Isoflurane and hepatic oxygenation.
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Animals↗
Biomedical subjects
D E Longnecker
Publications and source records attributed to D E Longnecker.
Effects of lidocaine concentration on distal capillary blood flow in a rabbit ear model.
The laser pulse doppler provides a noninvasive, reproducible method to measure the flux in distal capillary blood flow in a rabbit ear model. The distal capillary blood flow responds proportionally to changes in periarterial lidocaine concentration. The response is biphasic. Flow initially decreased from the baseline in all lidocaine concentrations between 0.5% and 10.0%. Proportional increases in distal blood flow above baseline are noted as the buffered lidocaine concentrations increase from 1.0% to 10.0%. Lidocaine concentration of 0.5% dose not increase distal blood flow above baseline.
Animals↗
The hemodynamic response to isoflurane is altered in genetically hypertensive (SHR), as compared with normotensive (WKY), rats.
The authors compared the hemodynamic effects of isoflurane anesthesia in normotensive (WKY) and genetically hypertensive (SHR) rats. Eighteen male SHR and 18 WKY rats were subdivided into conscious animals and those anesthetized with isoflurane, 1.2 vol% inspired. During brief isoflurane anesthesia, cannulae were placed in the left cardiac ventricle, the femoral artery, and the femoral vein. Central and regional hemodynamics were determined with 85Sr-labeled microspheres (15 +/- 1 micron) using the reference sample technique in both conscious and anesthetized animals. Isoflurane anesthesia caused similar reductions in mean arterial blood pressure (MAP) in all rats. This was due to a significant decrease in systemic vascular resistance in WKY rats, whereas MAP declined due to a significant decrease in cardiac output in SHR rats. In the anesthetized WKY rat, the decrease in total systemic vascular resistance resulted from significant decreases in vascular resistance of the brain and nonrespiratory skeletal muscles. In the anesthetized SHR rat, both decreases (cerebellum, hepatic artery) and increases (GI tract, skin, diaphragm) in regional vascular resistances occurred, resulting in no net change in total systemic vascular resistance. In both SHR and WKY rats, isoflurane redistributed blood flow in favor of the brain at the expense of blood flow to the GI tract, diaphragm, and skin. Blood flows to the liver, GI tract, and skin were significantly less in the anesthetized SHR as compared with WKY rats. It is concluded that isoflurane influences central and regional hemodynamics differently in hypertensive, as compared with normotensive, rats.
Anesthesia, Inhalation↗
Alpine anesthesia: can pretreatment with clonidine decrease the peaks and valleys?
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Anesthesia, General↗
Carotenoid compound crocetin improves cerebral oxygenation in hemorrhaged rats.
The carotenoid compound crocetin has been shown to increase oxygen diffusivity in vitro. In the present study the effect of crocetin on tissue oxygenation was examined in the cerebral cortex of rats subjected to hemorrhage. Twelve male Sprague-Dawley rats were anesthetized with pentobarbital and ventilation was controlled (PaCO2 = 33 mm Hg). A craniotomy was performed and the animals were hemorrhaged (20% of estimated total blood volume). Six of 12 animals then received a bolus of crocetin (2 U in 0.1 ml saline); the remaining animals received saline (0.1 ml i.v.) only. Values for mean arterial pressure. PO2, PCO2, pH, and hematocrit did not differ in rats that received either saline or crocetin. Tissue oxygen tension (PtO2) was measured at approximately 170 locations in the parietal cerebral cortex of each rat by a platinum-oxygen microelectrode technique. Results were compared by PtO2 frequency histograms. Crocetin as compared with saline treatment resulted in a right shift of the PtO2 frequency distribution and a significant decrease in the frequency of occurrence of low PtO2 values. The average of individual median PtO2 values was significantly greater in crocetin-treated animals as compared with those receiving saline (7.6 +/- 1.7 vs. 3.2 +/- 1.2 mm Hg, respectively). The results suggest that the carotenoid compound crocetin improves tissue oxygenation in the cerebral cortex of hemorrhaged rats.
Animals↗
The addition of nitrous oxide to halothane decreases renal and splanchnic flow and increases cerebral blood flow in rats.
