Biomedical subjects

H Habazettl

Publications and source records attributed to H Habazettl.

At least 37 records · Page 2Linked to original sources

PubMed1997

Comparative effects of hypotension due to isoflurane, nitroglycerin, and adenosine on subendocardial microcirculation: observation of the in situ beating swine heart under critical stenosis.

BACKGROUND: Although isoflurane may cause subendocardial hypoperfusion in the presence of coronary stenosis because of its coronary arteriolar dilatory effects, it is not known how the subendocardial microcirculation is affected. The authors examined the effects of isoflurane on poststenotic subendocardial microvessels with coronary stenosis. METHODS: The authors observed subendocardial microvessels in in situ beating swine hearts with or without critical stenosis of the left anterior descending coronary artery (LAD) with a needle-type videomicroscope during isoflurane- (ISO-H), adenosine- (ADE-H), and nitroglycerin- (NTG-H) induced hypotension (mean arterial pressure, 55 mmHg). Regional myocardial function, oxygen balance, and lactate metabolism in the region perfused by the LAD also were determined. RESULTS: In swine with stenosis, there were no differences in heart rate, cardiac output, and LAD blood flow among the three types of hypotension. Regional lactate production and anterior interventricular venous pO2 were similar during ISO-H and NTG-H but higher during ADE-H. With videomicroscopy, about half as many subendocardial microvessels could be visualized during ADE-H as with ISO-H and NTG-H. The average decrease in the systolic diameter of subendocardial microvessels of greater than 100 microm was 9 +/- 6% during ISO-H and 12 +/- 5% during NTG-H, but no consistent phasic diameter changes were observed during ADE-H. In swine without stenosis, a systolic diameter decrease was observed during all three types of hypotension. CONCLUSIONS: These findings suggest that hypotension induced by isoflurane or nitroglycerin preserves phasic diameter changes in subendocardial microvessels in the presence of critical coronary stenosis, whereas that induced by adenosine does not.

Adenosine↗

PubMed1996

Improvement in functional recovery of the isolated guinea pig heart after hyperkalemic reperfusion with adenosine.

The aim of this study was to examine the effect of initial hyperkalemic reperfusion (HKR), with and without added adenosine, on coronary flow, myocardial function, and endothelium-dependent and endothelium-independent coronary vascular function. Cardioplegic arrest was induced in 40 isolated guinea pig hearts by infusing oxygenated cardioplegic (high in potassium ion) Krebs solution for 5 minutes. Hearts were then stored at room temperature for 3.5 hours. On reperfusion, hearts were divided into four groups of 10 hearts each: control, reperfusion with regular Krebs solution (4.6 mmol/L potassium chloride); base hyperkalemic reperfusion, initial reperfusion with 37 degrees C oxygenated, cardioplegic Krebs solution for 5 minutes; hyperkalemic reperfusion with addition of 1 mmol/L adenosine during HKR; and hyperkalemic reperfusion with addition of 5 mmol/L adenosine. Coronary reserve (adenosine bolus 2 mmol/L) and responses to acetylcholine (1 mumol/L) and nitroprusside (100 mumol/L) were examined before and after ischemia and reperfusion. Flow did not return to preischemic values in any group after reperfusion. Adenosine treatment during initial reperfusion increased coronary flow (percentage of baseline +/- standard error of the mean) from 57% +/- 4% in control and 45% +/- 3% in hearts with hyperkalemic reperfusion to 79% +/- 3% and 83% +/- 5% in hearts with hyperkalemic reperfusion also treated with, respectively, 1 mmol/L adenosine and 5 mmol/L adenosine (p < 0.05). At 30 and 60 minutes of reperfusion, however, flow remained elevated only in the group treated with 5 mmol/L adenosine. Coronary reserve and responses to acetylcholine and nitroprusside were equivalently depressed in all groups after reperfusion. Recovery of left ventricular systolic and diastolic function was improved in all groups after hyperkalemic reperfusion (54% +/- 4% of preischemic value) compared with control (39% +/- 3%), and recovery was further enhanced in the group treated with 5 mmol/L adenosine (60% +/- 4%). In this ex vivo model, hyperkalemic reperfusion improved myocardial function after cardioplegic arrest and the addition of 5 mmol/L adenosine improved coronary flow. Adenosine may counteract the potassium chloride-induced vasoconstriction that occurs during hyperkalemic reperfusion and may thus improve coronary flow and myocardial function. Postischemic depression of endothelium-dependent or endothelium-independent vascular functions, however, was not alleviated by hyperkalemic reperfusion with or without adenosine.

