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C Ince

Publications and source records attributed to C Ince.

At least 19 recordsLinked to original sources
PubMed1999

Microvascular oxygen pressure in the pig intestine during haemorrhagic shock and resuscitation.

1. The aim of this study was to investigate the relation between microvascular and venous oxygen pressures during haemorrhagic shock and resuscitation in the pig intestine. To this end microvascular PO2 (microPO2) was measured by quenching of Pd-porphyrin phosphorescence by oxygen and validated for the intestines. In addition, mesenteric venous blood gasses, blood flow, ilial CO2 production and global haemodynamics were also measured. 2. In one group (n = 11), moderate shock was induced by withdrawal of 40% of the circulating blood volume. Seven of these animals were resuscitated with a crystalloid solution and four with the withdrawn blood. In a second group of three animals, a more severe shock was induced by withdrawal of 50% of the circulating blood volume; these animals were not resuscitated. 3. Baseline mesenteric venous PO2 and microPO2 values were similar (60 +/- 9 and 60 +/- 11 mmHg, respectively). During moderate shock, microPO2 dropped significantly below mesenteric venous PO2 (26 +/- 10 versus 35 +/- 8 mmHg). After resuscitation with crystalloid solution, microPO2 and mesenteric venous PO2 rose to 44 +/- 9 and 44 +/- 6 mmHg, respectively. In the group that received the withdrawn blood, values were 41 +/- 9 and 53 +/- 12 mmHg, respectively. Severe shock resulted in a drop in the mesenteric venous PO2 (n = 3) to a value similar to that seen in the moderate shock group, but the gut microPO2 dropped to a much lower value than that of the moderate shock group (15 +/- 5 versus 26 +/- 10 mmHg). 4. The results indicate that the oxygenation of the microcirculation of the gut can become lower than the venous PO2 under conditions of haemorrhagic shock.

Animals↗
PubMed1999

Microcirculatory oxygenation and shunting in sepsis and shock.

OBJECTIVE: To review optical spectroscopic techniques for assessment of the determinants of tissue oxygenation and to evaluate the notion that the disturbances in oxygen pathways in sepsis can be accounted for by enhanced functional shunting of parts of the microcirculation. DATA RESOURCES: Experimental data from previous research and the literature were analyzed. STUDY SELECTION: The data selected pertained to a) whether cellular distress in sepsis is caused by tissue hypoxia or disturbed metabolic pathways, b) optical spectroscopic techniques used to study microcirculatory oxygenation, and c) possible mechanisms underlying shunting of the microcirculation in hypoxemia and sepsis. STUDY SYNTHESIS: Despite resuscitation of oxygen-derived variables, signs of regional tissue hypoxia persist in sepsis. The mechanisms underlying this condition are expected to be associated with oxygen pathways in the microcirculation. Optical spectroscopic techniques are providing new insights into these mechanisms. These include absorption spectroscopy for hemoglobin saturation of erythrocytes, reduced nicotinamide adenine dinucleotide fluorescence for tissue mitochondrial bioenergetics, and palladium-porphyrin phosphorescence for microvascular PO2. Reduced nicotinamide adenine dinucleotide videofluorescence studies have shown the heterogeneous nature of hypoxia. Measurement of gut microvascular PO2 in pigs has shown the development of a PO2 gap between microvascular PO2 and venous PO2 during hemorrhage and endotoxemia, with a larger gap occurring in sepsis than in hemorrhage. It is hypothesized that this difference is caused by the enhanced shunting of the microcirculation present in sepsis. CONCLUSIONS: Microcirculatory distress may form one of the earliest stages in the progress of sepsis to multiple organ failure, and shunting of the microcirculation may be an important contributing factor to this development. To evaluate the severity of microcirculatory distress and the effectiveness of resuscitation strategies, new clinical technologies aimed at the microcirculation will need to be developed. It is anticipated that optical spectroscopy will play a major role in the development of such tools.

Humans↗
PubMed1999

PO2 measurements in the rat intestinal microcirculation.

