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Biomedical subjects

L H Smaje

Publications and source records attributed to L H Smaje.

47 records · Page 3Linked to original sources
PubMed1973

The effect of chronic duct ligation on the vascular and secretory responses of the cat's submaxillary gland.

1. The object of the present experiments was to re-investigate the role of kallikrein in functional hyperaemia in the submaxillary gland of the cat. Kallikrein concentration in the gland and saliva was reduced by ligation of the duct for 2-3 days before the acute experiment, at which time the duct was cannulated proximal to the ligation and blood flow and salivation measured.2. Despite the fall in kallikrein concentration, a normal two-phase vascular response was obtained on continuous stimulation of the chorda-lingual nerve at 1-5 Hz and the progressive increase in blood flow to a constant level characteristic of 10 and 20 Hz stimulation was also seen. Quantitatively, the increase in blood flow following a 10 sec stimulation was reduced to about 75% of control values at all stimulation frequencies used and the maintained vasodilatation was reduced when using continuous stimulation at 1 Hz but not at 10 and 20 Hz.3. The supersensitivity to the vasodilator properties of bradykinin, previously reported to follow duct ligation, was confirmed.4. The increased blood flow produced by chorda-lingual nerve stimulation could be delayed by circulatory arrest. Evidence was obtained suggesting that the vascular response to chorda stimulation delayed by arterial occlusion was not mediated by kallikrein alone.5. It was concluded that kallikrein was not the sole mediator of functional hyperaemia in the cat submaxillary gland but that a combination of vasodilator nerves and kallikrein release explained more phenomena than either hypothesis alone.

Acetylcholine↗
PubMed1973

Spontaneous salivation in the rabbit submandibular gland.

1. Salivation has been studied in the submandibular gland of the rabbit. A very slow spontaneous salivation took place when all possibility of nerve influence had been excluded. Salivation was not due to ultrafiltration.2. The ;spontaneous' saliva had a mean K concentration of 148 mM and Na concentration of 46 mM. With increasing salivation rate produced by parasympathetic nerve stimulation, K concentration fell to a plateau level of about 30 mM whilst Na concentration fell rapidly to reach the low value of 3 mM, then began to rise again at the higher flow rates.3. Ligation of the submandibular duct produced a reversal of the ion concentrations in spontaneous saliva. By 4 days K concentration was lower and that of Na higher than control values until by 2 weeks the effect was maximal with mean concentrations of 25 mM for K and 153 mM for Na.4. Ouabain increased the spontaneous salivation rate and ethacrynic acid slowed or prevented it altogether. On the basis of the known sites of action of these drugs it is postulated that two pumps are involved in the regulation of spontaneous salivation. There appears to be basal activity of an acinar mechanism pumping NaCl into the lumen, taking water with it. This pump is activated directly or indirectly by the intracellular Na concentration which itself is controlled by an Na-K exchange pump.5. Excitation of the sympathetic trunk produced a small, though definite, increase in salivation rate. There was evidence that myoepithelial cells might also be involved in the sympathetic response and that they were activated by alpha receptor stimulation. Salivation evoked by sympathetic nerve stimulation would seem to be a response to beta receptor stimulation, but the possibility that activation of both alpha and beta receptors was required could not be excluded entirely.

Animals↗
PubMed1972

Dependence of functional vasodilatation in the cat submaxillary gland upon stimulation frequency.

1. Submaxillary gland blood flow and salivation have been measured in anaesthetized cats and the chorda-lingual nerve has been stimulated at different frequencies.2. At low stimulation frequencies (1-5 Hz) there was a large transient increase in blood flow followed by a more modest maintained increase which lasted as long as stimulation continued. Stimulation at 10-20 Hz also produced a rapid initial increase in flow but at these frequencies the subsequent decline was not seen and a gradual further increase to a maintained level was observed.3. Atropine in small doses depressed both the transient and the maintained response to low frequency stimulation but at 10-20 Hz the maintained vasodilatation was unaffected by the drug.4. The transient increase in potassium concentration in saliva and venous blood draining the gland was not correlated with the vascular response.5. In conclusion, further details have been provided concerning the vascular response to chorda-lingual nerve stimulation and its sensitivity to atropine. Functional vasodilatation is not secondary to potassium release and is not due to a direct interaction between rate of saliva production and rate of blood flow although the vasodilatation does appear to be related in part to the acompanying salivation.

