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P C Hüttemeier

Publications and source records attributed to P C Hüttemeier.

13 recordsLinked to original sources
PubMed1997

Extracellular glutamate and dopamine measured by microdialysis in the rat striatum during blockade of synaptic transmission in anesthetized and awake rats.

We investigated the effect of high dose tetrodotoxin (TTX) on microdialysis measurements of extracellular striatal glutamate and dopamine in normal female rats. Both halothane-anesthetized rats with acutely implanted microdialysis probes and awake rats with microdialysis probes implanted for 24 h were tested. Glutamate levels in awake rats were 45% higher than those of anesthetized rats. Extracellular glutamate remained TTX-insensitive regardless of TTX concentration, anesthesia, or time lapsed after probe implantation. In contrast, TTX reduced dialysate dopamine in all TTX concentrations tested. We speculate that the lower glutamate levels in anesthetized rats reflect the effect of anesthesia. Because glutamate is involved, either as a reactant or a product in a variety of reactions critical to intermediary metabolism in the brain, basal dialysate glutamate levels might indirectly reflect brain metabolism. Further, we conclude that extracellular glutamate collected during non-stimulated conditions is TTX-insensitive. The fact that glutamate levels are TTX-independent does not rule out that glutamate is synaptic in origin but rather demonstrates that it is not nerve impulse-dependent. However, the brain interstitial glutamate pool accessible to the microdialysis probe during control conditions is most likely isolated from the synapse, and therefore does not impose a neurotoxic potential.

Anesthesia↗
PubMed1993

Calcitonin gene-related peptide mediates hypotension and tachycardia in endotoxic rats.

Circulating calcitonin gene-related peptide (CGRP) concentrations are elevated in experimental and clinical sepsis. CGRP causes hypotension and tachycardia, suggesting that the peptide might mediate the acute circulatory changes in sepsis. To test this hypothesis we administered Escherichia coli endotoxin (8 mg/kg iv) to Nembutal- (pentobarbital sodium; 50 mg/kg) anesthetized rats. Endotoxin caused hypotension and tachycardia within 60 min that stabilized for 90 min. After 2 h more severe hypotension developed, and 80% of rats died spontaneously after 3 h. In other endotoxic rats we administered 20 nmol of the CGRP receptor antagonist hCGRP (8-37) intravenously at 60 min. hCGRP (8-37) transiently reversed tachycardia (from 469 +/- 11 to 407 +/- 7 beats/min, P < 0.05) and increased mean blood pressure (from 63 +/- 4 to 93 +/- 11 mmHg, P < 0.05) over 30 min, after which hemodynamics and survival rates were no different from untreated animals. The results suggest that CGRP plays an important role in the acute circulatory changes of endotoxemia. More detailed work is necessary to determine the effects of CGRP antagonism on cardiac function, regional blood flow, and overall survival rates in sepsis.

Animals↗
PubMed1989

Right and left ventricular performance during endotoxin-induced pulmonary hypertension in sheep.

We investigated right and left ventricular performance by radionuclide angiocardiography in anaesthetized and instrumented sheep following a (1.5 micrograms/kg) sublethal Escherichia coli endotoxin infusion. Six animals served as controls and five were pre-treated with intravenous Ibuprofen (12 mg/kg). In control sheep an acute five-fold increase of pulmonary vascular resistance (PVR) resulted in a significant decrease of right ventricular ejection fraction (RVEF) and stroke volume. Left ventricular ejection fraction (LVEF) was unchanged as was pulmonary capillary wedge pressure (PCWP). The calculated right and left ventricular end-diastolic volumes (RVEDV; LVEDV) changed significantly in opposite directions during the acute increase of PVR. Right ventricular end-diastolic pressure increased significantly paralleled by an increase of RVEDV. The decrease of LVEDV with an unchanged PCWP suggested a decrease of left ventricular compliance. Pre-treatment with Ibuprofen resulted in complete cardiovascular stability after endotoxin.

Animals↗
PubMed1988

Ventilation-perfusion inequality during endotoxin-induced pulmonary vasoconstriction in conscious sheep: mechanisms of hypoxia.

In sheep low-dose endotoxin infusion causes transient thromboxane-mediated pulmonary vaso- and bronchoconstriction. These changes are paralleled by a decrease of arterial PO2. To elucidate the mechanisms of hypoxia we analysed ventilation-perfusion (VA/Q) distributions by the multiple inert gas elimination technique before and after endotoxin infusion in six conscious sheep. We found that hypoxia after endotoxin could be explained by both a VA/Q inequality and a simultaneous decrease in the mixed venous oxygen tension. The latter was due to a decrease of cardiac output. True shunt did not contribute to hypoxia as it was unchanged.

Animals↗
PubMed1984

Regional blood flow and pulmonary thromboxane release after sublethal endotoxin infusion in sheep.

Fifteen minutes after intravenous Escherichia coli endotoxin (EN) infusion the sheep lung transiently releases into the systemic circulation up to 12 micrograms of thromboxane A2 (TxA2)/min measured by radioimmunoassay as its metabolite thromboxane B2 (TxB2). To determine whether lung thromboxane release alters regional blood flow (RBF) we injected microspheres before and 20, 30, and 100 minutes after EN infusion in 13 awake sheep. In seven untreated control sheep (group 1) pulmonary vascular resistance (PVR) increased threefold at 20 and 30 minutes after EN infusion, coinciding with a large transpulmonary blood concentration gradient of TxB2. There was no measured RBF change to any systemic tissue or organ except the right ventricle at 20 minutes after EN infusion, when blood flow per gram of tissue doubled. In six sheep (group 2) treated with intravenous ibuprofen before EN infusion there was no increase in PVR, plasma TxB2, or blood flow to the right ventricle, and no difference of RBF to any other organ or tissue when compared to group 1. TxA2 is a potent local pulmonary vasoconstrictor but it rapidly hydrolyzes. Its short half-life and the circulatory delay in systemic arterial delivery prevent TxA2 from acting as a circulating vasoconstrictor.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Pure oxygen breathing increases sheep lung microvascular permeability.

