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Biomedical subjects

D Grundy

Publications and source records attributed to D Grundy.

At least 127 records · Page 7Linked to original sources
PubMed1986

A permissive role for the vagus nerves in the genesis of antro-antral reflexes in the anaesthetized ferret.

1. The role of the vagus nerves in the genesis of antro-antral reflexes was investigated in the urethane-anaesthetized, splanchnectomized ferret. 2. Antral distension stimulated antral contractions with a threshold volume of 3.5 +/- 0.9 ml (corresponding to an intra-antral pressure of 0.27 +/- 0.11 kPa) by a vagal-dependent mechanism as indicated by the attenuated response seen during vagal blockade by cooling. Atropine (1 mg/kg) abolished the antral response to distension. 3. In vagotomized animals, close arterial infusions of acetylcholine at a dose sufficient to return antral motility to basal levels led to the reappearance of the reflex. Low-frequency electrical stimulation of the preganglionic vagal neurones had a similar effect. These effects were also abolished by atropine (1 mg/kg). 4. Hexamethonium (10-25 mg/kg) suppressed the potentiating effect of acetylcholine, indicating a ganglionic site of action. The attenuated response to antral distension seen in vagotomized animals in the absence of exogenous acetylcholine or electrical vagal stimulation was not sensitive to hexamethonium but abolished by atropine (1 mg/kg). 5. The results are consistent with the vagus performing a permissive role in the genesis of antro-antral reflexes mediated through local enteric pathways.

Acetylcholine↗
PubMed1986

The response to isoniazid of action tremor in multiple sclerosis and its assessment using polarised light goniometry.

Isonicotinic acid hydrazide (isoniazid) was evaluated in five patients as a treatment for the control of severe cerebellar action tremor occurring in multiple sclerosis. Oral doses of isoniazid BPC were increased every 2 weeks from 300 mg to 1200 mg daily over an 8 week period. Four patients reported considerable symptomatic benefit at doses ranging from 600 mg to 900 mg daily. Polarised light goniometry demonstrated a two to three-fold reduction of tremor in these patients when standard methods of clinical assessment showed only marginal improvement.

Adult↗
PubMed1986

Evidence for a non-cholinergic excitatory innervation in the control of colonic motility.

The colon of the ferret anesthetized with urethane exhibits two distinct types of motility patterns. These were abolished or considerably reduced by blocking nervous conduction in the vagus nerves by cooling to below 4 degrees C. Atropine transiently abolished motility which on its return was also found to be sensitive to vagal integrity. Electrical stimulation of either the cut central or peripheral end of a branch of the abdominal vagus caused large amplitude contractions of the colon which were not blocked by atropine or by atropine and a combination of alpha- and beta-adrenoceptor blocking agents. These results are consistent with either two separate motor pathways to the colon in the vagus nerve, one cholinergic, the other non-adrenergic, non-cholinergic, or a single pathway with the effects mediated by a primary and a co-transmitter. They also demonstrate that "spontaneous activity" is driven in part by both cholinergic and non-cholinergic mechanisms.

Animals↗
PubMed1985

The effect of intraluminal tryptophan and phenylalanine on small intestinal motility in the conscious dog.

The effect of D- and L-isomers of tryptophan and phenylalanine on fasting motor activity of canine jejunum were investigated. Only L-tryptophan had any effect on jejunal motility. The concentration of L-tryptophan required to elicit a motor effect in 50% of animals was estimated at 28 mM. 50 mM-L-tryptophan stimulated jejunal motility after a latency of 4.5 +/- 0.7 min. The pattern of motility was similar to that evoked by feeding but continued for only 41 +/- 5 min and failed to disrupt the normal timing of the interdigestive migrating motor complex (m.m.c.). The duration of the subsequent phase II of the complex was, however, significantly reduced. Multiple infusion of L-tryptophan also failed to disrupt the timing of the m.m.c. These data are consistent with the hypothesis that specific breakdown components of protein digestion are implicated in the stimulation of postprandial motor activity. The mechanisms involved in the motor response to L-tryptophan are discussed.

Animals↗
PubMed1984

Vagal control of colonic motility in the anaesthetized ferret: evidence for a non-cholinergic excitatory innervation.

Spontaneous colonic motility in the urethane-anaesthetized ferret consists of two distinct types of contraction which correspond to the patterns recorded myoelectrically in conscious animals. This motility was abolished or greatly reduced when nervous conduction was prevented in the cervical vagi by cooling to below 4 degrees C. On rewarming the nerves the colonic motility returned, after a short latency, to the pre-cool level. Atropine transiently abolished colonic motility. On its return the motility was significantly reduced but still sensitive to vagal integrity. Thus the atropine-resistant colonic motility was also abolished or markedly reduced by cooling the cervical vagi to below 4 degrees C. On rewarming there was a longer latency for the return of motility compared to that before atropinization. Electrical vagal stimulation produced, after a short latency, large-amplitude colonic contractions. Following atropine, the short-latency response to electrical vagal stimulation was replaced in the majority of animals by a long-latency response whose characteristics were quite different from those of the cholinergic response. These results are consistent with the vagus containing two functional motor pathways to the colon, one to cholinergic post-ganglionic neurones and the other operating via a non-cholinergic mechanism.

Animals↗
PubMed1984

Vago-vagal reflexes to the colon of the anaesthetized ferret.

Electrical stimulation of the central end of the vagal communicating branch in the thorax at frequencies between 2 and 20 Hz elicited, after a latency of 7.2 +/- 0.8 s, large-amplitude colonic contractions. 5 Hz stimulation gave near maximal contractions and, because vomiting was more likely to occur at higher stimulus frequencies, was used as the standard stimulus for subsequent experiments. At this frequency the peak colonic contraction was 6.5 +/- 0.9 kPa. Following atropine the characteristics of the response to central vagal stimulation differed from that seen before atropinization. The latency was longer (45.7 +/- 8.2 s) and the amplitude greatly attenuated (0.7 +/- 0.2 kPa). Cooling the vagus nerves to 2 degrees C at a level either above or below the site of stimulation completely abolished both the cholinergic and the atropine-resistant colonic responses to central vagal stimulation. These results are consistent with the vagus containing two motor pathways to the colon which are reflexly stimulated by a vagal afferent input. The functional significance of these reflexes is discussed.

Animals↗
PubMed1983

The response of the pancreas of the anaesthetized cat to secretin before, during and after reversible vagal blockade.

Cooling the cervical vagi of the anaesthetized splanchnectomized cat to 2 degrees C caused a 54.4 +/- 8.8% inhibition of pancreatic electrolyte secretion stimulated submaximally with pure secretin. On rewarming the vagi there was a prolonged increase in secretion rate over and above the control rate which existed before cooling. The increase lasted about 90 min. There were no changes in acid/base status due to interference of the lung inflation reflex which could account for the inhibition of secretion and the subsequent rebound. Cold block of the cervical vagi increased the transpancreatic electrical conductance, indicating that vasodilation had occurred and therefore eliminated a vasomotor cause for the inhibition. Electrolyte secretion was also inhibited by bilateral vagal section. Atropine only partially prevented the inhibitory response to vagal cooling. A cholinergic mechanism, therefore, accounted for some but not all of the response to vagal cooling. It is concluded that even in the fasted, anaesthetized animal vagal impulses facilitate the action of secretin on the pancreas. This facilitation is only partially cholinergic; the major part of the response is due to some non-cholinergic transmitter substance. Such a mechanism may be necessary to potentiate the action of the very small amounts of secretin which appear to be released during a meal.

Acid-Base Equilibrium↗