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Biomedical subjects

D Delbro

Publications and source records attributed to D Delbro.

At least 55 records · Page 3Linked to original sources
PubMed1985

P2-purinoceptors mediate both vasodilation (via the endothelium) and vasoconstriction of the isolated rat femoral artery.

The distribution of P1- and P2-purinoceptors in isolated rat femoral artery was studied by comparing responses to ATP, alpha, beta-methylene ATP and adenosine, both when endothelial cells were intact and when they had been removed by mechanical rubbing (as confirmed by histochemical staining and abolition of relaxations to acetylcholine). alpha, beta-Methylene ATP and ATP (but not adenosine or acetylcholine) contracted preparations at resting tone. alpha, beta-Methylene ATP was significantly more potent than ATP. The potency of both alpha, beta-methylene ATP and ATP was significantly increased in the absence of the endothelium. These contractions were unaffected by tetrodotoxin, phentolamine and methysergide in concentrations sufficient to abolish contractions to perivascular nerve stimulation, noradrenaline or 5-hydroxytryptamine. Acetylcholine, ATP and adenosine relaxed arteries whose tone had been raised by 10(-6) M noradrenaline. Removal of the endothelium abolished relaxations to ATP (contractions were seen instead) and acetylcholine, but not to adenosine. alpha, beta-Methylene ATP further contracted the high tone preparation and was again more potent when the endothelium was absent. ATP and alpha, beta-methylene ATP were more potent as contractile agents when noradrenaline was present. These results confirm that endothelial cells can mediate vasodilation. They also show that ATP can act at P2-purinoceptors at two locations in the isolated rat femoral artery; one on the endothelium leading to vasodilation, and the other on the smooth muscle leading to vasoconstriction. P1-Purinoceptors, however, appear to be located on the smooth muscle only and mediate vasodilation. At the smooth muscle P2-purinoceptor, alpha, beta-methylene ATP is more potent than ATP, whereas at the endothelial P2-purinoceptor, the reverse is true.

Adenosine↗
PubMed1985

Blockade of substance P receptors inhibits non-nicotinic, non-adrenergic colonic contractions induced by stimulation of the lumbar sympathetic nerves to the feline large intestine.

Experiments were performed on chloralosed cats, pretreated with guanethidine and hexamethonium and with ligated adrenals. The motility of an arterially isolated colonic segment was monitored by a volumetric method. Colonic contractions were induced either by electric stimulation of the centrally cut lumbar splanchnic nerves, or by close i.a. injections of acetylcholine (ACh). Close i.a. injections of substance P (SP) were performed in order to test the degree of SP-receptor blockade. Blockade of colonic SP-receptors, either by close i.a. administration of large amounts of SP itself or by Spantide, a competitive SP-receptor antagonist, markedly reduced or abolished the neurally induced colonic contractions, while responses to ACh were unchanged. These results indicate a role for SP, or a closely related peptide, as an intermediate neurotransmitter in the neurally induced colonic responses. Thus, the present study gives support to the hypothesis that non-nicotinic, non-adrenergic colonic contractions, in response to electric stimulation of sympathetic nerves, are due to an antidromic activation of sensory neurons with peripheral excitatory collaterals which release SP, in turn activating the colonic smooth muscle, mainly via a muscarinic mechanism.

Acetylcholine↗
PubMed1985

Non-nicotinic, non-adrenergic excitatory motor fibres in the preganglionic sympathetic supply to the feline colon. An axon reflex arrangement associated to thin sensory neurons, involving substance P?

