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J. Golonka, M. Krobicki, A. Waśkowska, M. Cieszkowski & A. Ślączka reply: We welcome the comments by our Slovakian colleagues and their critique of our results, particularly as we have discussed and published papers together several times about our ideas, sometimes, more or less, disputable (Aubrecht et al.2003, 2006; Krobicki et al.2003; Krobicki, Aubrecht & Golonka, 2003; Golonka et al.2006; Pieńkowski et al.2008). We are pleased to see such warm reaction to our work/paper, which is focused on one of the rudimentary questions in the Pieniny Klippen Belt (PKB) area. How many/what kind of olistoliths/olistostromes occur within the inner structure of the PKB, and when and why did they originate mostly during the Palaeogene part of the Mesozoic–Cenozoic history of this region? We expected this discussion earlier. The content of our paper was presented at the 6th Meeting of the Central European Tectonic Studies Group (CETeG) in Upohlav, Pieniny Klippen Belt, Slovakia (Cieszkowski et al.2008), and later, at the XIX Congress of the Carpathian–Balkan Geological Association in Thessaloniki, Greece (Cieszkowski et al.2010; Golonka et al.2010). Some ideas were also briefly mentioned in the paper by Cieszkowski et al. (2009) in a journal issue edited by D. Plašienka. We assume that the comments are based on recent investigation, because the authors list the grants received to conduct the research. Therefore, the submitted comments sometimes present a point of view different from that published previously by some of the authors of the comments (RA, JM) (see Aubrecht et al.2003; Krobicki, Aubrecht & Golonka, 2003; Wierzbowski et al.2006; Pieńkowski et al.2008). The statement, ‘Certainly there are many still unresolved problems in the geology of the PKB, and it ought to be said that the co-authors of this discussion also do not fully agree with all interpretations formulated and illustrated by the first author’ perhaps explains this controversy. Of course, we agree that ‘there are many still unresolved problems in the geology of the PKB’. We also agree with the statement ‘olistostromes and olistoliths are quite frequent, but not omnipresent’. We depicted the distribution of the olistoliths and their relationship to the non-olistolith tectonic units of the PKB in Golonka et al. (2015, figs 3, 8). [ABSTRACT FROM PUBLISHER]

Postprandial pancreatic secretion results from the interaction of neural and hormonal factors but their contribution to the net postprandial secretion is unknown. Recent description of highly specific and potent cholecystokinin (CCK) receptor antagonists allows the determination of the physiological role of CCK in the postprandial pancreatic secretion. In six dogs with chronic pancreatic fistulae, the blockade of CCK receptors by non-peptidal agent (L-364,718) caused little change in basal pancreatic secretion, but decreased significantly (p less than 0.05) by about 60% the pancreatic protein response to meat feeding and virtually abolished the pancreatic responses to CCK-8 and bombesin. The pancreatic protein responses to pentagastrin, reaching about 37% of CCK maximum, was also significantly reduced but this effect was less pronounced than that observed in tests with CCK-8 or bombesin stimulation. In contrast, cholinergically stimulated pancreatic secretion, reaching about 40% of CCK maximum, was unaffected by L-364,718. Cholecystokinin antagonism also failed to affect the postprandial and bombesin induced increments in plasma CCK and gastrin concentrations, but significantly reduced the PP responses to CCK-8 bombesin and meat feeding possibly as a result of the removal of the CCK mediated release of PP. We conclude that CCK plays a crucial role in the mediation of the postprandial and bombesin induced pancreatic secretion and in the PP release. [ABSTRACT FROM PUBLISHER]

Background: Recent studies clearly demonstrate that Helicobacter pylori (H. pylori) infection of the stomach causes persistent elevation of ammonia (NH3) in gastric juice leading to hypergastrinemia and enhanced pancreatic enzyme secretion., Methods: The aim of this study is to evaluate the influence of NH4OH on plasma gastrin level and exocrine pancreatic secretion in vivo in conscious dogs equipped with chronic pancreatic fistulas and on secretory activity of in vitro isolated acini obtained from the rat pancreas by collagenase digestion. The effects of NH4OH on amylase release from pancreatic acini were compared with those produced by simple alkalization of these acini with NaOH., Results: NH4OH given intraduodenally (i.d.) in increasing concentrations (0.5, 1.0, 2.0, 4.0, or 8.0 mM/L) resulted in an increase of pancreatic protein output, reaching respectively 9%, 10%, 19%, 16% and 17% of caerulein maximum in these animals and in a marked increase in plasma gastrin level. NH4OH (8 x 0 mM/L, i.d.) given during intravenous (i.v.) infusion of secretin (50 pmol/kg-h) and cholecystokinin (50 pmol/kg-h) reduced the HCO3 and protein outputs by 35% and 37% respectively, as compared to control obtained with infusion of secretin plus cholecystokinin alone. When pancreatic secretion was stimulated by ordinary feeding the same amount of NH4OH administered i.d. decreased the HCO3- and protein responses by 78% and 47% respectively, and had no significant effect on postprandial plasma gastrin. In isolated pancreatic acini, increasing concentrations of NH4OH (10(-7)-10(-4) M) produced a concentration-dependent stimulation of amylase release, reaching about 43% of caerulein-induced maximum. When various concentrations of NH4OH were added to submaximal concentration of caerulein (10(-12) M) or urecholine (10(-5) M), the enzyme secretion was reduced at a dose 10(-5) M of NH4OH by 38% or 40%, respectively. Simple alkalization with NaOH of the incubation medium up to pH 8.5 markedly stimulated basal amylase secretion from isolated pancreatic acini, whereas the secretory response of these acini to pancreatic secretagogues was significantly diminished by about 30%. LDH release into the incubation medium was not significantly changed in all tests indicating that NH4OH did not produce any apparent damage of pancreatic acini and this was confirmed by histological examination of these acini., Conclusions: 1. NH4OH affects basal and stimulated pancreatic secretion. 2. The excessive release of gastrin may be responsible for the stimulation of basal pancreatic enzyme secretion in conscious animals, and 3. The inhibitory effects of NH4OH on stimulated secretion might be mediated, at least in part, by its direct action on the isolated pancreatic acini possibly due to the alkalization of these acini.

