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Biomedical subjects

N Lund

Publications and source records attributed to N Lund.

At least 37 records · Page 2Linked to original sources
PubMed1991

Rabbit skeletal muscle PO2 during hypodynamic sepsis.

We measured skeletal muscle tissue PO2 (PtO2) in anesthetized rabbits (n = 7) following infusion of an intravenous bolus of E coli endotoxin. An array of surface PO2 microelectrodes was placed over the hindlimb biceps femoris muscle and sufficient readings were obtained to construct a PtO2 histogram. Changes in the histogram standard deviation were used to characterize micro-circulatory maldistribution. Systemic O2 consumption (VO2) was measured by the expired gas method. Cardiac output (Q) and systemic O2 transport (TO2) were calculated. Samples of arterial, right atrial (ra), and hindlimb venous blood, from a catheter placed in the infrarenal portion of the vena cava, were simultaneously obtained for measurement of blood gases and saturations. Following the administration of endotoxin, there were decreases in Q and TO2 of approximately 50 percent. The VO2 initially decreased 23 percent, but returned to baseline levels 30 minutes after endotoxin administration. Systemic O2 extraction ratio (ERO2 = VO2/TO2) increased from 0.32 +/- .03 to 0.54 +/- .07 (p less than 0.01), whereas hindlimb ERO2 increased from 0.42 +/- .03 to 0.60 +/- .02 (p less than 0.01). The arithmetic mean of the PtO2 histograms decreased after endotoxin infusion (43 +/- 4 to 7 +/- 2 mm Hg; p less than 0.01), but PLO2 remained at baseline levels (35 +/- 2 vs. 33 +/- 2 mm Hg; p = NS). The standard deviation of the PtO2 histograms remained constant during the experiment. This finding supports the notion that skeletal muscle microcirculatory heterogeneity does not increase during endotoxin induced hypodynamic sepsis.

Animals↗
PubMed1991

Effects of dopamine and dobutamine on skeletal muscle oxygenation in normoxemic rats.

The effects of two vasoactive drugs, dopamine and dobutamine, on skeletal muscle tissue oxygenation were studied in a normoxemic rat model. It is usually claimed that drugs may increase or decrease oxygen delivery to tissues. However, this claim is only valid on the global level. Our interest is directed towards individual organs. Two groups of rats (n = 7 each) were studied. One group received dopamine, the other dobutamine. Blood gases, hematocrits, and mean arterial blood pressures were measured in addition to tissue pO2. Infusion of dopamine 2.5 micrograms/kg/min resulted in a statistically significant decrease in skeletal muscle pO2. Higher doses of dopamine, and all doses of dobutamine, did not influence pO2 at all. The results raise the question of whether blood flow to vital organs may be negatively affected by dopamine 2.5 micrograms/kg/min. Direct measurements of tissue oxygenation are warranted in, e.g., the liver and gut.

Animals↗
PubMed1990

[Gluteal compartment syndrome].

The gluteal compartment syndrome is a condition which has rarely been described. Most frequently, it is caused by violent injury. A case which was precipitated by intramuscular injection in connection with anticoagulation treatment and which involved the sciatic nerve is described.

Buttocks↗
PubMed1990

Skeletal muscle PO2 during hypoxemia and isovolemic anemia.

We subjected anesthetized mechanically ventilated rabbits (n = 6) to sequential exchanges of blood for a 6% dextran solution and compared their responses with those obtained in a previous study on progressive hypoxemia (n = 7). Right atrial PO2 (PVO2)RA and hindlimb PO2 (PVO2)limb, measured at the level of the iliac bifurcation, were compared with tissue PO2 (PtiO2) histograms obtained with an array of surface microelectrodes placed over the biceps femoris muscle. Systemic O2 consumption (VO2) was measured with the expired gas method. Cardiac output and systemic O2 transport (TO2) were calculated. Six exchanges of blood for dextran produced decreases in hemoglobin from 10.8 +/- 0.4 to 2.7 +/- 0.2 g/dl (P less than 0.001). Critical TO2 (TO2crit), defined as the level of TO2 associated with initial decreases in control VO2, was similar for anemia and hypoxemia (40.5 +/- 5.6 and 40.1 +/- 5.3 ml.min-1.kg-1, respectively). At any given TO2 other than control TO2, the levels of (PVO2)RA and (PVO2)limb were greater in anemia than in hypoxemia (P less than 0.01), but the mean and the distribution of the PtiO2 histograms were similar in both conditions. Mean PtiO2 was significantly less than (PVO2)RA or (PVO2)limb, except for those values obtained during the control period. These results confirm our previous finding that PVO2 is not an accurate index of PtiO2 under conditions of tissue hypoxia. Furthermore, similar PtiO2 levels during anemia and hypoxemia suggest that VO2 is limited by decreases in O2 diffusion from the capillaries to the cells.

