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Biomedical subjects

S Holbeck

Publications and source records attributed to S Holbeck.

5 recordsLinked to original sources

Dextran, gelatin, and hydroxyethyl starch do not affect permeability for albumin in cat skeletal muscle.

OBJECTIVE: To evaluate the effects of the three commercially available colloid solutions, 6% dextran 70, 6% hydroxyethyl starch (HES) 200/0.5, and 3.5% urea-linked gelatin on permeability for human albumin in a skeletal muscle in vivo model by evaluating their effects on the reflection coefficient for albumin. DESIGN: Controlled laboratory study. SETTING: University research laboratory. SUBJECTS: Eighteen adult cats. INTERVENTIONS: The autoperfused and denervated calf muscles of the cat hindlimb were placed in a plethysmograph. The transvascular fluid absorption induced by an increase in the colloid osmotic pressure following a fixed intravenous bolus of human albumin was analyzed, first before start of, and then during an intra-arterial infusion to, the muscle preparation of the synthetic colloid to be analyzed. Capillary filtration coefficient as a measure of microvascular fluid permeability (conductance) was analyzed before and after start of the synthetic colloid. MEASUREMENTS AND MAIN RESULTS: Arterial blood flow, arterial and venous blood pressures, total vascular resistance, tissue volume changes, capillary filtration coefficient, and plasma volume were measured before and during the colloid infusion. According to the Starling fluid equilibrium, the ratio between the reflection coefficients for albumin on two occasions (before and after infusion of the synthetic colloid) can be calculated from the maximum osmotic absorption rates induced by a fixed intravenous bolus infusion of albumin and from the capillary filtration coefficients. Obtained data were adjusted for different plasma volume at the two occasions. We found that none of the three synthetic colloids analyzed had any significant effect on the reflection coefficient for albumin. CONCLUSION: An effect on albumin microvascular permeability of the synthetic colloids dextran 70, HES 200/0.5, and urea-linked gelatin could not be shown by a method analyzing their effect on the reflection coefficient for albumin.

Analysis of Variance↗

Effects on capillary fluid permeability and fluid exchange of albumin, dextran, gelatin, and hydroxyethyl starch in cat skeletal muscle.

OBJECTIVE: To evaluate the peripheral hemodynamic effects in a skeletal muscle in vivo model of the four commercially available colloid solutions, 20% human albumin, 6% dextran-70, 6% hydroxyethyl starch 200/0.5 (HES), and 3.5% urea-linked gelatin. DESIGN: Controlled laboratory study. SETTING: University research laboratory. SUBJECTS: Fifteen adult cats. INTERVENTIONS: The isolated, autoperfused, and denervated calf muscles of the cat hindlimb were placed in a plethysmograph. The colloids tested were given intra-arterially to the muscles in increasing rates of clinically relevant doses. MEASUREMENTS AND MAIN RESULTS: Arterial blood flow, arterial and venous blood pressures, total vascular resistance, tissue volume changes, and capillary filtration coefficient were measured before, during, and after the colloid infusions. The altered capillary filtration coefficient reflects a change in capillary fluid permeability. The capillary filtration coefficient was decreased by albumin and dextran, not affected by HES, and increased by urea-linked gelatin. Albumin induced transcapillary fluid absorption, gelatin induced transcapillary filtration, and no transcapillary fluid exchange was observed with dextran and HES. After discontinuation of the infusions, HES and gelatin induced a rebound transcapillary filtration. No such effect was seen after dextran and albumin. All colloids increased muscle blood flow. CONCLUSION: We conclude that capillary fluid permeability is decreased by albumin and dextran, unchanged by HES, and increased by gelatin. This and the differences in the rebound effect may contribute to the differences in the plasma volume expanding properties of the respective colloid. The increased blood flow induced by the colloids was more an effect of reduced vascular tone than of lowered blood viscosity.

Albumins↗

HLA class II typing using oligonucleotide probes.

A DQ beta locus-specific oligonucleotide probe is used to identify DQ beta alleles present in six insulin-dependent diabetes mellitus (IDDM) multiplex families. Results of genotyping using this technique agree with those from cDNA probes and are often clearer. Allele-specific oligonucleotide probes for the DR beta locus are used to identify subtypes (Dw4 and Dw14) of the DR4 specificity in five IDDM multiplex families. This distinction cannot be made with available cDNA probes.

Blotting, Southern↗

HLA DQ beta 3.2 identifies subtypes of DR4+ haplotypes permissive for IDDM.

The HLA class II-related susceptibility to type I insulin-dependent diabetes mellitus (IDDM) is examined in 94 multiplex families sorted by the presence or absence of a DR4+ haplotype in at least one diabetic family member. The families with DR4+ haplotypes are then sorted by the presence or absence of a DR4-linked DQ beta 3.2 allele. Further analysis assumes each multiplex family to represent a single diabetic genetic event and identifies the HLA class II haplotype(s) present in all affected members. The DQ beta 3.2 allele is present in over 95% of the multiplex families where DR4+ haplotypes segregate with IDDM, implying a major permissive role in determining susceptibility to IDDM.

Diabetes Mellitus, Type 1↗

Prostacyclin reduces microvascular fluid conductivity in cat skeletal muscle through opening of ATP-dependent potassium channels.

Prostacyclin is suggested to reduce microvascular permeability, but the cellular mechanisms mediating this response in the microvascular endothelial cells are still unknown. Considering that prostacyclin relaxes vascular smooth muscle cells via opening of ATP-dependent potassium channels, and opening of ATP-dependent potassium channels in the endothelial cells is suggested to influence microvascular permeability, this study was designed to test (1) if ATP-dependent potassium channels are involved in the regulation of microvascular hydraulic permeability, (2) if the permeability-reducing effect of prostacyclin is mediated through opening of ATP-dependent potassium channels, and (3) if cAMP is involved in this process. An autoperfused cat calf hindlimb was used as experimental model, and microvascular hydraulic permeability (conductivity) was estimated by a capillary filtration coefficient (CFC) technique. The potassium channel opener PCO-400 (0.5 microg x min(-1) per 100 g muscle, intra-arterially), prostacyclin (1 ng x min(-1) per kg body weight, intravenously) and the cAMP analogue dibutyryl-cAMP (24 microg x min(-1) per 100 g muscle, intra-arterially), decreased CFC to 77, 72 and 69% compared to control, respectively (p < 0.01). The decrease in CFC obtained by these substances was completely restituted after the start of a simultaneous infusion of the ATP-dependent potassium channel blocker glibenclamide (6 microg x min(-1) per 100 g muscle, intra-arterially; p < 0.01). Infusion of glibenclamide alone increased CFC to 107% of control (p < 0.05). In conclusion, the ATP-dependent potassium channels contribute to the regulation of microvascular hydraulic conductivity, and the prostacyclin permeability-reducing effect may act through this mechanism via increase in intracellular cAMP.

Adenosine Triphosphate↗