane. Propofol was administered to maintain a steady-state serum concentration of 3 microg.ml(-1). Desflurane and isoflurane were administered at age-corrected 1 MAC. Hemodynamic stability was maintained. Transcranial Doppler sonography was used to measure Vmca. Hemodynamic variables as well as Vmca were measured 30 min after skin incision and repeated 30 min after each change in anesthetic maintenance agent. RESULTS: The mean age and weight was 2.3 +/- 1.3 years and 13.0 +/- 3.7 kg, respectively. The Vmca (mean) increased by 35% from 37.7 +/- 10.5 cm s(-1) to 57.8 +/- 14.6 cm s(-1) (P < 0.0001) when propofol was changed to desflurane but was unaffected when desflurane replaced isoflurane. CONCLUSION: When propofol is changed to desflurane, cerebral blood flow velocity increases significantly in normal children. This cerebral vasodilatory effect may have important implications in the neurosurgical setting.     

Transcutaneously measured near-infrared spectroscopic liver tissue oxygenation does not correlate with hepatic venous oxygenation in children

PURPOSE: To compare transcutaneous near-infrared spectroscopic (NIRS) measured liver tissue oxygenation with hepatic vein oxygen saturation (SvhO2) in children undergoing cardiac catheterization. METHODS: A NIRS optode (containing an emitter and a receiver of near-infrared light) was placed directly below the right costal arch above the palpable liver in 40 children aged 0.02 to 7.28 yr (median: 1.8 yr). Spatially resolved spectroscopic measured tissue oxygenation index (TOI) was recorded using the NIRO-300. Paired blood samples from the hepatic vein were taken under radiological control for determination of SvhO2 in a co-oxymeter. TOI values were compared with hepatic vein oxygenation, with simultaneously obtained arterial oxygen saturation (SaO2), inferior vena cava SO2 and hemoglobin concentration using simple linear and multi-regression analysis. RESULTS: TOI values ranged from 35% to 73% (58.6 +/- 8.4%); SvhO2 from 32% to 80% (58.4 +/- 14.4%), and arterial SO2 from 54% to 100% (90.0 +/- 11.4%). TOI and hepatic vein oxygen saturation failed to correlate (r = 0.052/P = 0.752). A regression model containing arterial saturation (Delta R2 = 0.177) and the ratio of pulmonary to systemic resistance (Delta R2 = 0.095) explained 27.3% of the observed variance in TOI. In this model, hepatic vein oxygen saturation was no longer significant; explaining only 3.4% of the variance. No other variable retained a significant association. CONCLUSION: Transcutaneously measured NIRS tissue oxygenation with an optode placed over the palpable liver does not correlate with SvhO2. The value is dominated by non-hepatic variables such as arterial saturation and vascular resistances.     

Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism in fentanyl anesthetized patients with peripheral vascular disease

The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 micrograms.kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 +/- 20 (SEM) micrograms.kg-1.min-1, to reduce mean arterial blood pressure by approximately 20% (23 +/- 2% SEM, from 82 +/- 3 to 63 +/- 3 SEM mmHg) during a 20-min period. Systemic and pulmonary vascular resistance indices decreased by 36 +/- 3 and 32 +/- 6% (SEM), and cardiac index increased by 18 +/- 5%. Heart rate, ventricular filling pressures, and whole body oxygen consumption were not affected by adenosine. Despite the reduced mean arterial blood pressure, coronary sinus flow increased by 128 +/- 26% (SEM) in parallel with a 96 +/- 11% (SEM) increase in coronary sinus oxygen content. Left and right ventricular stroke work indices, as well as myocardial oxygen consumption, were maintained. ECG (12-lead) demonstrated signs of ischemia in one subject, while myocardial lactate uptake was unchanged in all subjects. In conclusion, adenosine-induced hypotension in patients with peripheral vascular disease increased cardiac index without affecting myocardial work, whole body, and myocardial oxygen consumptions. The marked increase in coronary sinus blood flow, indicating coronary vasodilation, was not related to increased myocardial work. Further information regarding myocardial effect of adenosine in patients with ischemic heart disease is warranted.     

Intracoronary propofol attenuates myocardial but not coronary endothelial dysfunction after brief ischaemia and reperfusion in dogs

We have investigated the effects of propofol on recovery of regional mechanical and coronary endothelial function and on lipid peroxidation in post-ischaemic myocardium in dogs. The animals were assessed for 180 min during reperfusion after 15-min of occlusion of the left anterior descending coronary artery (LAD). They were treated with intracoronary (i.c.) propofol 5 or 20 micrograms/ml of coronary flow or vehicle (control group) for 60 min, beginning 30 min before LAD occlusion. Propofol significantly enhanced recovery of regional contractile function (70% and 81% of baseline segment shortening in the propofol 5 and 20 micrograms ml-1 groups, respectively, compared with 51% in controls at 3 h of reperfusion). However, LAD flow responses to i.c. acetylcholine were similarly attenuated regardless of treatment with propofol throughout reperfusion. The increase in malondialdehyde induced by ischaemia-reperfusion was significantly suppressed by both doses of propofol. These results demonstrated that in vivo, propofol ameliorated dysfunction of the myocardium but not of the coronary endothelium resulting from brief ischaemia and reperfusion; the protection may be related, at least in part, to its ability to reduce lipid peroxidation.      