Acetylcholine↗

PubMed1996

Initial reperfusion with 2,3 butanedione monoxime is better than hyperkalemic reperfusion after cardioplegic arrest in isolated guinea pig hearts.

OBJECTIVE: Initial warm cardioplegic reperfusion is widely used to ameliorate cardiac reperfusion damage after cardioplegic arrest. However, undesired effects of the high potassium concentration of the cardioplegic perfusate may limit the beneficial effect of this treatment. Contraction uncoupling by a negative inotropic and vasodilating agent such as 2,3-butanedione monoxime (BDM) may be superior to warm cardioplegic reperfusion in reducing reperfusion damage. Thus, initial reperfusion with BDM was compared with hyperkalemic reperfusion (HKR) after global ischemia of Langendorff-perfused guinea pig hearts. METHODS: Cardiac arrest was induced in 16 hearts using hyperkalemic Krebs' solution and hearts were stored unperfused at 37 degrees C for 40 min. Two groups were studied: HKR, initial reperfusion with 37 degrees C oxygenated hyperkalemic Krebs' for 5 min, and BDM, addition of 20 mM BDM to normokalemic Krebs' for 5 min. RESULTS: BDM increased reactive coronary reflow (128 +/- 8%; all data mean +/- SEM of baseline) much more than HKR treatment (65 +/- 5%). O2 consumption was reduced more by HKR (28 +/- 1%) than by BDM (42 +/- 4%), but the O2 supply/consumption ratio was higher with BDM. During perfusion with normal Krebs' solution, flow stabilized at about 75% of baseline in both groups. Post-ischemic responses to adenosine, serotonin, and nitroprusside were depressed to a similar degree in both two groups. Recovery of left ventricular developed pressure was better in BDM (69 +/- 2%) than in HKR (61 +/- 3%)-treated hearts. Reperfusion dysrhythmias were markedly reduced after BDM reperfusion. CONCLUSIONS: These data indicate that treatment in the initial 5-min reperfusion period with BDM is more effective than hyperkalemic reperfusion in reducing reperfusion damage.

Animals↗

PubMed1996

[Interaction of adenosine with leukocytes and thrombocytes].

Platelets and polymorphonuclear granulocytes (PMN) contribute to post-ischemic myocardial reperfusion damage. However, to elicit any deleterious actions, they first need to become adherent to the vascular endothelium. Numerous studies have documented an A2-receptor mediated platelet-stabilizing action of adenosine and an A2-dependent antiinflammatory effect on PMN themselves. Intriguingly, an A1-receptor mediated chemotactic action of adenosine on isolated PMN has also been reported. A1-receptors are more sensitive towards adenosine than A2-receptors, and interactions between platelets and leukocytes could alter the net-adhesive potential. Furthermore, the endothelial cells also express adenosine A1- and A2-receptors. In the situation of ischemia and reperfusion both, the intracoronary concentration of adenosine and the shear forces, vary with time. We have, therefore, investigated the influence of adenosine on intracoronary adhesion of PMN and platelets, applied to isolated heart preparations (guinea pig), both separately and in combination, and determined the resultant effect on postischemic myocardial pump function. At submicromolar adenosine concentrations, as found after brief ischemia (15 min stopped-flow or 30 min low-flow), adenosine enhanced intracoronary PMN retention by preferentially stimulating endothelial A1-receptors. The effect required the intermediate formation of platelet activating factor (PAF) and occurred via CD11/CD18 adhesion molecules on the PMN. Higher, i.e., micromolar levels of adenosine, in contrast, inhibited PMN adhesion via an A2-receptor dependent mechanism. Thrombin-induced platelet adhesion was inhibited by adenosine at high shear rates by both A1- and A2-receptor dependent mechanisms. However, adenosine was not protective at low shear rates, or at high flow in the presence of PMN. Pertinently, adhesion of either PMN or platelets, alone or in combination, regularly caused deterioration of post-ischemic myocardial function. Thus, depending on its concentration and on the phase of ischemia/reperfusion, adenosine may elicit cardioprotective or detrimental effects in the reperfused myocardium, which makes general prognosis of its role in such situations difficult. However, in the course of every reperfusion, the adenosine levels will inevitably fall into the proadhesive range. Thus, prophylactic inhibition of A1-receptor effects may be beneficial.