Experiments were performed on chloralosed cats with ligated adrenals. The peripheral ends of the preganglionic sympathetic nerves to the colon were stimulated and colonic motility was monitored by a volumetric method. Electric nerve stimulation with various intensities elicited inhibitory motor responses and occasionally contractions. Hexamethonium and/or guanethidine blocked all inhibitory actions and revealed pure excitatory responses at high stimulation intensities. These colonic contractions were inhibited by atropine. However, atropine-resistant contractions were sometimes observed, predominantly in the colorectal region. Thoracic sympathetic nerves affected the motility in the proximal colon only, while lumbar sympathetic nerves acted on both proximal and distal parts. Strength-duration relationships and sensitivity to local heating suggest that the excitatory responses are due to an antidromic activation of thin, possibly afferent nerve fibres. Small doses of substance P injected close i.a. induced colonic contractions unchanged by hexamethonium and/or guanethidine but sensitive to atropine. The neurally-induced colonic contractions are suggested to be due to an antidromic activation of thin sensory neurons which in the periphery release substance P, in turn activating cholinergic motor neurons, thus constituting an axon reflex arrangement. The possibility of a similar axon reflex mechanism, associated to thin afferents, activating adrenergic inhibitory neurons at the prevertebral ganglionic level is discussed.

Animals↗
PubMed1985

On the transmission of sacral parasympathetic nervous influence on distal colonic and rectal motility in the cat.

Experiments were performed on cats anaesthetized with chloralose and treated with adrenoceptor blocking agents. Distal colonic and rectal motility were selectively recorded by a volumetric method. The effects of muscarinic and ganglionic nicotine receptor blockade on motor responses induced by graded efferent electrical pelvic nerve stimulation (PNS) were studied. Stimulation at low current strength evoked contractions in both the colon and the rectum, which were sensitive to atropine and to hexamethonium. High intensity stimulation elicited distal colonic contractions resistant to both atropine and hexamethonium. Similar excitatory responses to high strength PNS were also observed in the rectum, though not in all experiments. Stimulation at intermediate intensities evoked distal colonic and rectal relaxations which were resistant to atropine but blocked by hexamethonium. The results indicate that PNS influences colonic and rectal motility by activation of at least three discrete non-adrenergic nervous pathways: (1) low-threshold excitatory fibres involving nicotinic and muscarinic transmission, (2) high-threshold excitatory fibres with a non-muscarinic, non-nicotinic transmission mechanism, (3) inhibitory fibres with an intermediate stimulus intensity threshold, exerting their effect by a non-muscarinic mechanism involving a nicotinic step.

Animals↗
PubMed1984

Atropine-sensitive gastric smooth muscle excitation by mucosal nociceptive stimulation--the involvement of an axon reflex?

Experiments were performed in chloralosed cats where gastric motility was recorded by the "volume method". Mucosal and serosal nociceptive stimulations were accomplished by local heating to 45-52 degrees C. Heating generally elicited gastric relaxations, mainly due to activation of extrinsic inhibitory reflexes, but mucosal heating sometimes caused contractile responses which were resistant to nicotinic and adrenergic blockade. The contractions were, however, blocked by atropine and, further, could not be demonstrated after degeneration of splanchnic afferents. On the basis of these and earlier results it is suggested that the gastric contractions induced by mucosal nociceptive stimulation are due to axon reflexes, conveyed by splanchnic afferents that, possibly via release of substance P, make non-nicotinic reflex contacts with intramural excitatory cholinergic neurons.

Animals↗
PubMed1983

Inhibition of antidromically induced stimulation of gastric motility by substance P receptor blockade.

Electrical stimulation of the feline vagal or splanchnic nerves after hexamethonium blockade of nicotinic ganglionic transmission produces gastric contractions, suggesting antidromic activation of thin afferents. The present experiments were performed to examine whether substance P is involved as a transmitter in such gastric responses. Cats were anesthetized with chloralose, laparotomized and the adrenals were ligated. The left greater splanchnic nerve, proximal to the celiac ganglion, and the left or right cervical vagal nerve were dissected, cut and placed on electrodes for peripheral stimulation. Gastric motility was monitored with a balloon. Hexamethonium was administered i.v. as well as i.a. to the stomach. Nerve stimulations produced powerful gastric contractions, which were antagonized by large doses (approximately 0.8 mumol) of substance P administered i.a. to the stomach. Similarly, the gastric contractions elicited by vagal or splanchnic nerve stimulations were reduced to at least 60% of control by the specific substance P antagonist (D-Pro2, D-Trp7,9)-SP administered i.a. (0.4-1.3 mumol). The present results support the concept that substance P is associated with gastric excitatory motor responses, possibly elicited by antidromic activation of thin afferent nerve fibres.