Postprandial pancreatic secretion results from the interaction of neural and hormonal factors such as cholecystokinin (CCK), gastrin and gastrin releasing peptide (GRP), but their contribution to the net secretion is not established. Recent description of highly specific and potent hormonal receptor antagonists allows the determination of the physiological role of CCK, gastrin and GRP. In six dogs with chronic pancreatic fistulas, the blockade of CCK receptors by L-364, 718, gastrin receptors by L-365, 260 or GRP/bombesin receptors by nonapeptide RC-3095 failed to affect basal or sham-feeding induced pancreatic secretion indicating that none of these hormonal peptides plays a major role in this secretion. In contrast, the pancreatic response to ordinary feeding (which includes cephalic, gastric and intestinal phases), that was accompanied by a significant increment in plasma CCK and gastrin levels, was strongly inhibited (by over 50%) by L-364, 718 and slightly (by 20-30%) by L-365, 260 but not by RC-3095. Each antagonist was given at a dose that eliminated the secretory response to CCK, gastrin or GRP, respectively. We conclude that specific receptor antagonists are useful tools in assessing the physiological role of gut hormones in the control of pancreatic secretion and that none of the peptides tested appears to be involved in the cephalic phase. However, CCK plays a major role in the postprandial stimulation of pancreatic secretion.

Background: Endogenous nitric oxide has been implicated in the control of mesenteric circulation, but its role in the control of pancreatic blood flow and exocrine pancreatic secretion has not been studied., Methods: Secretory studies were performed on conscious dogs with chronic pancreatic fistulas, and changes in pancreatic blood flow were measured by laser Doppler flowmetry in anesthetized animals., Results: Infusion of NG-nitro-L-arginine did not affect basal pancreatic protein secretion but suppressed an increase of this secretion induced by L-arginine but not that induced by glyceryl trinitrate. Sham-feeding, meal feeding, and infusion of secretin plus cholecystokinin induced pancreatic protein outputs reaching, respectively, 30%, 74%, and 50% of cerulein maximum in these dogs. Infusion of NG-nitro-L-arginine caused a profound inhibition of these secretions, whereas the addition of L-arginine reversed this inhibition in part. NG-nitro-L-arginine or L-arginine added to the incubation medium of isolated canine pancreatic acini did not affect basal or cholecystokinin-induced amylase release. In anesthetized dogs, infusion of NG-nitro-L-arginine caused a significant reduction in the pancreatic blood flow both while resting and following stimulation with secretin plus cholecystokinin but did not affect this flow in animals treated with glyceryl trinitrate. Addition of L-arginine attenuated the decrease in pancreatic blood flow and the increase in systemic blood pressure caused by NG-L-nitro-arginine., Conclusions: Endogenous NO affects pancreatic secretion probably through the changes in the vascular bed.

In dogs with gastric fistulas and vagally denervated Heidenhain pouches, omeprazole, a benzimidazole derivative infused intravenously or given intraduodenally, dose-dependently inhibited gastric acid secretion, which had been induced by histamine, pentagastrin, or urecholine. It also suppressed gastric acid response to physiologic stimulants such as sham-feeding and gastric peptone meal without affecting serum gastrin level. The inhibition of histamine-induced acid secretion was accompanied by a parallel reduction in the mucosal blood flow, but no significant alteration in the ratio (R) value, indicating that omeprazole primarily affected gastric acid secretion but did not limit gastric mucosal microcirculation. Omeprazole, infused into the Heidenhain pouch, caused a dose-dependent inhibition of the Heidenhain pouch response to intravenous histamine without any significant change in the acid response of the main stomach and plasma concentrations of the drug. This indicates that omeprazole may exhibit local inhibitory action on the oxyntic glands. Omeprazole did not affect gastric mucosal integrity or the rate of alkaline secretion from the gastroduodenal mucosa or the pancreas stimulated by duodenal acidification or secretin.

This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of them caused a dose-dependent inhibition of acid secretion from the gastric fistula (GF) and Heidenhain pouches (HP) stimulated by pentagastrin and bethanechol, telenzepine being 5-9 times more potent than pirenzepine and equipotent with atropine. All antimuscarinics were also effective inhibitors of acid responses to sham feeding and ordinary feeding. The inhibitory effect of telenzepine and pirenzepine were not accompanied by any major alterations in plasma gastrin or somatostatin but those of atropine were related to significant increase in plasma gastrin and to significant decrease in plasma somatostatin levels, suggesting the involvement of M2 receptors in the cholinergic control of these hormones. All three antimuscarinics were effective inhibitors of pepsin secretion induced both from the GF and HP by all secretagogues used. Neither telenzepine nor pirenzepine administered in various doses affected the heart rate while atropine caused a significant increase in heart rate confirming that the former agents are selective M1 receptor antagonists. This study provides evidence that telenzepine is more potent than pirenzepine in the inhibition of gastric secretion induced by pentagastrin, bethanechol, sham-feeding and ordinary feeding and that, unlike atropine, it does not increase plasma gastrin responses to meat feeding. In fact, telenzepine and pirenzepine alike reduced plasma gastrin concentrations under these conditions. No influence of these antimuscarinics on plasma somatostatin levels was observed.