Adenosine↗

PubMed1995

Isotonic versus hypertonic initial hyperkalemic reperfusion after cardioplegic arrest in isolated hearts.

In 24 isolated perfused guinea-pig hearts, 40 min of hyperkalemic arrest and ischemia at 37 degrees C were followed by 5 min of either isotonic or hypertonic initial hyperkalemic reperfusion (HKR). Hearts were divided into 3 groups: HKR, 5 min initial reperfusion with isotonic hyperkalemic Krebs' solution; Mannitol, initial reperfusion with hypertonic (450 mosm für 1 min and 330 mosm for 4 more min) hyperkalemic Krebs' solution modified by addition of mannitol; NaCl, same as Mannitol group but using NaCl instead of mannitol to increase osmolarity. In isotonic HKR hearts, postischemic peak reflow was 98 +/- 11% of pre-ischemic control. Subsequently coronary flow stabilized at 75% of control. Left-ventricular developed pressure (LVDP) recovered to 60% of control. Hypertonic reperfusion increased peak reflow to 141 +/- 11% in the mannitol and to 121 +/- 12% in the NaCl groups, but had no effect on the subsequent reduction of coronary flow to 75% of control. Recovery of LVDP, dP/dtmax, dP/dtmin, the time constant of relaxation, and O2 consumption did not differ between groups. Postischemic flow responses to adenosine, acetylcholine, and nitroprusside were equivalently reduced in all groups. We conclude that the flow increase seen in the hypertonic reperfusion model of the study may be due to direct coronary vasodilation rather than the desired reduction of endothelial or perivascular cell edema by the hypertonic solutions.

Animals↗

PubMed1995

Does nitrous oxide affect coronary microcirculation? An intravital microscopic study in the canine heart.

The safe use of nitrous oxide, in particular in patients with coronary artery disease, has been questioned. This study was designed to determine whether nitrous oxide directly affects global coronary hemodynamic variables and coronary arteriolar microvessels in the absence of changes of myocardial oxygen consumption. In dogs the effects of nitrous oxide were evaluated during normotension (NT, intravenous [IV] piritramid, nitrogen/oxygen; and NT/N2O, IV piritramid, nitrous oxide/oxygen) and during hypotension (MAP 60 mm Hg) (HT, IV piritramid, halothane, nitrogen/oxygen; and HT/N2O, IV piritramid, halothane, nitrous oxide/oxygen). The diameter of coronary arteriolar microvessels (range, 20-450 microns) was assessed by intravital fluorescence microscopy. Myocardial blood flow was determined by radioactive microspheres. Systemic and coronary hemodynamics, as well as arteriolar microvessel diameters, were comparable between NT and NT/N2O. During HT, nitrous oxide (HT/N2O) affected neither systemic nor coronary hemodynamics. Moreover, there was no obvious difference in the diameters of coronary microvessels between HT and HT/N2O. In conclusion, nitrous oxide, whether at normotensive or hypotensive conditions, neither influences coronary arteriolar tone nor reduces or redistributes myocardial blood flow.

Animals↗

PubMed1995

One-day hypothermic preservation of isolated hearts with halothane improves cardiac function better than low calcium.