Animals↗
PubMed1971

Myoepithelial cell activation in the submaxillary salivary gland.

1. Pressure in the duct of the submaxillary gland of the cat was recorded under chloralose anaesthesia. Single pulses applied to the parasympathetic nerve caused a pressure rise.2. Salivation was just detectable in about half of the animals when an open tube was connected to the duct and single pulses applied to the nerve. Applying a back pressure of 1-4 mm Hg renders the duct less distensible and under these circumstances secretion of 1-3 mul. fluid was always seen. An alternative method of detecting salivation based on the pressure record itself also showed that salivation occurred in response to the stimulus and that salivation was responsible for the pressure rise observed.3. Single pulses applied to the cervical sympathetic trunk produced a small fall in pressure. In a short series of pulses this was followed by a slow rise which then slowly decayed. It was tentatively concluded that the initial fall was secondary to the accompanying vasoconstriction but the subsequent effects were due to myoepithelial cell contraction.4. Close arterial injection of bradykinin caused a pressure rise which could best be explained by myoepithelial cell contraction.5. It is concluded that the myoepithelial cells of the submaxillary gland of the cat do not receive a parasympathetic motor innervation but it is probable that they are innervated by the sympathetic nervous system and contract in the presence of bradykinin.

Anesthesia, General↗
PubMed1968

Secretion of kallikrein and its role in vasodilatation in the submaxillary gland.

1. The effects of parasympathetic (chorda) and sympathetic nerve stimulation on the concentration and output of kallikrein secreted in saliva from the cat's submaxillary gland were compared. Sympathetic stimulation always produced a much higher concentration (up to 500 times) and output (up to 390 times) of kallikrein than parasympathetic stimulation. In the dog, in which sympathetic nerve stimulation produces little or no secretion from the submaxillary gland, there was also a marked increase in the secretion of kallikrein when sympathetic was superimposed on parasympathetic secretion. This effect did not occur, however, in the rabbit's submaxillary gland.2. It was possible to deplete the cat's submaxillary gland of kallikrein, either by ligation of the duct for several days or by duct ligation and sympathetic nerve stimulation, so that it was undetectable either in the gland or in saliva after stimulation of the chorda. Such glands, nevertheless, responded to chorda stimulation with a normal atropine-resistant vasodilatation.3. There is a close parallelism between the rate of secretion of salvia and vasodilatation over a range of frequencies of chorda stimulation, but the output (and concentration) of kallikrein in saliva is distinctly different for the same frequencies of nerve stimulation.4. Our results are consistent with the view that vasodilator nerves exist in the parasympathetic nerves to the submaxillary gland. We suggest that they are cholinergic in nature despite the fact that chorda vasodilatation is resistant to atropine. It is further suggested that neither the kallikrein-kinin system nor adrenergic vasodilator nerve fibres play a significant role in chorda vasodilatation.

Animals↗
PubMed1966

Vasodilatation in the submaxillary gland of the rabbit.

1. In the rabbit, in contrast to the cat and dog, the vasodilatation and the secretion in the submaxillary gland which accompany parasympathetic nerve stimulation are correspondingly sensitive to atropine block. 2. It is concluded that true vasodilator nerve fibres to the submaxillary gland exist in the chorda tympani nerve of the rabbit. 3. The vasodilatation which follows sympathetic vasoconstriction in the submaxillary gland of the rabbit is small and variable. The possibility that this after-dilatation is due to an adrenergic neurotransmitter agent acting on beta-vascular receptors is discussed.

Animals↗