Comparison of the effect of somatostatin on gastrointestinal function in the conscious and anaesthetized cat and on the isolated cat pancreas.

Albinus, Margittá; Blair, E. L.; Case, R. M.; Coy, David H.; Gómez-Pan, A.; Hirst, Barry H.; Reed, J. D.; Shaw, B.; Smith, Porsha L.; Smy, J R

doi:10.1113/jphysiol.1977.sp011893

Cited by 40 publications

(12 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mean Ra in the conscious cat is similar to values reported in the anaesthetized cat with vagus and splanchnic nerves sectioned (Reed & Smy, 1971). These results suggest that the significantly lower acid output in response to the same dose of pentagastrin in the anaesthetized compared with the conscious cat (Albinus et al 1977) is unlikely to be the simple result of a limiting MBF in the anaesthetized preparation.…”

Section: Psupporting

confidence: 78%

Communications

1981

The Journal of Physiology

View full text Add to dashboard Cite

It has recently been suggested that the inactivation of calcium currents in molluscan neurones may depend on calcium entry, rather than membrane potential as such (Tillotson, 1979). We have studied calcium current in identified, voltageclamped neurones of the snail bathed in sodium-free saline containing 25 mm CaCl2, 10 KCl, 5 MgCl2, 5 Tris-HCl, with 75 mm TEA-Cl and 2 mM-4-aminopyridine to reduce potassium currents as much as possible.Under these conditions inward calcium currents turn offexponentially over the first 100 msec at potentials up to + 20 mV. At these potentials the currents do not inactivate completely, even during pulses up to 1 see in duration. With potentials more positive than + 20 mV the current becomes outward at the end of a 400-msec pulse. Cadmium ions (1-2 mM) completely abolished the inward current and, for potentials above +30 mV, also reduced the net outward current at the end of a 400-msec pulse, suggesting that some of this outward current was calcium-activated.The rate of decline of the calcium current was dependent on its size. When the current was reduced by reducing [Ca]o from 25 to 5 mm the decline was slowed. (For a pulse to 0 mV the time constant changed from 46 to 88 msec.) The inactivation was also studied in two-pulse experiments. A 250 msec pre-pulse of variable voltage was followed after a 100-msec interval by a test pulse to 0 mV. The inward current during the test pulse was reduced as the pre-pulse became more positive in the range -30 to + 30 mV, but then increased with further depolarization, approaching the value for no pre-pulse when the pre-pulse was + 110 to + 120 mV.This result may be interpreted in terms of calcium entry causing calcium inactivation, or alternatively in terms of the calcium entry leading to a Ca-activated potassium current instantaneously activated by depolarization during the test pulse. Such Ca-activated K currents have been shown to be voltage-dependent (Gorman & Hermann, 1979), and it might therefore be expected that such an effect would increase with increasing test pulse potential. This second explanation is less likely as the relationship between test pulse current relative to that with no pre-pulse

show abstract

Section: Psupporting

confidence: 78%

Communications

1981

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…It has been reported that the chloralose-anaesthetized acutely surgically prepared cat secretes significantly less acid than the conscious gastric fistula cat in response to pentagastrin 8,ug kg-1 hr-1 (Albinus et al 1977 (Emis & Grossman, 1967). Whether this effect would be marked at the dose of pentagastrin used, which produces acid secretion approaching maximum, is not known.…”

Section: Discussionmentioning

confidence: 99%

“…The precise mechanism whereby the surgical procedures alter the gastric acid response to stimuli requires further investigation. However, it is obvious that care must be taken in interpreting the results from anaesthetized acutely prepared animals, especially in the light of the evidence that somatostatin in the cat (Albinus et al 1977) and atropine in the cat (Blair, Harper, Lake & Reed, 1961;Konturek, Radecki, Demitrescu & I)embinski, 1974) and dog …”

Section: Discussionmentioning

confidence: 99%

“…The majority of these studies have been carried out using the dog. Whilst studying the effects of somatostatin on gastrointestinal function, we observed that this peptide inhibited acid secretion in the conscious but not in the acutely surgically prepared anaesthetized cat (Albinus, Blair, Case, Coy, Gomez-Pan, Hirst, Reed, Schally, Shaw, Smith & Smy, 1977 or 10 #sg kg body wt.-, or as an infusion of 1 or 8 jug kg-' h-' in 0-9 % saline in a volume of 12 ml. h-1.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The effect of anaesthesia on pentagastrin stimulated gastric acid secretion in the cat.