BACKGROUND: Halothane exerts a potent negative inotropic effect on the heart and mimics many of the cardiac effects of lowered extracellular CaCl2. Reduced slow inward Ca2+ current and sarcoplasmic reticular effects on intracellular Ca2+ are likely involved. The authors reported previously that halothane protects against hypoxic and ischemia reperfusion injury in isolated hearts. The aim of this isolated heart study was to compare protective effects of halothane and low CaCl2 (0.5 mM) administered during 1 day of hypothermic perfusion on return of normothermic perfusion. METHODS: Guinea pig hearts (n = 66) were isolated and perfused at 37 degrees C with a Krebs' solution, gassed with 96% O2, 4% CO2, and containing 2.5 mM Ca2+, and 4.5 mM K+. Heart rate, isovolumetric left ventricular pressure, coronary flow, %O2 extraction, O2 consumption rate, and relative cardiac efficiency (EFF = heart rate.left ventricular pressure/O2 consumption rate) were measured in five groups of hearts: time controls (no hypothermia); 1.5, and 3% halothane delivered by vaporizer; cold controls (hypothermia only); and 0.5 mM CaCl2. Halothane was administered, or CaCl2 was decreased 0.5 h before hypothermia at 3.8 +/- 0.1 degrees C, during hypothermia for 22 h, and for 0.5 h after rewarming to 37.0 +/- 0.1 degrees C. Hearts were perfused at 25% of initial coronary flow during hypothermia. RESULTS: All groups had similar ventricular function and vasodilator responses before hypothermia. During normothermic reperfusion after hypothermia, both concentrations of halothane protected better than low CaCl2. Values, expressed as a percent of initial values in the five groups (time control, 3% halothane, 1.5% halothane, cold control, and 0.5 mM CaCl2, were respectively: 90 +/- 6, 54 +/- 6*, 48 +/- 5*, 27 +/- 8, 27 +/- 4% for left ventricular pressure; 84 +/- 5, 61 +/- 4*, 62 +/- 6*, 40 +/- 5, 34 +/- 5% for EFF; and 102 +/- 3, 63 +/- 3*, 66 +/- 3*, 55 +/- 2, 42 +/- 2% for coronary flow (*P < 0.05 halothane vs. 0.5 mM CaCl2). The coronary flow response to endothelium-dependent (acetylcholine) and endothelium-independent (nitroprusside) vasodilators was also greater after halothane than after 0.5 mM CaCl2. CONCLUSIONS: Halothane administered during hypothermia restores left ventricular pressure, cardiac efficiency, basal coronary flow, and flow responses better than low CaCl2. Although halothane and low CaCl2 both reduce intracellular Ca2+, contractile force, and metabolic demand, the better protective effect of halothane is not likely simply due to a reduction in contractile function and metabolic rate before or initially after hypothermia because these were reduced much more by low CaCl2 than by halothane.

Anesthetics↗

PubMed1994

Preservation of regional myocardial function and myocardial oxygen tension during acute ischemia in pigs: comparison of selective synchronized suction and retroinfusion of coronary veins to synchronized coronary venous retroperfusion.

OBJECTIVES: The efficacy of selective synchronized suction and retroinfusion of coronary veins was compared with synchronized coronary venous retroperfusion in preventing ischemic reduction of regional myocardial function and myocardial oxygen tension. BACKGROUND: Because incomplete protection by synchronized coronary venous retroperfusion during ischemia might result from nonselective retroinfusion and only passive drainage of the veins, a suction device was added to a retroinfusion system. METHODS: Regional myocardial function (ultrasonic crystals) and myocardial oxygen tension (polarographic electrodes) were studied in 30 pigs during 10-min occlusion of the left anterior descending coronary artery (ischemia), followed by reperfusion. During ischemia, group A (n = 10) was supported by selective synchronized suction and retroinfusion; group B (n = 10) was supported by synchronized coronary venous retroperfusion, and group C (n = 10) was not supported by retroinfusion. RESULTS: In group A, subendocardial segment shortening decreased from 21 +/- 4% (mean +/- SD) before ischemia to 11 +/- 5% during ischemia. In contrast, systolic dyskinesia was observed in group B (-2 +/- 4%, p < 0.001) and group C (-2 +/- 5%, p < 0.001). During ischemia, the decrease in intramyocardial oxygen tension was less pronounced in group A (41 +/- 15 vs. 27 +/- 12 mm Hg) than in group B (40 +/- 10 vs. 19 +/- 10 mm Hg, p = 0.1) or group C (33 +/- 11 vs. 12 +/- 8 mm Hg, p = 0.002). During ischemia, myocardial surface oxygen tension was preserved > 0 mm Hg only in group A. CONCLUSIONS: Preservation of regional myocardial function and myocardial oxygen tension was substantially higher by selective synchronized suction and retroinfusion of coronary veins than by synchronized coronary venous retroperfusion in pigs.

Animals↗

PubMed1994

Heterogeneous microvascular coronary vasodilation by adenosine and nitroglycerin in dogs.