Sheep that breathe pure oxygen via a tracheostomy develop progressive respiratory failure and die within four days. The characteristic terminal findings include an increased water content of the lung, a decrease in lung compliance, and severe hypercarbia. To sequentially assess alterations of lung transvascular fluid dynamics during prolonged oxygen breathing the authors measured lung lymph flow (Q lymph), protein transport (Q protein), and pulmonary vascular pressures in five sheep with chronic lung lymph fistulas. No significant changes of lung transvascular fluid dynamics occurred during the first 60 hours of oxygen breathing, although an increasing trend of Q lymph and Q protein was demonstrable. However, after 72 hours of oxygen breathing, Q lymph, Q protein, and extravascular lung water had increased significantly without any change of pulmonary vascular pressures. The authors conclude that the toxic effects of oxygen on the lungs of sheep include a delayed but marked increase of pulmonary microvascular permeability to protein and fluid.

Animals↗
PubMed1982

Thromboxane and pulmonary hypertension following E. coli endotoxin infusion in sheep: effect of an imidazole derivative.

We assessed the effect of a specific thromboxane synthetase inhibitor (an imidazole derivative) on pulmonary hemodynamics and the concentrations of TxB2 (TxA2), 6-keto-PGF1 alpha (PGI2), and PGF2 in pulmonary lymph and transpulmonary blood samples following intravenous administration of E. coli endotoxin (1 microgram/kg) in sheep. In control animals the rise in pulmonary artery pressure correlated with increases in plasma and lymph TxB2 concentrations and large transpulmonary concentration gradients of this metabolite were measured. In imidazole treated animals both pulmonary hypertension as well as increases in plasma and lymph TxB2 concentrations were substantially reduced. In contrast, peak concentrations of 6-keto-PGF1 alpha (PGI2) and PGF2 alpha were severalfold higher than those measured in control animals. This suggests a shunting of endoperoxide metabolism towards prostacyclin and primary prostaglandins and documents the specificity of the thromboxane synthetase inhibitor. Our study provides evidence that endotoxin-induced pulmonary hypertension is mediated by pulmonary synthesis of TxA2.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Effect of lung thromboxane generation on regional blood flow during sheep bypass.

Acute pulmonary artery hypertension and an increased plasma concentration of thromboxane B2 (TXB2), the stable metabolite of the potent vasoconstrictor thromboxane A2, occur within minutes of the onset of venovenous (VV) partial bypass in the awake sheep. To search for systemic vasoconstriction, we assessed systemic blood flow distribution by radioactive microspheres and correlated the changes to alterations in plasma TXB2 and 6-keto-F1 alpha concentration. In 10 control sheep mean plasma TXB2 concentration increased from 0.39 ng/ml prebypass to about 1.1 ng/ml at 8 and 16 min of bypass. Despite marked pulmonary vasoconstriction with a threefold elevated resistance, the blood flow to the heart, brain, and kidney were unchanged at 8 and 16 min of bypass. However, hepatic vascular resistance increased twofold at 8 min of bypass. Indomethacin treatment (10 mg/kg) of six sheep blocked the increase of both pulmonary and hepatic vascular resistance as well as reduced TXB2 levels below 0.1 ng/ml. Thus VV bypass induces transient and selective vasoconstriction of the lung and liver mediated by vasoconstrictor eicosanoids.

Animals↗
PubMedDate not supplied

In vivo diffusion-weighted magnetic resonance microscopy of rat spinal cord: effect of ischemia and intrathecal hyperbaric 5% lidocaine.

BACKGROUND AND OBJECTIVES: Pathophysiologic mechanisms underlying persistent neurologic deficits after continuous spinal anesthesia using hyperbaric 5% lidocaine are still not well understood. It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier. In this study, we use diffusion-weighted magnetic resonance microscopy to characterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal cord. The parameter measured with DWM, is an "apparent diffusion coefficient," (ADC), which can be used to exclude the presence of ischemia. METHODS: Female Fischer CDF rats were used. Group 1 (n = 5) was exposed to ischemia, group 2 (n = 7) was exposed to intrathecal 5% hyperbaric lidocaine, and group 3 (n = 5) was exposed to intrathecal 7.5% glucose. Diffusion-weighted MR images in group 1 were acquired before and after ischemia induced by cardiac arrest and in groups 2 and 3 rats prior to and during perfusion of the spinal catheter with either 5% hyperbaric lidocaine or 7.5% glucose. RESULTS: Ischemia decreased the ADC by 40% in gray matter and by 30% in white matter of spinal cord. Continuous intrathecal anesthesia with hyperbaric 5% lidocaine did not affect the spinal cord ADC. Further, 7.5% intrathecal glucose had no effect on ADCs in gray or white matter of spinal cord. CONCLUSIONS: Ischemia reduced the ADC in both spinal cord white and gray matter. Hyperbaric 5% lidocaine did not affect the spinal cord ADC during the first 1.5 hours. We suggest that 5% hyperbaric lidocaine does not induce irreversible neurologic deficits by causing spinal cord ischemia.

Anesthetics, Local↗