Propofol, but not thiopentone or etomidate, enhances isoflurane-induced coronary vasodilatation in dogs

Purpose

To test the hypothesis that thiopentone, propofol, and etomidate alter the coronary vascular effects of abruptly administered isoflurane.

Methods

Dogs (n = 6) received inspired isoflurane 5% in the presence of thiopentone (20 mg·kg^?1 induction dose and 20 mg·kg^?1·hr^t-1 infusion), propofol (5 mg·kg^?1 induction dose and 40 mg·kg^?1·hr^?1 infusion), etomidate (2 mg·kg^?1 induction dose and 5 mg·kg^?1·hr^?1 infusion), or isoflurane (1.0 MAC) anaesthesia in a random fashion. Haemodynamics were assessed in the conscious state, during baseline anaesthesia, and at 30 sec intervals for five minutes after beginning isoflurane 5%.

Results

Rapidly administered isoflurane caused greater (P < 0.05) reductions in coronary vascular resistance in thiopentoneor propofol-than in isoflurane-anaesthetized dogs. Isoflurane produced greater (P < 0.05) increases in the ratio of coronary blood flow velocity to pressure-work index (an index of myocardial oxygen consumption; +109 ± 19 % during isoflurane alonevs + 182 ± 27 % change from baseline during propofol and isoflurane) consistent with relatively greater direct coronary vasodilatation during baseline propofol than during baseline isoflurane anaesthesia. Isoflurane caused larger increases in coronary blood flow velocity in dogs anaesthetized with etomidate concomitant with higher coronary perfusion pressure and pressure-work index than in those anaesthetized with isoflurane alone.

Conclusions

The results suggest that thiopentone, propofol, and etomidate each uniquely modify the coronary vascular responses to abrupt administration of high inspired concentrations of isoflurane in chronically instrumented dogs.     

Lower esophageal contractility predicts movement during skin incision in patients anesthetized with halothane, but not with nitrous oxide and alfentanil

The frequency of spontaneous lower esophageal contractions (SLEC) has been proposed as one measure of anesthetic depth. The authors tested the hypothesis that SLEC frequency can predict movement in response to skin incision during halothane or nitrous oxide/alfentanil anesthesia. The incidence of movement during skin incision was compared with the frequency of spontaneous lower esophageal contractions in 20 healthy patients anesthetized with halothane. Esophageal contractility was determined using the Lectron 302, which senses the pressure in a water-filled balloon positioned in the distal esophagus. Absence of SLEC in the 6 min preceding incision correlated with no movement, with one exception (n = 9). All but one patient having greater than or equal to 2 SLEC in the 6 min preceding skin incision moved (n = 8) (P less than 0.01). Sixteen additional patients anesthetized with nitrous oxide (70%) and alfentanil demonstrated no correlation between SLEC frequency and movement. These data suggest that the frequency of spontaneous lower esophageal contractions, and its ability to predict movement, depends on anesthetic type.     

Doxazosin,but not amlodipine decreases insulin resistance in patients with chronic renal failure: a prospective,randomized-controlled study

Insulin resistance (IR) in chronic renal failure (CRF) is well-known. In this randomized-controlled study, we aimed to compare the effect of doxazosin and amlodipine on IR in patients with CRF. Fifteen patients with CRF (male/female: 5/10, mean age: 46 +/- 13 years) and 9 controls (male/female: 3/6, mean age: 35 +/- 8 years) were included. Patients and controls had no family history of diabetes mellitus. Homeostasis model assessment (HOMA) was calculated as a marker of IR. Patients were grouped randomly to doxazosin (n = 8; 2-4 mg/day) and amlodipine (n = 7; 5-10 mg/day) arms. Baseline biochemical analysis (fasting serum glucose, BUN, creatinine, uric acid, cholesterol and cholesterol subgroups) and parameters related with insulin metabolism (insulin, C peptide, HOMA) were similar between amlodipine and doxazosin groups. There was no difference in age, gender and body mass index among study groups. The follow-up time was 12 weeks. Patients with CRF had higher HOMA (1.83 +/- 0.55 vs 1.00 +/- 0.36, p = 0.001), fasting insulin (8.06 +/- 1.98 vs 4.46 +/- 1.31 IU/l, p < 0.001) and serum triglyceride levels (197 +/- 136 vs 112 +/- 67 mg/dl, p = 0.04) as compared to controls. Serum HDL cholesterol levels were significantly lower in patients with CRF than controls (40 +/- 10 vs 57 +/- 14 mg/dl, p = 0.02). HOMA significantly decreased after doxazosin (1.91 +/- 0.45 vs 1.41 +/- 0.21, p = 0.02), however, no difference was found after amlodipine. Also, fasting insulin levels were decreased after a 12-week doxazosin therapy from 8.17 +/- 1.22 vs 6.58 +/- 0.84 IU/l, p = 0.02), but no change was seen after amlodipine. Lipid parameters did not significantly change during the study period in 2 groups. No adverse effect requiring drug discontinuation was observed during the 12-week period in the study groups. In conclusion, doxazosin decreases IR in patients with CRF, whereas amlodipine has no effect. This may be of advantage in the treatment of hypertension in this group of patients for preventing some long-term complication of IR.