We investigated the effects of adenosine and nitroglycerin (NTG) on coronary microvessel diameters (intravital fluorescence microscopy) and coronary perfusion (radioactive microspheres). Measurements were performed during baseline conditions (intravenous piritramid) and during controlled hypotension (mean arterial pressure approximately 60 mmHg) induced by halothane, adenosine, and NTG. Coronary vascular resistance (CVR) remained unchanged during halothane (-7%) but decreased during adenosine (-76%) and NTG (-29%). Coronary arteriolar diameters increased during all experimental steps. In the smallest vessels (20-40 microns), diameters increased by 14, 43, and 42% during halothane-, adenosine-, and NTG-induced hypotension, respectively. Diameter increases were less pronounced in larger vessels. The uniform action of adenosine and NTG in 20- to 500-microns arterial vessels is in contrast to the pronounced differences in reduction of CVR. Preferential dilation of arterioles < 20 microns or recruitment of coronary microvessels by adenosine might account for the more pronounced decrease of CVR during adenosine. Intracoronary application of adenosine (0.8 mg.kg-1.h-1) and NTG (1, 5, and 25 micrograms.kg-1.h-1) equally caused near-maximum dilation of coronary arterioles > 100 microns. However, NTG dilation of arterioles < 100 microns was dose dependent and exceeded large-vessel dilation only with the highest concentration of NTG.

Adenosine↗

PubMed1993

Heparin-protamine reactions in pigs: role of oxygen-derived free radicals.

We tested the hypothesis that pulmonary hypertension and thromboxane A2 release after heparin neutralization by protamine are mediated by oxygen free radicals. Forty-five pigs in five groups were studied during general anesthesia. Group I animals received 250 IU heparin followed by 100 mg protamine after 15 min. Group II and group III animals received dimethyl sulfoxide (DMSO) and dimethylthiourea (DMTU) 30 min before heparin infusion. Group IV animals were given superoxide dismutase (SOD) 5 min before protamine. Group V served for testing the pulmonary vascular reactivity in DMTU-treated animals to a thromboxane A2 analogue (U-46619). Generation of oxygen free radicals by polymorphonuclear granulocytes (PMNs) was measured in vitro by chemiluminescence. Severe pulmonary hypertension and thromboxane A2 release after protamine were not prevented by either DMSO or SOD. DMTU reduced pulmonary vasoconstriction to U-46619 and protamine but not to TxA2 release, indicating that DMTU had unspecific vascular effects in group III. Heparin-protamine released no oxygen free radicals from isolated PMNs. The results indicate that oxygen free radicals do not have a key role in mediating pulmonary vasoconstriction after protamine neutralization of heparin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1993

PGI2 aerosol versus nitric oxide for selective pulmonary vasodilation in hypoxic pulmonary vasoconstriction.

Intravenous prostacyclin (PGI2) is a potent pulmonary vasodilator in pulmonary hypertension. However, dose-dependent systemic vasodilation, an increase in intrapulmonary shunt and hypoxemia limit its clinical application. Recently, inhaled nitric oxide (NO) has been reported to elicit selective pulmonary vasodilation, but its clinical use is restricted by its potential toxicity; furthermore, the feasibility of NO application in clinical practice seems difficult. Therefore, we investigated the effects of PGI2 aerosol on pulmonary and systemic circulation and compared the hemodynamic effects to those of inhaled NO. In 6 dogs, ventilation with a hypoxic gas mixture (FiO2 0.09-0.11) increased pulmonary vascular resistance (PVR) by 196% (HPV). Aerosolization of a PGI2 solution at a concentration of 430 ng/ml reduced hypoxia-induced increase of pulmonary artery pressure by 48% and PVR by 52% within 6-10 min without systemic vasodilation. The administered dose of PGI2 was 0.87 +/- 0.26 ng/kg/min. In 2 dogs, doubling the PGI2 concentration (860 ng/ml) did not enhance the vasodilatory effect. After termination of PGI2 inhalation, HPV was restored within 10-15 min. Inhaled NO (50 ppm) decreased the HPV-induced increase in PAP by 76% and in PVR by 73% within 5-10 min. Clinically relevant systemic vasodilation was not observed. It is concluded that inhalation of aerosolized PGI2 leads to selective pulmonary vasodilation in hypoxia-induced pulmonary hypertension. Aerosolized PGI2 at a concentration of 430 ng/ml was less potent than NO (50 ppm). However, due to the lack of known toxicity and its uncomplicated mode of application, inhaled PGI2 may be one alternative to inhaled NO in the treatment of acute pulmonary hypertension.

Administration, Inhalation↗

PubMed1992

Coronary microcirculation during halothane, enflurane, isoflurane, and adenosine in dogs.