Thirteen male Sprague-Dawley rats were anaesthetized with halothane and catheters were placed in the femoral artery and left ventricle. The animals breathed spontaneously through a tracheostomy throughout the investigation. After the surgical preparation, the inspired halothane concentration was maintained at 1.5 vol% (F/O2 = 0.3). After a 30-min stabilization period, strontium-85 radiolabelled microspheres (15 +/- 1 micron) were injected to the left ventricle for determination of cardiac output and regional blood flows. In six rats, nitrous oxide was then substituted for nitrogen in the inspired gas mixture. Ten min thereafter, 141Ce-labelled microspheres were injected and the haemodynamic measurements were repeated in all animals. The administration of the nitrous oxide to halothane-anaesthetized rats resulted in a decrease in cardiac output and decreases in blood flow to kidneys, liver, small bowel and spleen. Cerebral perfusion was increased.
Animals↗
Single versus divided doses of atracurium: does 0.05 + 0.10 equal 0.15?
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Atracurium↗
Cerebral oxygen tension in rats during deliberate hypotension with sodium nitroprusside, 2-chloroadenosine, or deep isoflurane anesthesia.
Thirty-four male Sprague-Dawley rats were divided into four groups: control animals and those receiving sodium nitroprusside (SNP), 2-chloroadenosine, or a high, inspired concentration of isoflurane to produce deliberate hypotension to a mean arterial blood pressure of 50 mmHg. Ventilation was controlled (FIo2 = 0.3); control animals and those treated with sodium nitroprusside or 2-chloroadenosine breathed isoflurane 1.4 vol%, whereas isoflurane, 3.9 vol%, was required to produce hypotension by deep anesthesia alone. Multiple tissue oxygen tension values (PtO2) were measured at intervals of 10 micron over a distance of 2 mm by advancing an oxygen microelectrode through the parietal cerebral cortex of all animals. The frequency of low tissue PO2 values (less than 10 mmHg) was increased with all forms of deliberate hypotension, but the magnitude of this change (a shift to the left in the frequency histogram) was significantly different among techniques. The shift toward lower PtO2 values during hypotension was least in animals receiving deep isoflurane anesthesia, intermediate in those receiving SNP, and greatest in those treated with 2-chloroadenosine. In rats, areas of the brain appear to be at risk for significant tissue hypoxia during hypotension produced by 2-chloroadenosine.
2-Chloroadenosine↗
Dose-dependent effects of bupivacaine on rat muscle arterioles.
The dose-dependent actions of bupivacaine on the microvasculature were evaluated by television microscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane. Mean arterial pressure was measured via a carotid artery cannula; heart rate was calculated from the phasic pressure trace. The cremaster muscle was suffused with a balanced electrolyte solution that was controlled for temperature, pH, PO2, PCO2, and osmolarity to provide a physiologic environment. Internal diameters of fourth-order arterioles were measured with an electronic vernier displayed on the video monitor. Arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of bupivacaine hydrochloride, and a 30-min recovery period. Bupivacaine 10(-1), 10(0), 10(1), and 10(2) micrograms X ml-1 produced progressive vasoconstriction to 82.7 +/- 2.9%, 75.0 +/- 5.6%, 71.0 +/- 7.0%, and 65.7 +/- 9.4% of control (P less than 0.05 for each), respectively. Bupivacaine, 10(3) and 2.5 X 10(3) micrograms X ml-1, did not alter arteriolar diameters significantly, although there was a tendency for vasodilation. In a second group of animals, arteriolar diameters were measured during intravenous bupivacaine infusion that produced stable plasma concentrations of 2.3 +/- 0.2 micrograms X ml-1. Vasoconstriction of 91.4 +/- 2.2%, of control (P less than 0.01) was observed. These results demonstrate that dose-dependent arteriolar constriction occurs even with blood bupivacaine levels that are at the upper limits of those expected to occur during regional anesthesia.
Administration, Topical↗
Lidocaine constricts or dilates rat arterioles in a dose-dependent manner.
