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Michael I Lindinger

Publications and source records attributed to Michael I Lindinger.

11 recordsLinked to original sources
PubMed2005

An improved method for constructing and selectively silanizing double-barreled, neutral liquid-carrier, ion-selective microelectrodes.

We describe an improved, efficient and reliable method for the vapour-phase silanization of multi-barreled, ion-selective microelectrodes of which the silanized barrel(s) are to be filled with neutral liquid ion-exchanger (LIX). The technique employs a metal manifold to exclusively and simultaneously deliver dimethyldichlorosilane to only the ion-selective barrels of several multi-barreled microelectrodes. Compared to previously published methods the technique requires fewer procedural steps, less handling of individual microelectrodes, improved reproducibility of silanization of the selected microelectrode barrels and employs standard borosilicate tubing rather than the less-conventional theta-type glass. The electrodes remain stable for up to 3 weeks after the silanization procedure. The efficacy of a double-barreled electrode containing a proton ionophore in the ion-selective barrel is demonstrated in situ in the leaf apoplasm of pea (Pisum) and sunflower (Helianthus). Individual leaves were penetrated to depth of approximately 150 microm through the abaxial surface. Microelectrode readings remained stable after multiple impalements without the need for a stabilizing PVC matrix.

Journal Article↗
PubMed2005

Association of maximum voluntary dietary intake of freeze-dried garlic with Heinz body anemia in horses.

OBJECTIVE: To characterize hematologic and clinical consequences of chronic dietary consumption of freeze-dried garlic at maximum voluntary intake in horses. ANIMALS: 4 healthy sex- and age-matched horses. PROCEDURE: An initial garlic dose (0.05 g/kg, twice daily) was fed to 2 horses in a molasses carrier as part of their normal ration and was gradually increased to maximum voluntary intake (0.25 g/kg, twice daily) over 41 days. Dietary supplementation then continued for a total of 71 days. Two control horses were fed molasses with no garlic with their ration. Blood samples were collected weekly and analyzed for hematologic and biochemical changes, including the presence of Heinz bodies. Recovery of affected blood values was followed for 5 weeks after termination of dietary supplementation with garlic. RESULTS: At a daily dose of > 0.2 g/kg, horses fed garlic developed hematologic and biochemical indications of Heinz body anemia, as characterized by increases in Heinz body score (HBS), mean corpuscular volume (MCV), mean corpuscular hemoglobin, platelet count, and serum unconjugated and total bilirubin concentrations and decreases in RBC count, blood hemoglobin concentration, mean corpuscular hemoglobin concentration, and serum haptoglobin concentration. Recovery from anemia was largely complete within 5 weeks after termination of dietary supplementation with garlic. Heinz body score and MCV remained high at the end of the 5-week recovery period. CONCLUSIONS AND CLINICAL RELEVANCE: Horses will voluntarily consume sufficient quantities of garlic to cause Heinz body anemia. The potential for garlic toxicosis exists when horses are chronically fed garlic. Further study is required to determine the safe dietary dose of garlic in horses.

Analysis of Variance↗
PubMed2004

Hematological and acid-base changes in men during prolonged exercise with and without sodium-lactate infusion.

An emerging technique used for the study of metabolic regulation is the elevation of lactate concentration with a sodium-lactate infusion, the lactate clamp (LC). However, hematological and acid-base properties affected by the infusion of hypertonic solutions containing the osmotically active strong ions sodium (Na(+)) and lactate (Lac(-)) are a concern for clinical and research applications of LC. In the present study, we characterized the hematological and plasma acid-base changes during rest and prolonged, light- to moderate-intensity (55% Vo(2 peak)) exercise with and without LC. During the control (Con) trial, subjects were administered an isotonic, isovolumetric saline infusion. During LC, plasma lactate concentration ([Lac(-)]) was elevated to 4 meq/l during rest and to 4-7 meq/l during exercise. During LC at rest, there were rapid and transient changes in plasma, erythrocyte, and blood volumes. LC resulted in decreased plasma [H(+)] (from 39.6 to 29.6 neq/l) at the end of exercise while plasma [HCO(3)(-)] increased from 26 to 32.9 meq/l. Increased plasma strong ion difference [SID], due to increased [Na(+)], was the primary contributor to decreased [H(+)] and increased [HCO(3)(-)]. A decrease in plasma total weak acid concentration also contributed to these changes, whereas Pco(2) contributed little. The infusion of hypertonic LC caused only minor volume, acid-base, and CO(2) storage responses. We conclude that an LC infusion is appropriate for studies of metabolic regulation.

Acid-Base Equilibrium↗
PubMed2004

Chronic metabolic acidosis increases mRNA levels for components of the ubiquitin-mediated proteolytic pathway in skeletal muscle of dairy cows.

Ruminants fed high-grain diets often are subjected to ruminal acidosis, which can lead to excessive absorption of lactate into the blood stream, thereby causing metabolic acidosis. Metabolic acidosis leads to body protein loss, mainly due to increased skeletal muscle degradation. Our objective was to determine the effects of metabolic acidosis on the messenger RNA (mRNA) abundance of genes encoding components of the ubiquitin-mediated proteolytic pathway in the skeletal muscle of lactating Holstein cows. Cows (n = 20) were assigned to one of two treatments: 1) control; or 2) NutriChlor 18-8, an HCl-treated supplement, which was fed to induce chronic metabolic acidosis. The longissimus muscle was biopsied before and after 10 d of treatments. Total RNA isolated from muscle tissue was hybridized with (32)P-labeled cDNA probes encoding for 14-kDa ubiquitin carrier protein E2 (14-kDa E2), ubiquitin, and C8 and C9 subunits of the 20S proteasome. Induction of metabolic acidosis increased (P < 0.05) skeletal muscle mRNA levels for ubiquitin (25%), 14-kDa E2 (34%), and the C8 subunit (20%); however, mRNA abundance for the C9 subunit was unaffected (P > 0.05). These results suggest that up-regulation of the ubiquitin-proteasome pathway is the mechanism by which metabolic acidosis stimulates muscle wasting in ruminants.