We investigated the effects of clinically administered volatile anesthetics and of adenosine on the microvasculature of the in situ beating canine heart. Thirteen dogs were studied during general anesthesia with an opioid (piritramide), which was infused throughout the experiments. Measurements were obtained in each animal at control (piritramide only) and during hypotension (mean arterial pressure 60 mmHg) induced by halothane, enflurane, isoflurane, and adenosine. Using epiillumination and fluorescence microscopy, 354 arterial microvessels with diameters from 20 to 450 microns were examined through all experimental periods. Hypotension by halothane, enflurane, isoflurane, and adenosine reduced coronary vascular resistance by 13%, 23%, 40%, and 85%, respectively. Coronary venous PO2 was unchanged from control with halothane (+/- 0%) and enflurane (+7%) and significantly increased with isoflurane (+16%) and adenosine (+65%). Left ventricular blood flow decreased significantly during halothane (-35%) and enflurane (-23%); was unchanged from control during isoflurane (-9%); but significantly increased during adenosine (+397%). Coronary arterial and arteriolar diameters increased with all hypotensive agents. Vasodilation was least with halothane, intermediate with enflurane and isoflurane, and most pronounced with adenosine. Diameters increased considerably more in vessels with initial diameters below 100 microns as opposed to larger vessels. Calculation of microvascular segmental resistances revealed that the maximum conductance changes during volatile anesthetics were located in the vessel segments visualized by microscopy, i.e., in vessels larger than 20 microns. However, this was not the case with adenosine. We conclude that volatile anesthetics induce coronary vasodilation by preferentially acting on vessels with diameters from 20 microns to approximately 200 microns, whereas adenosine, in addition, has a pronounced impact on the small precapillary arterioles.

Adenosine↗

PubMed1992

Effect of leukopenia on pulmonary hypertension after heparin-protamine in pigs.

Heparin neutralization by protamine after cardiac surgery and cardiopulmonary bypass may be associated with complement activation, transient leukopenia, thromboxane A2 release, and severe pulmonary hypertension. The role of leukocytes in the heparin-protamine reaction was studied in leukopenic pigs (n = 9) and a control group (n = 8). Leukopenia was induced by pretreatment with cyclophosphamide (30 mg.kg-1.day-1) for 6-7 days. During general anesthesia and after catheterization, baseline recordings of hemodynamics were performed and blood samples were withdrawn. Heparin (250 IU/kg) was injected and measurements were repeated after 10 min. Protamine sulfate (100 mg) was then infused over 2 min and measurements were performed after 2, 5, and 15 min. Prostanoid concentrations were measured by radioimmunoassays. In additional in vitro experiments, the release of thromboxane B2 from washed platelets and leukocytes after heparin-protamine stimulation was measured. Pretreatment with cyclophosphamide reduced leukocyte counts by 95.5% and the number of neutrophils by greater than 99.9%. Protamine infusion increased mean pulmonary arterial pressure by 74 and 46% and pulmonary vascular resistance by 185 and 384% in control and leukopenic animals, respectively. Thromboxane B2 concentrations increased in both groups. Stimulation by heparin, protamine, or heparin and protamine in sequence did not induce any thromboxane A2 release from washed blood cells. It is concluded that leukocytes do not contribute to pulmonary hypertension after heparin-protamine.

Animals↗

PubMed1992

Modified retrograde orotracheal intubation technique for airway access in rabbits.

Anatomical features of the oral fissure and pharynx of rabbits make orotracheal intubation a difficult task with a high failure rate. We have developed a versatile technique for retrograde intubation of rabbits which consists of the following steps: (1) assessment of the trachea through a cervicotomy (2) insertion of a guidewire into its lumen, (3) delivery of the guide through the mouth, and (4) introduction of the orotracheal tube over the guide. This procedure was performed in 58 rabbits under pentobarbital anesthesia and resulted in successful orotracheal intubation in 56 animals. Awakening from anesthesia and extubation were uneventful. No complications related to this technique were observed during a follow-up period of 5-14 days. The described technique is a simple and safe method to access the airways of rabbits and can be useful in chronic experiments.

Anesthesia↗

PubMed1992

Systemic and regional hemodynamics of isoflurane and sevoflurane in rats.

