Search PubMed⌕ Search

Biomedical subjects

D E Longnecker

Publications and source records attributed to D E Longnecker.

At least 19 recordsLinked to original sources
PubMed1992

Effects of hypoxemia on regional blood flows during anesthesia with halothane, enflurane, or isoflurane.

Hypoxemia during anesthesia can cause severe morbidity and mortality. To determine how the volatile anesthetics alter the normal hemodynamic compensation for hypoxemia, we investigated the effects of various anesthetics on regional blood flows during normoxemia and during normocapnic hypoxemia (FIO2 0.12 for 20 min) in rats. Using the radioactive microsphere method, organ blood flows were determined in animals anesthetized with 1 MAC of halothane, enflurane, or isoflurane and in awake animals. Brain blood flow increased significantly with hypoxemia in awake animals. However, brain blood flow decreased in all anesthetized animals that were hypoxemic. Coronary blood flow also increased significantly with hypoxemia in awake animals. In the presence of volatile anesthetics, coronary blood flow decreased, a decrease that was unchanged with hypoxemia. Thus, there was a large difference in brain and coronary blood flows between awake hypoxemic and anesthetized hypoxemic animals. Hypoxemia did not alter the magnitude of renal, gastrointestinal tract, or total hepatic blood flows in awake animals. However, all three blood flows decreased significantly in anesthetized hypoxemic animals. We conclude that volatile anesthetics modify the compensatory responses to hypoxemia that occur in awake animals, resulting in decreased blood flow to vital organs.

Anesthesia, Inhalation↗
PubMed1992

The influence of hemorrhage on organ perfusion during deliberate hypotension in rats.

There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.

2-Chloroadenosine↗
PubMed1992

Endothelium-dependent circulatory control--a mechanism for the differing peripheral vascular effects of isoflurane versus halothane.

Several studies have suggested that halothane and isoflurane modify responses to endothelium-dependent vasodilators, indicating that the differing circulatory effects of these anesthetics may be, in part, attributable to alterations in endothelial cell control of vascular tone. This study was designed to determine the contribution of endothelium-derived relaxing factor (EDRF/NO) to circulatory control in indomethacin-treated rats anesthetized with equipotent concentrations (1 MAC) of either isoflurane (n = 6) or halothane (n = 8). Using radiolabelled microspheres, systemic and regional hemodynamics were measured in cerebrum, cerebellum, heart, kidney, gastrointestinal tract, spleen, liver, skeletal muscle, skin, ear, and white and brown fat. Cardiac output, mean arterial pressure (MAP), systemic vascular resistance (SVR), regional blood flows, and regional vascular resistances were determined before (control) and after administration of NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg) to inhibit EDRF/NO synthesis, and following L-arginine (300 mg/kg) to reverse the effects of L-NMMA. In both anesthetic groups, L-NMMA decreased cardiac output and increased MAP, SVR, and regional resistances in brain, heart, kidney, spleen, gastrointestinal tract, hepatic artery, skeletal muscle, skin, and white fat. L-arginine returned SVR and MAP to or below control values in both groups, although cardiac output remained decreased. During isoflurane as compared to halothane anesthesia, L-NMMA caused significantly greater increases in blood pressure (54 +/- 7% vs. 24 +/- 2%) and SVR (143 +/- 22% vs. 79 +/- 11%). In addition, rats anesthetized with isoflurane had significantly greater increases in vascular resistance in heart, kidney, gastrointestinal tract, hepatic artery, and skin after L-NMMA than did rats anesthetized with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1992

Inhibition of endothelium-derived relaxing factor-dependent circulatory control in intact rats.

The effects of the endothelium-derived relaxing factor (EDRF) inhibitors NG-monomethyl-L-arginine (L-NMMA) and methylene blue (MB) on resting hemodynamics and responses to vasodilators were studied in the intact rat anesthetized with pentobarbital sodium. L-NMMA infusions (100 mg/kg) significantly increased mean blood pressure by 48%; this effect was rapidly reversed by L-arginine (300 mg/kg). MB (50 mg/kg) decreased mean blood pressure by 24%. Both MB and L-NMMA significantly attenuated the vasodepressor responses to acetylcholine, ATP, and adenosine. By use of radiolabeled microspheres, it was determined that the blood pressure increase after L-NMMA was due to a marked increase in systemic vascular resistance (SVR; from 1.3 +/- 0.1 to 3.1 +/- 0.3 mmHg.ml-1.min-1) and decreased cardiac output. L-NMMA increased vascular resistance in brain, cerebellum, skin, skeletal muscle, ear, white and brown fat, kidney, spleen, hepatic artery, and gastrointestinal tract. Flow decreased in the skin, kidneys, ear, white and brown fat, gastrointestinal tract, portal venous circulation, and liver in response to L-NMMA. In contrast, MB decreased heart rate, blood pressure, and SVR significantly. MB increased blood flow and decreased vascular resistance in several organs, including the brain, and skeletal muscle. These results indicate that both MB and L-NMMA can inhibit agonist-induced EDRF-mediated vasodepressor responses. However, inhibition of agonist-induced responses did not predict the general and regional hemodynamic responses to L-NMMA or MB infusion.

Animals↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1985

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↗
PubMed1985

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↗
PubMed1985

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↗
PubMed1979

Influence of anaesthetic agents on the survival of rats following acute ischaemia of the bowel.

We compared the effects of ketamine and halothane anaesthesia on the survival of rats subjected to superior mesenteric artery occlusion. Survival was significantly greater with halothane. Animals anaesthetized with ketamine developed arterial hypocarbia during bowel ischaemic shock, while those receiving halothane did not. Arterial hypoxaemia was not present in either group. Haematocrits increased in both groups following bowel ischaemia. Excess lactate was increased significantly in non-survivors compared with survivors. The survival data contrast with previous results obtained after haemorrhagic hypotension and emphasize the need to consider differing therapeutic approaches in the various shock states.

Anesthesia, Inhalation↗