Albinus¹,

Blair²,

Hirst³

et al. 1978

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

SUMMARY1. The effect of Saffan (alphaxalone and alphadolone acetate) and Nembutal (pentobarbitone) anaesthesia on gastric acid secretion stimulated by I.v. bolus injections of pentagastrin was investigated in the gastric fistula cat. The effect of Saffan anaesthesia was also tested on i.v. near-maximal and sub-maximal infusions of pentagastrin.2. Neither anaesthetic reduced the acid secreted in response to bolus injections of pentagastrin. Increased acid secretion with the anaesthetic was noted at some doses of pentagastrin in both intact and vagotomized animals.3. Saffan anaesthesia had no effect on near-maximal gastric acid secretion stimulated by pentagastrin 8 ,g kg-1 hr-1 but increased the response to pentagastrin 1,ug kg-1 hr-1. 4. It is suggested that the differences in the acid secretary responses of the anaesthetized acutely prepared animal compared with the conscious animal are a consequence of the surgical procedures rather than the state of consciousness.

show abstract

“…It has been shown that somatostatin does not inhibit enzyme secretion in either isolated arterially perfused preparations or acinic cells in vitro (1,6,23,27,40,41), suggesting that the mechanism of inhibition of pancreatic exocrine secretion is indirect. Indeed, there is evidence that somatostatin is likely to exert the inhibitory effect via a central vagal site (19), the sympathetic nerve (22), an intrapancreatic cholinergic pathway (16), or the intrinsic pancreatic peptidergic neurons (26).…”

mentioning

confidence: 99%

Microinjection of exogenous somatostatin in the dorsal vagal complex inhibits pancreatic secretion via somatostatin receptor-2 in rats

Liao¹,

Li²,

Lu³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Previous studies have suggested that somatostatin inhibits pancreatic secretion at a central vagal site, and the dorsal vagal complex (DVC) is involved in central feedback inhibition of the exocrine pancreas. The aim of this study was to investigate the effect of exogenous somatostatin in the DVC on pancreatic secretion and the somatostatin receptor subtype(s) responsible for the effect. The effects of somatostatin microinjected into the DVC on pancreatic secretion stimulated by cholecystokinin octapeptide (CCK-8) or 2-deoxy-D-glucose (2-DG) were examined in anesthetized rats. To investigate the somatostatin inhibitory action site, a somatostatin receptor antagonist [SRA; cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr)] was microinjected into the DVC before intravenous infusion of somatostatin and CCK-8/2-DG. The effects of injection of a somatostatin receptor-2 agonist (seglitide) and combined injection of somatostatin and a somatostatin receptor-2 antagonist (CYN 154806) in the DVC on the pancreatic secretion were also investigated. Somatostatin injected into the DVC significantly inhibited pancreatic secretion evoked by CCK-8 or 2-DG in a dose-dependent manner. SRA injected into the DVC completely reversed the inhibitory effect of intravenous administration of somatostatin. Seglitide injected into the DVC also inhibited CCK-8/2-DG-induced pancreatic protein secretion. However, combined injection of somatostatin and CYN 154806 did not affect the CCK-8/2-DG-induced pancreatic secretion. Somatostatin in the DVC inhibits pancreatic secretion via somatostatin receptor-2, and the DVC is the action site of somatostatin for its inhibitory effect. somatostatin; pancreatic exocrine secretion; dorsal vagal complex; dorsal motor nucleus of the vagus nerve; somatostatin receptor antagonist; somatostatin receptor-2 agonist; cholecystokinin octapeptide; 2-deoxy-D-glucose

show abstract

Comparison of the effect of somatostatin on gastrointestinal function in the conscious and anaesthetized cat and on the isolated cat pancreas.

Cited by 40 publications

References 17 publications

Communications

Communications

The effect of anaesthesia on pentagastrin stimulated gastric acid secretion in the cat.

Microinjection of exogenous somatostatin in the dorsal vagal complex inhibits pancreatic secretion via somatostatin receptor-2 in rats

Contact Info

Product

Resources

About