The authors studied the effects of sevoflurane and isoflurane on systemic hemodynamics and regional blood flow distribution (microsphere technique) in 15 rats during general anesthesia with intravenous chloralose and controlled ventilation. Inhaled anesthetics were applied to reduce mean arterial blood pressure (MAP) to 70 mm Hg (1.66 vol% sevoflurane and 0.96 vol% isoflurane) and 50 mm Hg (MAP 50; 3.95 vol% sevoflurane and 2.43 vol% isoflurane). Control recordings were obtained with intravenous chloralose only. At a MAP of 70 mm Hg, both anesthetics reduced heart rate, cardiac output, and systemic vascular resistance to a similar degree. Isoflurane decreased systemic vascular resistance markedly at a MAP of 50 mm Hg and thereby maintained cardiac output at higher levels than sevoflurane. The left ventricular rate-pressure product decreased comparably with both anesthetics. Cerebral blood flow increased dose-dependently with both inhaled anesthetics but to a greater degree with isoflurane. Total hepatic blood flow remained unchanged from control at a MAP of 70 mm Hg but decreased at a MAP of 50 mm Hg. This was due to reductions of hepatic arterial and portal venous tributaries. Renal blood flow was reduced with only the high concentrations of the anesthetics. Myocardial blood flow was reduced at all concentrations of volatile anesthetic; however, the decrease was less with isoflurane. This would indicate a more pronounced coronary vasodilation by isoflurane as the rate-pressure product, as a measure of the actual left ventricular oxygen demand, decreased by comparable degrees with both anesthetics. Our results indicate that sevoflurane and isoflurane (each approximately 0.7 MAC) have no dissimilar systemic and regional hemodynamic effects at a MAP of 70 mm Hg in this animal model. At higher concentrations (approximately 1.7 MAC), cerebral blood flow was more with isoflurane than with sevoflurane and was associated with a more pronounced vasodilation in the myocardium.

Anesthesia, General↗

PubMed1992

Blood flow and tissue oxygen pressures of liver and pancreas in rats: effects of volatile anesthetics and of hemorrhage.

The object of this investigation was to compare the effects of volatile anesthetics and of hemorrhage at comparable arterial blood pressures on splanchnic blood flow (radioactive microspheres) and tissue oxygenation of the liver and pancreas (surface PO2 [PSO2] electrodes). In contrast to earlier studies, we did not use identical minimum alveolar anesthetic concentration multiples as a reference to compare volatile anesthetics; rather, we used the splanchnic perfusion pressure. Under general anesthesia (intravenous chloralose) and controlled ventilation, 12 Sprague-Dawley rats underwent laparotomy to allow access to abdominal organs. Mean arterial pressure was decreased from 84 +/- 3 mm Hg (mean +/- SEM) at control to 50 mm Hg by 1.0 +/- 0.1 vol% halothane, 2.2 +/- 0.2 vol% enflurane, and 2.3 +/- 0.1 vol% isoflurane in a randomized sequence. For hemorrhagic hypotension, blood was withdrawn gradually until a mean arterial pressure of 50 mm Hg was attained. Volatile anesthetics and hemorrhage reduced cardiac output, and hepatic arterial, portal venous, and total hepatic blood flows by comparable degrees. Mean hepatic PSO2 decreased significantly from 30.7 +/- 2.6 mm Hg at control to 17.4 +/- 2 and 17.5 +/- 2 mm Hg during enflurane and isoflurane (each P less than 0.05) anesthesia, respectively. The decrease to 11.5 +/- 2.5 mm Hg was more pronounced during halothane anesthesia. Hemorrhagic hypotension was associated with the lowest hepatic PSO2 (3.4 +/- 1.3 mm Hg) and the highest number of hypoxic (0-5 mm Hg 86%) and anoxic PSO2 values (0 mm Hg 46%). Pancreatic blood flow and oxygenation remained unchanged from control during halothane and enflurane administration, whereas isoflurane increased both variables. Hemorrhagic hypotension slightly reduced pancreatic flow (-8%) but significantly decreased PSO2 from 58 +/- 5 mm Hg at control to 36 +/- 3 mm Hg, with 7% of all measured values in the hypoxic range. Thus, volatile anesthetics preserved pancreatic but not hepatic blood flow and tissue oxygenation in this rat model. Despite comparable effects on perfusion, the PSO2 of the liver and pancreas was the least during hemorrhagic hypotension compared to that with the anesthetics. Because the volative anesthetic-induced hypotension has such a different effect on splanchnic tissue oxygenation compared with hemorrhagic-induced hypotension, the authors conclude that the method of inducing hypotension may have different effects on oxygenation of various tissues.

Anesthetics↗

PubMed1992

[Delay phenomenon of the jejunum. Studies of nutritional blood supply and oxygen supply of the jejunum of the rabbit].