The microvascular effects of varying concentrations of lidocaine were evaluated with the use of videomicroscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane and breathed room air spontaneously. Mean arterial pressure and heart rate were measured via a carotid artery cannula. The cremaster muscle was suffused with a balanced electrolyte solution and pH, temperature, PO2, PCO2, and osmolarity were controlled. Internal diameters of fourth-order arterioles in the cremaster muscle were measured with an electronic vernier system. In one group of animals (n = 7), arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of lidocaine hydrochloride, and a 10-min recovery period. Lidocaine hydrochloride, 10(0), 10(1), 10(2), 10(3), or 10(4) micrograms X ml-1, produced changes in arteriolar diameters to 88.9 +/- 0.9, 79.0 +/- 1.3, 67.5 +/- 2.4, 60.1 +/- 3.4, and 127.1 +/- 7.2 per cent of control, respectively (P less than 0.001). In a second group of animals (n = 4), fourth-order arteriolar diameters were measured during administration of intravenous lidocaine, 1.2 mg X kg-1 bolus plus 0.3 mg X kg-1 X min-1. Vasoconstriction to 91.3 +/- 0.9% of control was observed (P less than 0.001). These results demonstrate a biphasic dose-dependent response to lidocaine. At lesser concentrations, including those that occur in the plasma of patients during intravenous infusion or nerve blocks, dose-related vasoconstriction occurred. Lidocaine, 10(4) micrograms X ml-1, a concentration similar to that which occurs at the site of injection during infiltration, nerve block, or epidural anesthesia, produced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Topical↗
Effects of anesthetics on regional hemodynamics in normovolemic and hemorrhaged rats.
Twenty-nine male Sprague-Dawley rats were divided into four groups based on anesthetic exposure, i.e., awake animals and those receiving anesthesia produced by chloralose-urethan, pentobarbital, or by midcollicular brain stem transsection. Before and after hemorrhage (30% of the estimated blood volume), cardiac output (CO) and regional blood flows were measured by the microsphere method. Arterial blood gases and lactate (L) and pyruvate (P) were also determined. CO and regional blood flows were greatest and the L/P ratio was least in awake animals both before and after hemorrhage. In normovolemic rats, the frequency of altered values (as compared with those in awake animals) was similar for all anesthetic techniques, whereas the CO and regional blood flow responses to hemorrhage were altered less frequently in decerebrated animals. Decerebration may be the preferable procedure if the intent is to produce responses in anesthetized animals similar to those in awake rats. If the intent is to study hemodynamics in a specific organ, the selection of an anesthetic technique should be guided by the individual anesthetic effects on that particular tissue.
Anesthesia, General↗
The influence of naloxone on regional hemodynamics in hemorrhaged rats.
Naloxone increases arterial pressure in hemorrhaged animals, but its effects on organ blood flows are not well established. We measured central and regional hemodynamics immediately before and 25 min or 55 min after hemorrhage in 33 anesthetized rats. Fifteen minutes after the beginning of hemorrhage, animals received either vehicle (n = 17) or naloxone (n = 16), 10 mg/kg, intravenously. At 25 min, animals treated with naloxone had a greater blood flow to the left cerebral hemisphere than those receiving vehicle, but all other measurements were similar. At 55 min, the mean arterial pressure and heart rate were greater in animals treated with naloxone, but blood flow was increased to the spleen only. Vascular resistance values were greater in the gastrointestinal tract and less in the spleen in animals receiving naloxone. The data confirmed that, in anesthetized rats, naloxone increased mean arterial pressure and splenic blood flow and transiently increased cerebral blood flow, but other regional flows and cardiac output were similar to those in rats receiving vehicle only.
Analysis of Variance↗
Captopril reduces the dose requirement for sodium nitroprusside induced hypotension.
The authors studied 12 patients who required deliberate hypotension for spinal fusion operations in order to investigate the efficacy of captopril for reducing dose requirement for sodium nitroprusside (SNP). Six patients, selected at random, were pretreated with captopril, 3 mg/kg po, and the remaining six patients served as controls. All patients received a similar anesthetic technique, consisting of thiopental 3 mg/kg, pancuronium 0.1 mg/kg, morphine 0.5 mg/kg, plus nitrous oxide 70% in oxygen. SNP was used to maintain mean arterial pressure (MAP) at 50-55 mmHg during deliberate hypotension lasting 140 +/- 13 minutes (mean +/- SE). Patients who received captopril required less SNP than untreated patients both early during hypotension (1.4 +/- 0.5 micrograms X kg-1 X min-1 vs. 4.8 +/- 0.8 micrograms X kg-1 X min-1, P less than 0.05), as well as late during hypotension (2.2 +/- 0.2 micrograms X kg-1 X min-1 vs. 5.6 +/- 0.6 micrograms X kg-1 X min-1, P less than 0.05). Whole blood cyanide was significantly lower in the patients pretreated with captopril than the untreated controls both early in the hypotensive period (2.7 +/- 0.6 mumol/l vs. 13 +/- 4 mumol/l, P less than 0.05) and also late in the hypotensive period (3.7 +/- 0.8 mumol/l vs. 30 +/- 10 mumol/l, P less than 0.05). MAP was reduced by captopril pretreatment both following induction of anesthesia (64 +/- 4 mmHg captopril vs. 80 +/- 4 mmHg control, P less than 0.05) and during surgery before deliberate hypotension (86 +/- 5 mmHg captopril vs. 100 +/- 4 control, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Photodegradation of sodium nitroprusside: biologic activity and cyanide release.
