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Biomedical subjects

D Delbro

Publications and source records attributed to D Delbro.

At least 37 records · Page 2Linked to original sources
PubMed1991

The effects of atropine or benzilonium on pelvic pouch and anal sphincter functions.

Anticholinergic drugs are used on an empirical basis for treatment of functional disturbances after restorative proctocolectomy, but their mode of action on ileal pouch performance is mainly unknown. We studied the acute effects of atropine or benzilonium on pouch characteristics and anal sphincter function in 20 patients with a pelvic pouch. Pouch volume was increased by 27% by atropine at distension with 20 cm H2O (p less than 0.01). Benzilonium tended to have a similar effect, but the changes did not reach statistical significance (p = 0.06). Pouch contractility, as reflected by volume fluctuations and pressure changes during distension, was almost abolished by both drugs. Sensory thresholds for sense of filling and, particularly, urge were raised. Resting anal pressure was slightly lowered, whereas no significant effect was found on maximal squeeze pressure. In conclusion, anticholinergics appear to have specific properties of action on small-intestinal reservoirs, constituting possible explanations for the empirically observed beneficial effects of anticholinergic treatment of functional disturbances after restorative proctocolectomy.

Adult↗
PubMed1989

Effects of dopamine on intestinal hemodynamics and motility during epidural analgesia in the cat.

The effects of dopamine on intestinal blood flow (IBF) and intestinal contraction rate (ICR), and on mean arterial pressure (MAP) and heart rate (HR) were studied in eight cats before and during epidural analgesia (EDA). Before EDA, dopamine 5 and 10 micrograms.kg-1.min-1 had no effect on IBF, MAP and HR, but the higher infusion rate decreased ICR by 71 +/- 19% (mean +/- 1 s.e.mean) (P less than 0.01). EDA significantly increased IBF when intestinal arterial pressure was maintained at an unchanged level by means of a pump, and transiently increased ICR and intestinal tone, but reduced MAP by 46 +/- 8% (139 +/- 11 to 75 +/- 9 mmHg, P less than 0.01) and HR by 26 +/- 3% (248 +/- 7 to 184 +/- 8 beats.min-1, P less than 0.01). During EDA, dopamine increased IBF further, the response being similar at both infusion rates. 5 micrograms.kg-1.min-1 increased HR by 26 +/- 7 beats.min-1 (P less than 0.01) and MAP by 19 +/- 9 mmHg (ns). The corresponding values at 10 micrograms.kg-1.min-1 were 65 +/- 14 beats.min-1 (P less than 0.01) and 35 +/- 8 mmHg (P less than 0.01), respectively, Vascular autoregulation appeared to be unaffected by dopamine and EDA. The effect of dopamine on ICR was not significantly different to what was seen before EDA. It is concluded that the effects of dopamine on IBF, MAP and HR were markedly different during EDA as compared to before the block and that ICR was reduced by dopamine, while it was transiently increased by EDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia, Epidural↗
PubMed1989

Spinovagal reflex modulation of gastric motility in response to mucosal nociceptive stimulation in the anaesthetized rat.

In anesthetized rats treated with guanethidine, the pylorus was ligated. A catheter was inserted into the stomach via the mouth and anchored by a ligature around the cervical oesophagus. The catheter was used for instillation into the stomach of a fixed volume (9 ml) of either isotonic or 1 M NaCl and for the recording of intragastric pressure. Neurogenic modulation of gastric motility caused by either solution was analysed by studying the effect of the systemic administration of the ganglionic blocker hexamethonium on gastric tone and on phasic motor activity. Gastric motility was not significantly changed by hexamethonium in the animals that had been subjected to isotonic NaCl. After intragastric treatment with 1 M NaCl, however, hexamethonium caused increased gastric tone and decreased phasic motor activity. An analysis of these results suggests that 1 M NaCl activated vagal non-adrenergic, non-cholinergic relaxatory and cholinergic excitatory motor neurons, respectively. These chemically induced modulations of gastric motility were dependent on the spinal cord and, most probably, were due to activation of the mucosal sensory endings of the splanchnic nerves, leading to reflex spinovagal motor adjustments.

Animals↗
PubMed1988

Motor responses elicited by local electrical stimulation of the distal colon in the anaesthetized rat.

A method to study electrically induced distal colonic motility in the rat in vivo is reported. The animals were anaesthetized with methohexital and chloralose and were artificially ventilated. Motility of a segment (2 cm) of the distal colon was monitored as volume changes of an intraluminal balloon, introduced via the anus. Local electrical stimulation of the wall of the segment was achieved by means of a bipolar electrode folded around the gut. Stimulations produced reproducible contractile responses in a frequency dependent fashion. Stimulation characteristics resembled those of other autonomic neuro-effector systems. The adrenergic neuron-blocker, guanethidine, significantly lowered colonic tone, but had no other effects on spontaneous or electrically induced motility. Atropine significantly lowered colonic tone. After the administration of this compound the electrically induced contractions were significantly smaller with a shorter duration and, furthermore, appeared upon the cessation of stimulation ('off' or 'rebound' contraction). Following the administration of tetrodotoxin (TTX, given close i.a. via a cannula with its tip in distal aorta) basal colonic tone and the number of spontaneously occurring contractions increased. The amplitude and duration of the electrically induced responses were significantly attenuated and, furthermore, appeared as 'rebound' contractions which were preceded by a relaxation. Such TTX-resistant responses may be myogenic, but a neurogenic origin cannot be excluded. The present study showed that local electrical stimulation of the distal colon elicits cholinergic contractions, but also atropine- and TTX-resistant motor responses.