Anemia↗
PubMed1989

Relationship of venous PO2 to muscle PO2 during hypoxemia.

Anesthetized mechanically ventilated rabbits were subjected to progressive hypoxemia (n = 7) to determine the relationship of venous PO2 (PvO2) to skeletal muscle PO2 (PtiO2). Measures of arterial PO2 (PaO2), right atrial PO2 [(PvO2)RA], and hindlimb PO2 [(PvO2)limb], were obtained from the carotid artery, right atrium, and inferior vena cava, just above the level of the iliac bifurcation. Biceps femoris muscle PtiO2 was measured with a surface O2 microelectrode having eight measuring points. PaO2 was decreased from 90.3 +/- 5.4 to 26.8 +/- 0.8 Torr in five consecutive steps, followed by reoxygenation to 105.6 +/- 10.5 (SE) Torr. Measurements were obtained after each decrement in PaO2. A total of 128 measures of PtiO2 were obtained per experimental stage. The mean and distribution of the muscle PtiO2 histogram were determined. Measurements were compared with analysis of variance and the Newman-Keuls post hoc method. (PvO2)limb had similar values as the average muscle PtiO2 (PtiO2) for PaO2 values greater than 52.1 +/- 4.3 Torr, where (PvO2)limb became greater than PtiO2 (P less than 0.05). The lowest measures of (PvO2)limb and PtiO2 were 15.9 +/- 0.7 and 4.0 +/- 0.1 Torr, respectively (P less than 0.01). The PtiO2 histograms showed no evidence of increased microvascular heterogeneity with hypoxemia. We conclude that in hypoxemia PvO2 is greater than muscle PtiO2. This difference may be related to the establishment of significant physicochemical O2 gradients from erythrocyte to tissue cell.

Animals↗
PubMed1989

Serotonin as a modulator of skeletal muscle oxygenation: effects of ketanserin and ritanserin on oxygen pressure distributions.

Hyperoxemia induces disturbances in tissue oxygenation. The purpose of this study was to examine the influence of serotonin (5-HT) on skeletal muscle oxygenation during hyperoxemia. Two highly selective and pure 5-HT2 receptor antagonists with different T1/2, ketanserin (90 min). and ritanserin (40 h), were employed during measurements of skeletal muscle oxygenation, blood gases and hemoglobin oxygenation in a rabbit model. Surface oxygen pressure measurements were performed on the medial vastus muscle using an MDO oxygen electrode. The results are presented as oxygen pressures distributions (OPD's). Ketanserin was used in one group of 7 rabbits (K-group), and ritanserin in another 7 (R-group). Normal near-Gaussian OPD shapes during normoxemia (paO2 11 kPa) changed to abnormal (scattered) shapes during hyperoxemia (paO2 approx. 50 kPa). After injection of ketanserin (0.07 mg.kg-1 bw) or ritanserin (0.035 mg.kg-1 bw) OPD shapes normalized in 13/14 cases. In the K-group, after ninety minutes, OPD shapes had rescattered and were not completely normalized after an additional half dose of ketanserin (0.035 mg/kg-1 bw). In the R-group, OPD shapes remained normal without additional ritanserin administration. There was poor correlation between normalization of muscle tissue oxygenation and venous pO2 (PvO2) or avDO2. Hyperoxemia-induced disturbance in OPD shape was normalized both by ketanserin and ritanserin in a fashion possibly related to the T1/2 time of the respective 5-HT2 receptor antagonist. These results suggest that serotonin modulates skeletal muscle oxygenation.

Animals↗
PubMed1989

Cellular oxygen utilization during multiple organ failure.

Organ survival depends on adequate tissue oxygenation and normal metabolic function. In MSOF there are changes in O2 transport and cellular bioenergetics. These metabolic alterations may set in motion mechanisms of cellular damage that will affect microcirculatory control and the ability of the cell to maintain both function and homeostasis.

Adenosine Triphosphate↗
PubMed1988

Striated muscle tissue oxygenation and lactate levels during normo-, hyper- and hypocapnia. A study in the rabbit.