Acidosis↗
PubMed2003

Exercise-induced changes in plasma composition increase erythrocyte Na+,K+-ATPase, but not Na+-K+-2Cl- cotransporter, activity to stimulate net and unidirectional K+ transport in humans.

We tested the hypothesis that exercise-induced changes in plasma composition result in peak stimulation of erythrocyte unidirectional K+ (JK,in) and net K+ (JK,net) transport within the first 120 s. In experimental series 1 (7 men; 2 women), plasma [K+] was continuously measured in vitro (37 degrees C) after the addition of red blood cells (RBCs) obtained from rested subjects (resting RBCs) into an exercise-simulated plasma (ESP; increased plasma osmolality, [K+], [H+], [lactate] and [adrenaline] (epinephrine)), and JK,net calculated. In experimental series 2 (7 men; 4 women), resting RBCs were incubated in true exercise plasma (TEP) obtained after two 30 s bouts of high intensity leg cycling exercise to determine JK,net and JK,in (via RBC 86Rb accumulation). JK,net of resting RBCs increased from 0.9 +/- 28.7 in resting plasma to 285 +/- 164 mmol (l RBCs)-1 h-1 in ESP and to 178 +/- 60 mmol (l RBCs)-1 h-1 after 10 s in TEP. Both JK,net and JK,in peaked within 10 s of incubation and decreased rapidly during the initial 120 s. The use of inhibitors for the Na+,K+-ATPase (ouabain) and the Na+-K+-2Cl- cotransporter (NKCC; bumetanide) indicated that rapid increases in JK,in and JK,net upon incubation of resting RBCs in TEP were due primarily to increased Na+,K+-ATPase activity; the NKCC appeared to be involved only when the Na+,K+-ATPase was blocked. It is concluded that RBCs rapidly increase JK,in and JK,net in response to exercise-induced changes in plasma composition.

Adult↗
PubMed2002

Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion.

To test the hypothesis that lactate plays a central role in the distribution of carbohydrate (CHO) potential energy for oxidation and glucose production (GP), we performed a lactate clamp (LC) procedure during rest and moderate intensity exercise. Blood [lactate] was clamped at approximately 4 mM by exogenous lactate infusion. Subjects performed 90 min exercise trials at 65 % of the peak rate of oxygen consumption (V(O(2))(,peak); 65 %), 55 % V(O(2))(,peak) (55 %) and 55 % V(O(2))(,peak) with lactate clamped to the blood [lactate] that was measured at 65 % V(O(2))(,peak) (55 %-LC). Lactate and glucose rates of appearance (R(a)), disappearance (R(d)) and oxidation (R(ox)) were measured with a combination of [3-(13)C]lactate, H(13)CO(3)(-), and [6,6-(2)H(2)]glucose tracers. During rest and exercise, lactate R(a) and R(d) were increased at 55 %-LC compared to 55 %. Glucose R(a) and R(d) were decreased during 55 %-LC compared to 55 %. Lactate R(ox) was increased by LC during exercise (55 %: 6.52 +/- 0.65 and 55 %-LC: 10.01 +/- 0.68 mg kg(-1) min(-1)) which was concurrent with a decrease in glucose oxidation (55 %: 7.64 +/- 0.4 and 55 %-LC: 4.35 +/- 0.31 mg kg(-1) min(-1)). With LC, incorporation of (13)C from tracer lactate into blood glucose (L GNG) increased while both GP and calculated hepatic glycogenolysis (GLY) decreased. Therefore, increased blood [lactate] during moderate intensity exercise increased lactate oxidation, spared blood glucose and decreased glucose production. Further, exogenous lactate infusion did not affect rating of perceived exertion (RPE) during exercise. These results demonstrate that lactate is a useful carbohydrate in times of increased energy demand.

Adult↗
PubMed2002

K(+) transport and volume regulatory response by NKCC in resting rat hindlimb skeletal muscle.

This study tested the hypothesis that the NKCC is involved in volume regulation, specifically regulatory volume increase (RVI), in resting skeletal muscle. Neurally and vascularly isolated rat hindlimbs were perfused with a bovine erythrocyte perfusate containing (42)K or (86)Rb as markers of unidirectional K(+) flux across the sarcolemma. Compared to controls, perfusion with 120 microM bumetanide (a specific inhibitor of the NKCC) decreased J(in)K by 15+/-2%, indicating the functional presence of the NKCC. Experiments with ouabain (to block active K(+) transport by the Na,K ATPase) showed that the bumetanide-sensitive component of J(in)K comprised 35% of the total ouabain-sensitive J(in)K. Inhibition of NKCC resulted in a net loss of water by muscle. When hindlimbs were perfused with hypertonic (380 mOsm/L by addition of sucrose) perfusate for 20 min, after initially blocking K(+) channels with 1 mM barium, J(in)K rapidly (2-3 min) increased 2-fold followed by a rapid decline. This rapid, transient increase in J(in)K was abolished with bumetanide, confirming that perfusion with hypertonic perfusate stimulated NKCC activity and RVI. The hypertonic perfusate also resulted in temporally associated decreases in net water uptake by muscle. It is concluded that a functional NKCC is present in mammalian skeletal muscle and that it is involved in cell volume regulation.

Animals↗