Animals↗
PubMed1988

Pre- and postganglionic sympathetic nerve activity during induced hypotension with adenosine or sodium nitroprusside in the anesthetized rat.

The aim of this study was to examine the effects of adenosine (AD)-induced hypotension on preganglionic adrenal (aSNA) and postganglionic renal (rSNA) sympathetic nerve activity. rSNA (n = 10) and aSNA (n = 6) were recorded together with mean arterial pressure (MAP) and heart rate (HR) in chloralose-anesthetized, artificially ventilated rats. In each experiment, hypotension was induced by equihypotensive doses of AD (0.03-2.0 mg.kg-1.min-1) and sodium nitroprusside (SNP) (1-10 micrograms.kg-1.min-1). SNP induced a progressive reflex tachycardia and a reflex increase in rSNA to levels 159 +/- 35% above control at a MAP reduction of 55% of the normotensive control value. Equipotent doses of AD induced a decrease in HR and significantly less pronounced reflex increase in rSNA. The maximal increase in rSNA with AD was 55 +/- 19% at a MAP reduction of 30%. At higher infusions rates of AD, rSNA progressively declined toward the normotensive control values. However, AD elicited a progressive increase in preganglionic aSNA that was not significantly different from the increase seen during SNP infusion. It is concluded that AD-induced hypotension is associated with a suppression of postganglionic sympathetic nerve activity caused by an inhibition of ganglionic neurotransmission.

Adenosine↗
PubMed1987

Hypothalamic stimulation counteracts sympathetically mediated gastrointestinal inhibition in chloralose-anaesthetised cats.

The inhibitory motor effect of the sympathetic gastrointestino-gastrointestinal (GI-GI) reflex was studied in cats with isolated innervated ileal (Thiry-Vella) loops. They were subjected to acute experiments under chloralose-gallamine anaesthesia where gastric volume, arterial blood pressure and heart rate were continuously monitored. The cervical vagi were sectioned and used for efferent stimulation. The hypothalamus was systematically explored by means of stereotaxically guided electrodes. When the abdomen was undisturbed, gastric contractile responses to central stimulation were virtually absent, regardless of whether a vagally induced tone was present or not. Distension of the isolated intestinal loop induced marked inhibition of vagally induced gastric tone, indicating activation of the GI-GI reflex. Under these conditions, about 17% of the hypothalamic points induced gastric excitation, due to withdrawal of sympathetic tone. The GI-GI reflex can thus be inhibited from diencephalic levels. This inhibition is not linked to any distinct cardiovascular 'pattern'.

Animals↗
PubMed1987

Substance P-induced tachycardia in the anaesthetized rat.

In pentobarbital-chloralose-anaesthetized rats, pretreated with hexamethonium and atropine the mechanism by which substance P (SP) causes tachycardia was analysed. Substance P, when infused i.v. at doses between 0.49 nmol and 1.52 nmol elicited a marked, dose-dependent tachycardia, which was reduced to less than half by propranolol, 0.1 mg kg-1. Furthermore, the SP-induced tachycardia was reduced to about 1/10 of control by guanethidine. Further, the tachycardia, which could also be elicited in pithed rats, was antagonized by the SP-receptor blocker Spantide, but these results must be taken with care since Spantide itself caused a pronounced and long-lasting depressor response. It is hypothesized that SP causes tachycardia by exciting specific receptors on the stellate ganglia, which leads to an activation of adrenergic fibres to the sinus node.

Animals↗
PubMed1987

Depressor and pressor actions of purine nucleosides and nucleotides in the anaesthetized rat.

In pentobarbitone-chloralose anaesthetized rats, the effects of aortic administration of various purine compounds on systemic arterial pressure were investigated. All animals were pretreated with atropine and guanethidine to (largely) eliminate reflex neurogenic cardiovascular adjustments, and drugs influencing purine receptors, prostaglandin synthesis, etc. were used for analytical purposes. The compounds used were adenosine (AD) and its slowly degradable analogue, 2-chloroadenosine (2-chloro), adenosine-5'-triphosphate (ATP) and its slowly degradable analogues beta, gamma-methyleneATP (beta,gamma-meATP) and alpha,beta-methyleneATP (alpha,beta-meATP). Control cardiac output measurements before, at and after the peak pressure changes in some experiments revealed that they were at least 80% due to changes in systemic resistance, i.e. dominated by shifts in resistance vascular tone. Adenosine, 2-chloro, ATP and beta,gamma-meATP all elicited depressor (vasodilator) responses. 2-chloro was more potent than AD. Furthermore, the results suggest that the depressor action of ATP involves P1-purinoceptors, following the rapid degradation of ATP to AD, and probably also other mechanisms. The stable ATP analogues caused prompt pressor (vasoconstrictor) responses, where alpha,beta-meATP was more potent than beta,gamma-meATP. The latter compound also produced delayed (probably P1-purinoceptormediated) depressor actions, presumably via slow degradation to AD.