Animals↗
PubMed1982

Gastric atropine-sensitive excitation by peripheral vagal stimulation after hexamethonium. Antidromic activation of afferents?

Experiments were performed in chloralosed cats with ligated adrenals with recording of arterial blood pressure, heat rate and gastric volume, the latter with a balloon method. Electric activation of the peripheral cut vagus at low and high intensity induced gastric excitatory and relaxatory responses, respectively. Hexamethonium blocked the stimulation-bound bradycardia but now high intensities induced excitatory gastric responses, resistant to alpha- and beta-adrenergic blocking agents and naloxone but sensitive to atropine. Heating of the intact vagus, to selectively activate thin afferents, resulted in gastric inhibition, due to vago-vagal reflex activation. When the nerve had been proximally cut, local nerve heating induced excitatory gastric responses, with the same pharmacological characteristics as those caused by electric nerve stimulation. The observations suggest that the hexamethonium-resistant gastric excitatory responses to peripheral vagal stimulation are due to antidromic activation of thin afferents which are proposed to function in axon reflexes affecting gastric motility.

Animals↗
PubMed1982

Atropine-sensitive gastric excitation by stimulation of thoracic dorsal roots--antidromic activation of afferents?

In chloralosed cats, usually with ligated adrenals and paralysed with gallamine, the thoracic dorsal roots were electrically stimulated and gastric motor responses were recorded. Thoracic dorsal root stimulation regularly elicited gastric contractions after pretreatment with guanethidine and/or hexamethonium which were readily blocked by atropine. It was established that these gastric motor responses were due to peripheral stimulation of the dorsal root and not to spread to the ventral roots. Together with other results (Delbro & Lisander 1980) the findings suggest an antidromic activation of thin afferent fibres with excitatory collaterals to intramural cholinergic neurons which convey the gastric contractions.

Animals↗
PubMed1982

Hexamethonium-resistant gastric contractions by stimulation of the vagal nuclei. An antidromic activation of vagal afferents?

Experiments were performed in chloralosed cats, laparotomized with ligated adrenals and spinalized in the cervical region. Blood pressure, heart rate and gastric motility were monitored. Stimulations were performed in two brain stem regions, viz. a "control region" including the nucleus ambiguous and a "dorsal region" approximately corresponding to the dorsal vagal nucleus and the solitarius complex. From both regions were regularly elicited gastric motor responses that were either excitatory, biphasic or inhibitory in direction, and always associated with prompt bradycardia and hypotension. After hexamethonium blockade of the "conventional" efferent vagal excitatory and relaxatory fibres to the stomach, stimulation of the control region no longer augmented gastric motility, while gastric contractions which could be abolished by atropine or vagotomy were produced from the dorsal region. The bradycardia and hypotension responses from both regions were also blocked by hexamethonium and then stimulations often led to delayed pressor responses, resistant to both vagotomy and atropine. The present results, together with previous findings (Delbro et al. 1981, 1982) suggest that the hexamethonium-resistant gastric contractions, elicited by stimulation of the mentioned dorsal region of the brain stem, are due to antidromic activation of afferent gastric vagal fibres with excitatory collaterals to intramural cholinergic neurons.

Afferent Pathways↗
PubMed1980

The effect of Apamin on nonadrenergic, noncholinergic nervous vasodilatations in the cat small intestine.

The intestinal vasodilation evoked by mechanical mucosal stimulation or by transmural electrical field stimulation was abolished by close i.a. injection of Apamin, a polypeptide originally isolated from bee venom. Apamin also blocked the vasodilatation induced by close i.a. infusion of vasoactive intestinal polypeptide (VIP). It is suggested that Apamin is a VIP receptor antagonist.

Animals↗