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Biomedical subjects

J Chalmers

Publications and source records attributed to J Chalmers.

At least 199 records · Page 11Linked to original sources
PubMed1975

Observations on the induction of bone in soft tissues.

Using bone decalcified with 0-6 N hydrochloric acid as an inducing agent, the inductive capacity of different soft tissue sites was investigated. Muscle and fascia regularly permitted the induction of bone, while spleen, liver and kidney suppressed bone induction. Bone formation could be induced in these organs if living autologous fascia was implanted together with the inducing agent; while bone formation was inhibited when living autologous spleen tissue was implanted with the inducing agent to normally favourable sites. The administration of systemic heparin and the diphosphonate ethane-1-hydroxyl, 1-diphosphonic acid (EHDP) suppressed bone induction. It is suggested that for bone induction to occur in soft tissues, three conditions must be present: 1) an inducing agent; 2) an osteogenic precursor cell; and 3) an environment which is permissive to osteogenesis. The presence of osteogenic inhibitors in spleen, liver and kidney is postulated.

Animals↗
PubMedDate not supplied

Cardiovascular effects of intracisternal 6-hydroxydopamine and of subsequent lesions of the ventrolateral medulla coinciding with the Al group of noradrenaline cells in the rabbit.

The acute cardiovascular effects of intracisternal injections of 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine and the degree of neurotransmitter depletion achieved by such injections were studied. The two different vehicles used--0.2% ascorbic acid in 0.9% NaCl, or 0.9% NaCl--had little effect on the cardiovascular response to 6-OHDA injections but had a striking effect on levels of noradrenaline (NA) subsequently measured in the thoracic spinal cord. 6-OHDA (600 micrograms kg-1 free base) dissolved in normal saline depleted spinal cord NA to less than 1% of control levels whereas the same dose of 6-OHDA dissolved in ascorbate saline only depleted spinal cord NA to 24% of control levels. The degree of depletion of NA in medulla, pons and hypothalamus was similar in the two groups. Ascorbic acid also appeared to contribute to the non-specific toxicity of intracisternal injections of 6-OHDA. The hypertension and bradycardia that followed lesions of the ventrolateral medulla coinciding with the A1 group of noradrenergic cells (Al lesions) were attenuated in animals in which spinal cord NA had been depleted to 2% of control using 6-OHDA in normal saline. However, pretreatment with 6-OHDA in ascorbate saline, which only reduced spinal cord NA to 23% of control, had no effect on the cardiovascular response to Al lesions. It seems likely that the effects of Al lesions are mediated, at least in part, by NA projections descending within the spinal cord.

5,6-Dihydroxytryptamine↗
PubMedDate not supplied

Protective effect of methylcellulose and other polymers on insect cells subjected to laminar shear stress.

The relative sensitivity of two insect cell lines to laminar shear stress was determined, and the protective effect of polymers added to the growth media of two insect cell lines, Trichoplusia ni (TN-368) and Spodoptera frugiperda (SF-9), was evaluated. TN-368 and SF-9 cells were found to be equally sensitive to laminar shear stress. Methylcellulose [0.5% (w/v) Dow E4M Methocel] and dextran [4.5% (w/v)] increased the resistance of suspended cells to lysis due to laminar shear stress by factors of up to 76 and 28, respectively, compared to cells in media without additives. It was observed that the protective effect of Pluronic F-68 was concentration-dependent: 0.2% and 0.3% (w/v) F-68 increased the resistance of SF-9 cells to shear stress by factors of 15 and 42, respectively. However, increasing the concentration to 0.5% did not significantly increase the cells' resistance compared to 0.3% (w/v). F-68 at 0.2% only increased the resistance of TN-368 cells by a factor of 6. It is believed that the protection is a result of the polymer adsorbing to the cell membrane. None of the polymer additives tested had a significant effect on SF-9 or TN-368 growth rate.

Animals↗
PubMedDate not supplied

Effects of vasopressin on heart rate in conscious rabbits.

The effects of vasopressin on heart rate and on the baroreceptor-heart period reflex were assessed during graded intravenous infusions of arginine vasopressin. Infusions which elevated plasma arginine vasopressin to 200 pg/ml had no effect on blood pressure, but induced a fall in heart rate and cardiac output and an increase in peripheral resistance. These effects were unaltered by vagal blockade with methylscopolamine and cardiac sympathetic blockade with propranolol but were prevented by pretreatment with a specific vascular antagonist to vasopressin, d(CH2)5Tyr(Me)AVP. Baroreflex control of heart rate was studied during vasopressin infusion by monitoring the heart period responses to graded changes in mean arterial blood pressure produced by inflation of balloon occluders around the abdominal aorta and thoracic vena cava. Elevation of plasma arginine vasopressin to 50 pg/ml and 200 pg/ml had no significant effect on the slope or sensitivity of the baroreceptor-heart period reflex but increased the maximum bradycardia elicited in response to large increases in blood pressure. We conclude that at physiological levels, arginine vasopressin has a direct cardiodepressant action that is not dependent on cardiac vagal or sympathetic activity. Our results indicate that arginine vasopressin increases the maximum bradycardia that can be elicited through baroreceptor reflexes but does not alter the slope relating change in heart rate to change in blood pressure.

Animals↗
PubMedDate not supplied

Importance of central serotonin neurons in the hypotensive action of methyldopa in the rat.

Normotensive (WKY) and stroke prone spontaneously hypertensive (SHR-SP) rats were given methyldopa (200 mg/kg i.p.) daily for five days and their brains were then sectioned and processed with the Faglu method for catecholamine fluorescence. This treatment with methyldopa induced a green fluorescence not seen in control animals, in cells coinciding with the B1-B9 groups of serotonin neurons in the brainstem. Pretreatment with the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, i.c.v.), which is relatively specific for serotonin neurons, prevented the appearance of this green fluorescence in the serotonin cell groups of rats given methyldopa. Pretreatment with 5,7-DHT, i.c.v. approximately halved the magnitude of the hypotensive response to a single dose of methyldopa (80 mg/kg i.p.). We suggest that central serotonin nerves contribute to the hypotensive action of methyldopa. It is our hypothesis that methyldopa is taken up by these serotonin cells and that the green fluorescence reflects the production of alpha-methyldopamine, as a result of decarboxylation by the ubiquitous enzyme, L-aromatic amino acid decarboxylase.

5,7-Dihydroxytryptamine↗