Microvascular partial oxygen pressure (PO2) data measured with the quenched phosphorescence of palladium-porphyrin (Pd-porphyrin) with the use of optical fibers have provided new insight into the behavior of the microvascular oxygenation in models of shock. However, the actual microcirculatory compartment measured by this fiber technique has not yet been demonstrated. The purpose of this study was to investigate whether the PO2 of the intestines, as measured using a fiber phosphorometer, reflects the microvascular compartment. To this end, a new intravital phosphorometer with an improved sensitivity to high-PO2 levels (up to 180 mmHg) was developed and validated. With this setup, PO2 values were measured at different inspired oxygen fractions (15, 25, and 50% oxygen) in first-order arterioles, capillaries, and venules of the ileum of rats. Simultaneously, the PO2 was measured with an optical fiber attached to another phosphorometer. PO2 measurements with the fiber phosphorometer show excellent correlation with the PO2 in the capillaries and first-order venule vessels (r2 = 0.94, slope 0.99). We therefore conclude that values measured with the fiber phosphorometer correlate with the capillary and venular PO2.

Animals↗
PubMed1999

Regional ischemia in hypertrophic Langendorff-perfused rat hearts.

Myocardial hypertrophy decreases the muscle mass-to-vascularization ratio, thereby changing myocardial perfusion. The effect of these changes on myocardial oxygenation in hypertrophic Langendorff-perfused rat hearts was measured using epimyocardial NADH videofluorimetry, whereby ischemic myocardium displays a high fluorescence intensity. Hypertrophic hearts, in contrast to control hearts, developed ischemic areas during oxygen-saturated Langendorff perfusion. Reoxygenation of control hearts after a hypoxic episode resulted in a swift decrease of fluorescence in a heterogeneous pattern of small, evenly dispersed, highly fluorescent patches. Identical patterns could be evoked by occluding capillaries with microspheres 5.9 micrometer in diameter. Ten seconds after reoxygenation there were no more dysoxic areas, whereas reoxygenation in hypertrophic hearts showed larger ischemic areas that took significantly longer to return to normoxic fluorescence intensities. Hypothesizing that the larger areas originate at a vascular level proximal to the capillary network, we induced hypoxic patterns by embolizing control hearts with microspheres 9.8 and 15 micrometer in diameter. The frequency distribution histograms of these dysoxic surface areas matched those of hypertrophic hearts and differed significantly from those of hearts embolized with 5.9-micrometer microspheres. These results suggest the existence of areas in hypertrophic Langendorff-perfused hearts with suboptimal vascularization originating at the arteriolar and/or arterial level.

Animals↗
PubMed1998

NADH videofluorimetry to monitor the energy state of skeletal muscle in vivo.

BACKGROUND: Reduction of the cellular energy state during ischemia of the limbs is an important determinant for development of necrosis. Since energy conversion in the mitochondria is based on electron transport from NADH to molecular O2, the NADH/NAD+ redox couple reflects the mitochondrial redox state and cellular O2 requirement. The applicability of NADH videofluorimetry to monitor noninvasively changes in the energy state of intact resting skeletal muscle as a function of oxygenation was investigated in a rat model. MATERIALS AND METHODS: In mechanically ventilated rats (n = 6), NADH fluorescence images of the gracilis muscle were recorded under different oxygenation conditions. Induction of anoxic and ischemic hypoxia were verified by simultaneous measurement of tissue oxygen pressure and afferent blood flow. RESULTS: Anoxic hypoxia and ischemic hypoxia increased the NADH fluorescence intensity by 46.0 +/- 15.0 and 30.8 +/- 26.4%, respectively. The response time of NADH fluorescence intensity, tissue oxygen pressure, and afferent blood flow was similar during development of anoxic and ischemic hypoxia. Upon reperfusion and reoxygenation, however, NADH fluorescence intensity changed significantly earlier than tissue oxygen pressure as measured by an oxygen needle electrode. CONCLUSION: These results demonstrate that changes in NADH fluorescence intensity reflect oxygenation changes in intact skeletal muscle in vivo. Since NADH videofluorimetry, in contrast to oxygen needle electrode measurements, noninvasively visualizes temporal and regional changes in the energy state of skeletal muscle, this technique has the potential to improve clinical evaluation of ischemia/reperfusion injury and tissue viability.

Animals↗
PubMed1998

A novel method of evaluation of three heat-moisture exchangers in six different ventilator settings.