INTRODUCTION: Delay procedure has been shown to effectively improve microvascular perfusion in skin flaps. In analogy to skin, we have analyzed the effect of delay on regional blood flow and surface tissue PO2 of a proximal segment of the jejunum. METHODS: Under nembutal anesthesia (30 mg/kg BW) and mechanical ventilation a total of 15 rabbits were laparotomized. Regional blood flow of the jejunum was estimated using radioactive-labeled microspheres, and tissue PO2 was assessed by means of a platinum-multiwire surface electrode. In order to induce acute ischemia three consecutive jejunal arteries were ligated, and the proximal marginal vascular arch was temporarily occluded by a microvascular clip. Delay procedure was induced by 1) ligation of the jejunal arteries, 2) in situ-maintenance of the jejunal segment for two weeks followed by 3) relaparotomy and occlusion of the proximal marginal arch (n = 8). Regional blood flow of the jejunum and tissue PO2 were also assessed in sham-operated animals (n = 7). RESULTS: After acute ischemia regional blood flow (0.27 (0.05) ml x min-1 x g-1, mean (SEM)) and surface tissue PO2 (39 (3) mmHg) of the jejunal segment were found significantly (p < 0.05) reduced as compared to baseline (0.82 (0.12) ml x min-1 x g-1 and 66 (1) mmHg) and sham-operated animals (0.69 (0.12) ml x min-1 x g-1 and 62 (5) mmHg), respectively. In contrast, delay of the jejunal segment resulted in almost complete preservation of regional blood flow (0.56 (0.04) ml x min-1 x g-1) and surface tissue PO2 (65 (1) mmHg). CONCLUSION: We therefore like to propose that the jejunal delay phenomenon may be clinically used to reduce ischemic complications in jejunal transposition for esophagoplasty.

Animals↗

PubMed1992

[Anesthesiologic efficacy of propanidid as a liposome dispersion. An experimental study with rats].

BACKGROUND: Propanidid, an ultra-short-acting i.v. anaesthetic agent, was widely used in the 1960s. Reports of anaphylactoid reactions in patients associated with release of histamine following administration of the drug, however, led to withdrawal of this useful anaesthetic. Since the adverse side effects of the former solution could be attributed to the solvent cremophor, attempts have recently been made to produce a propanidid solution without addition of the solvent. We report on comparative investigations employing a new liposomal solution (B. Braun, Melsungen, FRG) and the conventional cremophor preparation with regard to anaesthetic properties, haemodynamic side effects, and electroencephalographic effects (EEG). METHODS: Sprague-Dawley rats (n = 46) were implanted with venous and arterial lines and epidural EEG electrodes during chloral-hydrate anaesthesia. The following day, arterial blood pressure (ABP), heart rate (HR), and EEG were monitored in awake animals and then after induction of anaesthesia by a bolus of the respective propanidid preparation, followed by an infusion period of 15 min in six different experimental groups. Animals of groups L-60, L-90, L-120, or C-60, C-90, or C-120 groups received 60, 90, or 120 mg.100 g-1.h-1 of the liposomal (L) or cremophor (C) preparation. During anaesthesia, the corneal reflex and nociception to tail-clamping were also tested. At termination of the infusion, blood samples were drawn for determination of plasma propanidid concentrations. RESULTS: Both preparations were similarly effective in induction and maintenance of anaesthesia in a dose-dependent manner; both similarly lowered ABP and HR. The corneal reflex and nociceptive responses to tail clamping were also comparably suppressed. However, whereas the liposomal preparation was well tolerated at higher dose levels, the cremophor preparation caused considerable dose-dependent mortality of 11%, 86%, and 86% in animals in groups C-60, C-90, and C-120, respectively. Both preparations were found to induce a burst-suppression pattern in the EEG associated with clonic seizures, with a lower incidence with the liposomal preparation (22% and 50% in groups L-90 and L-120) as compared to the cremophor preparation (100% and 89% in groups C-90 and C-120). A remarkable variability in propanidid plasma concentrations was found at the end of the infusion period, although no differences were observed between both preparations. Discontinuation of infusion of propanidid resulted in rapid awakening (less than 5 min), irrespective of whether the liposomal or conventional preparation was employed. CONCLUSION: The present findings demonstrate largely identical anaesthetic potencies of a new liposomal solution as compared to the conventional cremophor preparation of propanidid. The liposomal preparation, however, was superior as far as tolerance and incidence of clonic seizures was concerned. The present findings should prompt further studies on the suitability of liposomal propanidid as a short-acting anaesthetic agent in patients.

Anesthesia, Intravenous↗