2-Chloroadenosine↗
PubMed1987

Vago-vagal activation of naloxone-sensitive non-adrenergic, non-cholinergic jejunal contractions in the anaesthetized cat.

Experiments were performed on chloralose-anaesthetized cats, pretreated with guanethidine and with ligated adrenals and sectioned splanchnic nerves. The animals were paralysed and artificially ventilated. Jejunal motility was recorded by an intraluminal balloon, as volume changes at a constant pressure. Cervical or abdominal vagal afferent stimulation was performed before and after the administration of atropine. In both circumstances jejunal contractions were elicited. The latency of onset and the duration of the responses were significantly shorter before than after atropine. Strength-duration and frequency-response relationships, respectively, did not differ significantly prior and subsequent to atropine. Naloxone (0.05-0.5 mg kg-1 i.v.) blocked these reflexly induced atropine-resistant jejunal contractions, as did section of the contralateral vagus. Possible mechanisms of action of these putative opioid receptor-mediated neurogenic effects are discussed. The present study demonstrates that non-adrenergic, non-cholinergic, naloxone-sensitive jejunal contractions can be elicited as a vago-vagal reflex, where the receptive field seems to be located within the abdominal cavity.

Animals↗
PubMed1987

Vagal influence on gastroduodenal HCO3- secretion in the cat in vivo.

Gastric and duodenal secretions of HCO3- were studied simultaneously in chloralose-anesthetized cats. The adrenals were ligated, and the cervical vagal as well as the abdominal splanchnic nerves were cut. Gastric secretions of H+ and HCO3- were calculated from measurements of the pH and PCO2 in the luminal perfusate. A duodenal segment devoid of Brunner's glands and pancreaticobilary secretions was cannulated in situ and the alkaline secretion determined by continuous titration at luminal pH 7.4. Electrical stimulation in the distal direction for 10-15 min of the cervical vagal nerves resulted in a 6- to 10-fold increase in gastric H+ and in a 20-60% rise in gastric HCO-3 secretion. Duodenal HCO3- secretion increased by 65-155%. Gastric basal secretions of H+ and HCO3- were not affected by atropine or hexamethonium, but both agents inhibited basal duodenal HCO3- secretion. Hexamethonium abolished and atropine reduced the rise in all secretions in response to vagal nerve stimulation. Thus gastroduodenal mucosal HCO3- secretion is stimulated by vagal mechanisms involving action on nicotinic as well as on muscarinic receptors and possibly also noncholinergic neurotransmission.

Animals↗
PubMed1986

Bradykinin-induced atropine-sensitive gastric contractions. Activation of an intramural axon reflex?

Gastric motor responses, recorded as volume changes of an intragastric balloon, were induced by the close i.a. administration of bradykinin (0.75-4 micrograms) in chloralose-anaesthetized cats. The animals were vagotomized and the adrenals were ligated at the outset of the experiments. Prior to autonomic blocking agents bradykinin elicited relaxatory or biphasic motor responses. Following nicotinic ganglionic receptor blockade bradykinin caused predominantly gastric contractions. Such excitatory responses were antagonized by 80-100% by atropine, suggesting a dominant neurogenic component. An hypothesis is put forward that the observed gastric contractions result from a bradykinin-induced activation of an axon reflex arrangement confined to thin sensory nerve fibres which, by substance P release from intramural collaterals, excite postganglionic cholinergic motor neurones.

Animals↗
PubMed1986

Effect of alpha, beta-methylene ATP on distal colonic and rectal motility--a possible involvement of P2-purinoceptors in pelvic nerve mediated non-adrenergic, non-cholinergic contraction.

The possible involvement of purinoceptors in the parasympathetic nervous control of large intestinal motility was investigated in cats anaesthetized with chloralose and treated with adrenolytics. Distal colonic and rectal motor responses to efferent pelvic nerve stimulation (PNS) and drugs injected close i.a., were recorded by a volumetric method. Single dose i.a. injections of alpha, beta-methylene ATP (mATP) induced colonic and rectal contractions which were resistant to atropine, hexamethonium and indomethacin, as well as to the nerve blocking agent tetrodotoxin. Repeated injections of mATP were followed by attenuated motor responses and eventually complete tachyphylaxis to the compound developed. In the presence of atropine, or a combination of hexamethonium and atropine, contractions elicited by PNS were inhibited during mATP tachyphylaxis. In contrast, prior to such anticholinergic drugs, or in the presence of hexamethonium alone, pelvic nerve mediated contractions persisted despite mATP tachyphylaxis, which did not affect the colonic and rectal contractions evoked by acetylcholine or histamine. The results suggest that P2-purinoceptors are involved in non-adrenergic, non-cholinergic large intestinal excitatory motor responses to PNS.

Adenosine Triphosphate↗