Because the belief that cyanide is released from nitroprusside in vivo recently was challenged, the authors performed a series of experiments that examined the conditions under which nitroprusside is degraded. These experiments include an examination of the release of cyanide and nitric oxide from nitroprusside in vitro, the release of cyanide in vivo, and a comparison of the biologic activity of intact and degraded nitroprusside. Nitroprusside in aqueous solution degraded when exposed to white or blue light but not to red light. While light at 20 microW X cm-2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 microW X cm-2 produced 100% apparent photodegradation after 2 h exposure. At 10% apparent photodegradation, 10% of the nitrosyl ligand was recovered as free nitric oxide, and 0.4% of the cyanide ligand was recovered as free cyanide. Following a 2-h infusion of light-protected nitroprusside in seven patients, cyanide concentrations ranged from 1.4 to 45.5 microM and 0.09 to 3.2 microM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 microW X cm-2) for 4 h. Intact and photodegraded nitroprusside produced identical hypotensive responses in rats as would be expected, since the nitrosyl ligand was detected in solution following degradation, and it mediates this action. Cyanide was released from nitroprusside, both on its exposure to light in vitro and also in vivo. The latter was not an artifact of the assay for cyanide. Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.
Animals↗
Anesthetic influences on regional hemodynamics in normal and hemorrhaged rats.
Forty-six male Sprague-Dawley rats were divided in five groups: awake animals and those receiving ketamine, halothane, enflurane, or isoflurane anesthesia. Cannulae were inserted into the left femoral artery and vein and the left ventricle. Inspired concentrations of the volatile anesthetics were adjusted to achieve the minimal alveolar concentration (MAC) of each drug. Ketamine, 125 mg . kg-1, was injected intraperitoneally and then infused at a rate of 1 mg . kg-1 . min-1. All animals breathed spontaneously throughout the experiment (FIO2 = 0.3). Following a 2-h stabilization period, 30% of estimated blood volume was withdrawn gradually over 10 min. Immediately before and 20 min after hemorrhage, cardiac output and regional blood flows were measured by the microsphere method (85Sr, 141Ce-labeled 15-microns microspheres, respectively). Arterial blood samples were analyzed for PO2, PCO2, pH, lactate, and pyruvate at these times also. Prior to hemorrhage, cardiac output (CO) values were similar in awake rats and those receiving ketamine or isoflurane, but CO was reduced moderately by enflurane and to a greater extent by halothane. After hemorrhage, CO was greatest in awake animals and those receiving isoflurane, and awake rats tended to have the greatest organ blood flows. Values of lactate/pyruvate and excess lactate were least in awake animals. Overall results suggested that, in terms of cardiac output and regional blood flows, ketamine approximates the awake state most closely in normovolemic animals, whereas isoflurane anesthesia is most like the awake condition after hemorrhage.
Anesthetics↗
Effects of general anesthetics on the microcirculation.
The potent inhalation anesthetics (halothane, enflurane and isoflurane) have significant influences on the peripheral circulation. The changes in regional blood flows result from a combination of central circulatory effects on cardiac output and arterial pressure and from local microvascular changes in individual organs. The changes are drug-specific, organ-specific, and generally dose-related, so that no simple overall view is reliable and accurate. Some generalizations are possible, however. For example, each of the potent inhalation anesthetics reduces cerebral and cutaneous vascular resistance in a dose-related manner. Each reduces renal blood flow in humans in excess of the reduction in arterial pressure, implying that renal arteriolar constriction occurs with each drug. While the changes in organ blood flow do not result in tissue hypoxia when the circulation is normal, the anesthetics appear to have important microvascular influences during conditions of tissue ischemia such as coronary artery occlusion or hemorrhagic hypotension.
Anesthetics↗
Renovascular hypertension: effect of halothane and enflurane.
Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6-9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia. Principal responses were as follows: mean arterial pressure (MAP) was 193 +/- 4 mmHg awake and decreased to 114 +/- 3 mmHg and 135 +/- 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 +/- 3 mmHg and to 69 +/- 3 mmHg and 96 +/- 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 +/- 1.3 ng X ml-1 X h-1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia, Inhalation↗
Stress free: to be or not to be?
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Adrenal Cortex↗