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Biomedical subjects

C B Monson

Publications and source records attributed to C B Monson.

7 recordsLinked to original sources
PubMed1989

Thermoregulation in hypergravity-acclimated rats.

To determine the effect of hypergravity acclimation on thermoregulation, core temperature (Tc), tail temperature (Tt), and O2 consumption (VO2) were measured in control rats (raised at 1 G) and in rats acclimated to 2.1 G. When the animals were exposed to a low ambient temperature of 9 degrees C, concurrently with a hypergravic field of 2.1 G, Tc of rats raised at 1 G fell markedly by approximately 6 degrees C (to 30.8 +/- 0.6 degrees C) while that of the rats raised at 2.1 G remained relatively constant (falling only approximately 1 degree C to 36.4 +/- 0.3 degrees C). Thus prior acclimation to a 2.1-G field enabled rats to maintain Tc when cold exposed in a 2.1-G field. To maintain Tc, thermogenic mechanisms were successfully activated in the 2.1-G-acclimated rats as shown by measurements of VO2. In contrast, VO2 measurements showed that rats reared at 1 G and then cold exposed at 2.1 G did not activate thermogenic mechanisms sufficiently to prevent a fall in Tc. In other experiments, rats acclimated to either 1 or 2.1 G were found to lack the ability to maintain their Tc when exposed to a 5.8-G field or when exposed to prolonged cold exposure at 1 G. Results are interpreted as showing that when placed in a 2.1-G field, rats acclimated to 2.1 G can more closely maintain their Tc near 37 degrees C when cold exposed than can rats acclimated to 1 G. However, this enhanced regulatory ability of 2.1-G-acclimated rats over 1.0-G-acclimated rats is restricted to 2.1-G fields and is not observed in 1.0- and 5.8-G fields.

Adaptation, Physiological↗
PubMed1984

Impairment of thermogenesis and heat conservation in rats during 3 hours of 3-G exposure.

Heat conservation and production were studied in rats at 3 G and at 1 G. A closed-circuit system that includes a Krogh-type spirometer for the continuous measurement of oxygen consumption was used to determine heat production. At the same time, core temperature (Tc) and tail temperature (Tt) were also measured. During the first 20 min at 3 G, oxygen consumption increased by at most 18% in some of the rats and fell by up to 15% in the remaining rats. However, in all rats at 3 G, there was a fall of Tc during this time. Thus, the initial fall of Tc at 3 G was independent of concurrent changes in the rate of oxygen consumption. Furthermore, the rapid fall in Tc during the initial exposure to hypergravity was not due to reduced heat production (since oxygen consumption was variable and in some rats increased) but to an increase in heat loss. Even after 3 h at 3 G, when heat conservation mechanisms had recovered, the rate of oxygen consumption in rats was not significantly increased relative to the 1 G rate; hence thermogenesis was not activated to rewarm the animal.

Animals↗
PubMed1983

Hypergravic fields and parallel controllers for thermoregulation.

To test the proposal that mammals have parallel neurocontrollers for temperature regulation, Long-Evans hooded male rats were exposed to cold while in a 3-G field. When exposed to cold, these rats consumed 35% less oxygen/min at 3 G than they did when exposed to cold at 1 G. However, rats acclimated for 6 wk to 5 degrees C consumed oxygen at the same rate during cold exposure at 3 G as at 1 G. Because cold-acclimated rats generate heat primarily by nonshivering thermogenesis while rats acclimated to room temperature rely to a greater extent on shivering, the 35% decrease in oxygen consumption of cold-exposed room-temperature rats in 3-G fields may reflect an inactivation of shivering. These oxygen consumption measurements, together with measurements of core and tail temperatures of rats in 3-G fields, are consistent with the proposal that neurocontrollers for thermoregulation are arranged in parallel and can be uncoupled by hypergravic fields.

Acclimatization↗
PubMed1982

Scanning electron microscopy of cartilage in mice with hereditary chondrodysplasia.

Mice born with hereditary, recessive chondrodysplasia (cho/cho) are dwarfed because the cartilage model upon which the endochondral osseous skeleton develops is defective. The mutant's cartilage matrix lacks cohesiveness which apparently contributes to the absence of columnar alignment of proliferating epiphyseal chondrocytes in developing tubular (long) bones. The present communication reviews our current understanding of skeletal dysplasia as it relates to defective chondrogenesis, and presents observations made with the scanning electron microscope of cellular disarray and nonuniform size and distribution of collagen fibrils which confirm the existence of a matrix defect. Autoradiographic experiments on tibial cartilage, similar to those performed on sternal cartilage, confirm the normal pattern of sulfate labeling by mutant epiphyses.

Animals↗
PubMed1981

Ultrastructural studies of cartilage matrix in mice homozygous for chondrodysplasia.

UNLABELLED: The absence of columns of proliferative chondrocytes in mice with hereditary chondrodysplasia (cho/cho) has been attributed to a lack of structural integrity of the cartilage matrix. To determine whether the abnormality is related to defective interaction between proteoglycan and collagen, sternal cartilage from control and mutant fetuses at eighteen days of gestation was examined with autoradiographic and ultrastructural methods. The sulphate-labeling pattern in the mutant fetuses was normal, suggesting that the defect is not due to regional differences in proteoglycan synthesis. The presence of ruthenium red-stained matrix granules precipitated one collagen fibrils suggests that proteoglycan is capable of interacting with collagen in the mutant's matrix. The absence of a pericellular space and the presence of collagen fibrils adjacent to the external surface of the cell membrane suggests that the defect is due to precocious assembly of collagen monomers into fibrils, resulting in the absence of a normal network of interconnecting collagen fibrils and proteoglycan. Further studies are necessary to test this hypothesis. CLINICAL RELEVANCE: Because the phenotype of this mutation resembles certain forms of human skeletal dysplasia, mice with hereditary chondrodysplasia may serve as a model to elucidate the molecular mechanism for certain recessive disorders of chondrogenesis. In this regard, a much improved understanding of gene action is needed before effective treatment and corrective procedures can be applied to the eighty or more clinical forms of hereditary skeletal dysplasia.

Animals↗