The relationship between striated muscle tissue oxygenation during hyper- and hypocapnia, and lactate levels and venous pO2 (pvO2) was studied in a rabbit model. Seven rabbits were ventilated with constant volume during ether anesthesia, and arterial pCO2 (paCO2) was varied by addition of CO2. Muscle tissue oxygenation was measured with a multichannel electrode on the striated muscle surface, the results presented as oxygen pressure distributions (OPD:s). The principal result during hypercapnia (paCO2 9.9 kPa) was a tendency toward increased mean oxygen pressure (ptxO2) of the OPD; OPD shape was normal in 5/7 runs. Arterial lactates (aLa) decreased. During duplicate hypocapnia to paCO2 2.9 and 2.8 kPa ptxO2 decreased, but only in 4/14 runs were tissue oxygen pressures (ptO2) below 0.6 kPa found. OPD shape was scattered in 6/14 runs indicating disturbance in regulation of tissue oxygenation (but without signs of hypoxia). An increase in aLa was found, as well as a decrease in arterio-venous lactate difference (avDLa). Lacking direct blood flow measurements, these two results could not be interpreted as increased lactate efflux per se. Muscle lactates (mLa) were high but, on average, not higher than a control group. A decrease in pvO2 was seen during hypocapnia. Subgrouping OPD:s according to shape and presence of low ptO2 values did, however, suggest that lactate was released in cases with low ptO2 values: a covariation was seen in runs with low oxygen pressures between high arterial and muscle lactates, decreased avDLa and pvO2; runs with scattered OPD:s had only intermediately high lactates and low avDLa and pvO2 when compared to normally shaped OPD:s. In this study, hypercapnia influenced striated muscle tissue oxygenation only to a minor degree while hypocapnia influenced it more but not as much as expected. Only when low oxygen pressures were present in the OPD:s were there indications of peripheral lactate release.

Animals↗
PubMed1988

Surface oxygen pressure distributions in rabbit skeletal muscle: dependence on arterial pO2.

Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.

Animals↗
PubMed1987

The oxygen sensitivity of a multipoint antimony electrode for tissue pH measurements. A study of the sensitivity for in vivo PO2 variations below 6 kPa.

Monocrystalline micro antimony electrodes in a multipoint arrangement as described by Lund et al. were placed on the skeletal muscle surface of the rabbit. Tissue oxygen levels were measured simultaneously with the MDO (Mehrdraht Dortmund Oberfläche) oxygen electrode. The sensitivity for variations in tissue PO2 (PO2(t)) was evaluated for the antimony metal-metal oxide sensor. The sensitivity (delta E/delta log10 PO2)+/- SE was found to be 21.8 +/- 1.2 mV in the interval between 0.1 kPa and 1 kPa and 53 +/- 5 mV in the interval between 1 kPa and 6 kPa. These results are not consistent with the oxygen sensitivity of monocrystalline antimony described in vitro, but are in agreement with the findings of Nilsson & Edwall. A plausible explanation for the S-shaped oxygen sensitivity curve of antimony at oxygen levels below 10 kPa could be an interaction, at the electrode surface, between the dissolved oxygen and the oxygen bound to haemoglobin. If this is the case, the use of an antimony electrode would make possible the determination of the dissociation of oxyhaemoglobin in tissues.

Animals↗
PubMed1987

Capillary grouping in hamster tibials anterior muscles: flow patterns, and physiological significance.

We have used fluorescein-labeled albumin and epifluorescence videomicroscopy to visualize the organization and flow patterns in the capillaries of a postural muscle, the tibialis anterior, in the pentobarbital-anesthetized hamster. Video tape records were made of overlapping microscope fields comprising portions of the muscle up to two millimeters in length and as much as 180 micron in depth. Three-dimensional reconstructions made from these tapes incorporated observations on flow patterns and geometry of the microvessels. The microcirculation in the tibialis was found to be arranged in repeating modules or 'units', consisting of approximately 15 capillaries supplied by a common arteriole and drained by a common venule. The mean distance from arteriole to venule in a unit was 855 +/- 233 micron (X +/- SD) and the mean capillary length was 805 +/- 330 micron. Flow in the capillaries within a unit was almost entirely concurrent, and there was little interchange of blood flow between the capillaries of adjacent units. The flow in capillaries of adjacent units was both countercurrent and concurrent. For each capillary, a count of the adjacent capillaries with concurrent and countercurrent flow was made. The ratio of concurrent to countercurrent flow varied from 2.4 to 4.3, being greatest at the midpoint of the unit and least at the arterial and venous ends. Our observations suggest that the capillaries of striated muscle are arranged in modules which may function as the fundamental control and distribution elements in the microcirculation.