OBJECTIVE: The purpose of this study was to assess and compare the humidification, heating, and resistance properties of three commercially available heat-moisture exchangers (HMEs). To mimic clinical conditions, a previously validated, new, realistic experimental set-up and measurement protocol was used. DESIGN: Prospective, comparative experimental study. SETTING: Surgical Intensive Care Unit, University Hospital of Rotterdam. MATERIALS: An experimental set-up consisting of a patient model, measurement systems, and ventilator and three different HME types. INTERVENTIONS: The air flow, pressure in the ventilation circuit, pressure difference over the HME, and partial water vapour pressure and temperature at each side of the HMEs were measured. Measurements were repeated every 30 min during the first 2 h and every hour up to 24 h for each HME at six different ventilator settings. The mean inspiratory and maximum expiratory resistance, flow-weighted mean absolute humidity and temperature outputs, and humidification and heating efficiencies of HMEs were calculated. MEASUREMENTS AND RESULTS: The Dar Hygroster had the highest humidity output, temperature output, humidification efficiency, and heating efficiency values throughout the study (32.8 +/- 21. mg/l, 32.2 +/- 0.8 degrees C, 86.3 +/- 2.3%, and 0.9 +/- 0.01%, respectively) in comparison to the Humid-Vent Filter (25.3 +/- 3.2 mg/l, 31.9 +/- 0.8 degrees C, 72.2 +/- 5.3%, 0.9 +/- 0.02%, respectively) and the Pall Ultipor BB100 breathing circuit filter (23.4 +/- 3 mg/l, 28.3 +/- 0.7 degrees C, 68.8 +/- 5.9%, 0.8 +/- 0.02%, respectively). The inspiratory and expiratory resistance of the HMEs remained below clinically acceptable maximum values (2.60 +/- 0.04 and 2.45 +/- 0.05 cmH2O/l per s, respectively). CONCLUSION: The Dar Hygroster filter was found to have the highest humidity and temperature output of all three HMEs, the Humid-Vent filter had a satisfactory humidity output only at low tidal volume flow rate and minute volume settings, whereas the Pall Ultipore BB 100 never achieved a sufficient humidity and temperature output.

Hot Temperature↗
PubMed1998

Low-volume resuscitation with a hemoglobin-based oxygen carrier after hemorrhage improves gut microvascular oxygenation in swine.

Using palladium-porphyrin quenching of phosphorescence, we investigated the influence of diaspirin cross-linked hemoglobin (DCLHb) on gut microvascular oxygen pressure (microPO2) in anesthetized pigs. Values of gut microPO2 were studied in correlation with regional intestinal as well as global metabolic and circulatory parameters. A controlled hemorrhagic shock (blood withdrawal of 40 mL/kg) was followed by resuscitation with either a combination of lactated Ringer's solution (75 mL/kg) and modified gelatin (15 mL/kg)(lactR/Gel) or 10% DCLHb (5 mL/kg). After resuscitation, gut microPO2 was similarly improved in the lactR/Gel group (from 25 +/- 10 mm Hg to 53 +/- 8 mm Hg) and the DCLHb group (from 23 +/- 9 mm Hg to 46 +/- 6 mm Hg), which was associated with increased gut oxygen delivery. However, the improvement after resuscitation with DCLHb was sustained for longer periods of time (75 vs 30 min). Mesenteric venous PO2 was increased after resuscitation with lactated Ringer's solution and modified gelatin but not with DCLHb, which was associated with an increased gut oxygen consumption in the latter group. We conclude that measurement of microPO2 by the palladium-porphyrin phosphorescence technique revealed DCLHb to be an effective carrier of oxygen to the microcirculation of the gut. Also, this effect can be achieved with a lower volume than is currently used in resuscitation procedures.

Animals↗
PubMed1998

Red blood cell rigidification during cyclosporin therapy: a possible early warning signal for adverse reactions.

In a previous retrospective study with kidney-transplant patients, immunosuppressive treatment with Cyclosporin A (CsA) was found to be associated with impaired red blood cell (RBC) deformability. The aim of the present study was to evaluate and substantiate a possible causal relationship between the use of CsA and its effect on RBC deformability in a prospective study on non-transplant patients. Blood samples of 12 patients with psoriasis were taken before and after 2, 4, 8, 12 and 16 weeks of treatment with CsA (3-5 mg/day). Red cell deformability, expressed as Elongation Index (EI), was measured with the Laser-assisted Optical Rotational Cell Analyzer (LORCA), a new ektacytometric instrument. Mean values +/- SD for EI found after 16 weeks of treatment with cyclosporin (0.570 +/- 0.008) were significantly (p < 0.001) lower than the value before treatment (0.589 +/- 0.011). A dose-response relation could not be established within the small range of CsA doses used in this study. Irrespective of the dose, however, a significant correlation (r = -0.55; p = 0.0001) between duration of treatment and decrease in EI was demonstrated. In vitro incubation of blood with cyclosporin was not able to reproduce this effect, suggesting that a direct effect of the drug on RBCs is unlikely. Despite its use in relatively low doses, CsA causes a reduction in RBC deformability, an effect that increases during the course of treatment. It is suggested that this slow, but continuously increasing, RBC rigidification plays a role in the early pathogenesis of the adverse nephrotoxic complications frequently associated with this immunosuppressive regimen.