Animals↗
PubMed1987

High-energy phosphates and surface oxygen pressure fields in skeletal muscle after high-energy trauma.

The effect of a high energy missile trauma on energy metabolism and tissue oxygenation in uninjured parts of skeletal muscle was studied in anaesthetized pigs up to 72 hours after the trauma. High energy phosphates (HEP) were measured in muscle biopsies, and muscle tissue oxygenation was measured as muscle surface oxygen pressure fields by an oxygen electrode. In the traumatized group significantly decreased levels of HEP were found in spite of normal tissue oxygenation 72 hours after the trauma. In the control group both the HEP and the muscle tissue oxygenation were unchanged compared to the pretrauma situation. Decreased synthesis of HEP due to tissue hypoxia or inadequate nutrition could not account for the difference between the control and the trauma group. It was suggested that hypermetabolism induced by the high energy trauma caused increased utilization and thereby decreased concentrations of the HEP 72 hours after the trauma. It was also concluded that the general posttraumatic metabolic changes found in uninjured parts of the muscle tissue differed from the local changes of traumatized muscle described by other investigators, and therefore probably were caused by other mechanisms.

Adenosine Diphosphate↗
PubMed1986

Skeletal muscle oxygen pressure fields during controlled hypotension with adenosine and sodium nitroprusside. A comparative study in the rabbit.

The MDO (Mehrdraht Dortmund Oberfläche) multiwire oxygen electrode was used for studies of oxygen pressure fields in eight rabbit skeletal muscle preparations during controlled hypotension with adenosine and sodium nitroprusside (SNP). Tissue oxygen histograms were constructed from 120 simple tissue oxygen pressures (PtO2) samples that were collected during 5 min. Statistical analysis between histograms was performed with the two-sample Kolmogorov-Smirnov test. Mean arterial blood pressure was reduced to 60 mmHg with both drugs, corresponding to a 42-43% reduction during the 25-min hypotension period. SNP-induced hypotension caused significant reduction of muscle oxygenization (compared to normotensive controls) in six of the animals, while this occurred on three occasions during adenosine administration. When comparing the histograms during hypotension, the tissue oxygenation during adenosine infusion was higher than during SNP in five and equal to SNP in three animals. Low tissue oxygen pressure values (0-0.6 kPa) were four times more frequent during SNP than during adenosine hypotension, although systemic arterial oxygen pressures were unaffected. We conclude that controlled hypotension with adenosine preserves tissue oxygen pressures better than hypotension induced by SNP.

Adenosine↗
PubMed1986

Effects of increases in the inspired oxygen fraction on brain surface oxygen pressure fields in pig and man.

In six patients undergoing neurosurgical operation, brain surface oxygen pressure was studied during an increase of the inspired oxygen fraction (FiO2). The eight-channel oxygen surface electrode (MDO-electrode) was placed directly on the brain cortex. FiO2 was increased to four levels, from baseline level 0.21 to 0.3, 0.5, 0.7 and 1.0, respectively. During these four stages and FiO2 0.21, brain surface oxygen pressure (PtO2) was measured. The physiological variables such as blood pressure, PaCO2, pH and temperature were stable throughout the study. The results are presented as mean values +/- s.d. and a PtO2 histogram for each FiO2-level. Already at an FiO2 of 0.3 (at a PaO2 of 16.3 +/- 3.4 kPa) scattered histograms were seen in five of six patients. A scattered histogram indicates disturbed microcirculation. At the FiO2 levels of 0.5, 0.7 and 1.0, all histograms were scattered. The PtO2 values did not increase proportionally to PaO2 at FiO2 levels 0.3, 0.5 or 0.7. But at FiO2 1.0 four patients had normal mean PtO2 values and two patients very high mean PtO2 values. It is possible that the four patients with normal PtO2 values succeeded in regulating the cerebral microcirculation as a response to the high FiO2 leading to a high PaO2 (60.1 +/- 6.4 kPa). The same study was initially done on six pigs in which the regional cerebral blood flow (rCBF) was also measured. MDO-electrode measurements at different FiO2-levels gave the same results as in the patients. rCBF decreased when FiO2 was increased.

Adult↗