Cyclosporine↗
PubMed1997

(Semi-)quantitative analysis of reduced nicotinamide adenine dinucleotide fluorescence images of blood-perfused rat heart.

In vivo analysis of the metabolic state of tissue by means of reduced nicotinamide adenine dinucleotide (NADH) fluorimetry is disturbed by tissue movements and by hemodynamic and oximetric effects. These factors cause changes in the absorption of ultraviolet (UV) excitation light by the tissue. Many different methods have been used in the literature to compensate measured NADH fluorescence intensities for these effects. In this paper we show on theoretical grounds that the ratio of NADH fluorescence intensity and UV diffuse reflectance intensity provides a (semi-)quantitative measure of tissue NADH concentrations. This result is corroborated by experiments with tissue phantoms in which absorption and back-scattering properties were varied. Furthermore, we have verified the validity of this compensation method in isolated Langendorff-perfused rat heart preparations. In this preparation oximetric effects (of blood and tissue) are the major determinants of the metabolism-dependent UV diffuse reflectance change. Hemodynamic effects accompanying compensatory vasodilation are negligible. Movement artifacts were eliminated by simultaneously recording fluorescence and reflectance images, using a CCD camera with a biprism configuration. The results show that the NADH fluorescence/UV reflectance ratio can be used to monitor the mitochondrial redox state of the surface of intact blood-perfused myocardium.

Animals↗
PubMed1997

Nitric oxide causes dysfunction of coronary autoregulation in endotoxemic rats.

OBJECTIVE: This study tested the hypothesis that overproduction of endogenous nitric oxide (NO) during endotoxemia may modulate coronary autoregulation and myocardial reactive hyperemia. METHODS: Hearts of endotoxin-pretreated rats and controls were isolated and arranged for perfusion in a Langendorff preparation. Autoregulation was studied by examining flow-pressure relations during stepwise changes in perfusion pressure. The contribution of nitric oxide was examined by perfusion with N omega-nitro-L-arginine (NNLA), an inhibitor of nitric oxide synthesis and methylene blue (MB), an inhibitor of soluble guanylate-cyclase. RESULTS: Endotoxin-treated hearts showed massive coronary vasodilatation and autoregulatory function was impaired at perfusion pressures from 20 to 60 mmHg. Both NNLA and MB reduced coronary flow, improved autoregulation and eliminated differences in coronary flow and autoregulation between the control and endotoxin-treated group. Vasoconstriction with vasopressin, a direct smooth muscle constrictor, could not eliminate differences in autoregulation between groups. Reactive hyperemia following coronary occlusion in endotoxin-treated hearts showed decreased duration, flow repayment and repayment ratio. In the presence of NNLA or MB, however, no significant differences in reactive hyperemic flow patterns were present. CONCLUSIONS: These observations suggest that massive coronary vasodilatation due to increased myocardial NO synthesis can result in autoregulatory dysfunction and altered myocardial reactive hyperemia during endotoxemia.

Animals↗
PubMed1996

In vivo structural studies of the hippocampus in normal aging and in incipient Alzheimer's disease.

Population trends indicate that in the near future the size of the elderly population will increase. This will result in a large increment in the numbers of persons suffering mild to severe levels of cognitive impairment. While considerable efforts continue to be made to explain brain changes associated with Alzheimer disease (AD), little is known of the brain changes in aging without dementia or so-called normal aging. Pathologic studies suggest that the medial temporal lobe is informative in the examination of the early brain changes related to AD. However, pathologic studies only offer a single observation and considerable uncertainty exists regarding the likelihood of progression of disease and the development of dementia. Several structural neuroimaging studies have recently investigated this anatomy and recent reports are encouraging for a medial temporal lobe based diagnosis for age-related cognitive impairments. We will present our findings on the MRI anatomy of the hippocampal formation as well as data bearing on the use of hippocampal formation imaging in the diagnosis of AD and as a predictive marker for future dementia. Our findings suggest an anatomically specific relationship between hippocampal volume and secondary memory performance. Because these observations apply to nondemented and normal elderly subjects, we are encouraged that the anatomy of age-related cognitive impairments can be reliably recognized and possibly put to use in therapeutic studies.

Aged↗