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Biomedical subjects

R Crowe

Publications and source records attributed to R Crowe.

88 records · Page 5Linked to original sources
PubMed1979

Comparative pharmacological and histochemical evidence for purinergic inhibitory innervation of the portal vein of the rabbit, but not guinea-pig.

1 Intramural nerve stimulation elicited a powerful relaxation of the longitudinal muscle of the rabbit portal vein in the presence of atropine and guanethidine, but not of the guinea-pig portal vein.2 Intramural nerve stimulation of the rabbit portal vein produced a 13 fold increase in release of (3)H-adenyl compounds after preloading with [(3)H]-adenosine. About 50% of this release was abolished by guanethidine. All release was abolished by tetrodotoxin. No significant release of radioactive compounds was observed during intramural nerve stimulation of the guinea-pig portal vein in the presence of guanethidine, although there was a 6 fold increase in release of radioactivity in the absence of drugs.3 Histochemical studies using quinacrine, which binds ATP showed a fine fluorescent nerve plexus, nerve bundles, and ganglion cells in the rabbit portal vein, but not in the guinea-pig portal vein. This plexus was still present after chemical sympathectomy with 6-hydroxydopamine.4 Adenosine 5'-triphosphate (ATP) relaxed the rabbit portal vein, but usually produced a biphasic response, consisting of a contraction followed by a relaxation, of the guinea-pig portal vein.5 Prostaglandins E(1) and E(2) caused contraction of the rabbit portal vein. Indomethacin, a prostaglandin synthesis inhibitor, potentiated the relaxations of the rabbit portal vein produced by both non-adrenergic, non-cholinergic nerve stimulation and ATP.6 High concentrations of antazoline and phentolamine, which antagonize purinergic responses in the guinea-pig taenia coli, caused a loss of basal tone so that it was not possible to assess their effects on the responses of the portal vein to either non-adrenergic, non-cholinergic nerve stimulation, or ATP.7 Comparison of the results on the portal vein of the rabbit and guinea-pig provides support for the view that: (i) quinacrine fluorescence can be used to localize purinergic nerves and that the rabbit portal vein is supplied by these nerves; (ii) ATP is released from adrenergic nerve fibres, although, based on histochemical analysis, about 3 to 7 times less than is released from purinergic nerve fibres.

Animals↗
PubMed1979

Postpartum mania.

Twenty-one patients with bipolar affective disorder (20 manic episodes, one depressive episode) during the postpartum period were evaluated. They were compared to an unselected group of womicantly more Schneiderian symptoms and fewer recurrences of illness within the three-year periofectively ill relatives than the controls. The practical significance of these findings with rey of the bipolar syndrome.

Adult↗
PubMed1978

Quinacrine fluorescence of Merkel cells in Xenopus laevis.

It has been shown by electron microscopy that, in Xenopus laevis, Merkel cells are usually situated near the ducts of the skin glands. Cells which fluorescence in ultra-violet light after treatment of the skin with quinacrine can be identified with these Merkel cells by their position, shape and size. The method indicates the presence of purine nucleotides, probably ATP. This result is consistent with the view that "large opaque vesicles" are sites of ATP storage.

Animals↗
PubMed1978

The familial prevalence of anxiety neurosis.

A family history study of 112 anxiety neurotics and 110 surgical controls showed that the morbidity risk for anxiety neurosis among first-degree relatives of neurotics was 18% compared to 3% among control relatives. Relatives of anxiety neurotics were also shown to be at higher risk for the development of alcoholism. Female relatives were found to be at greater risk than male relatives, reflecting their increased susceptibility to the illness. These data confirm previous findings of an increased familial prevalence of anxiety neurosis.

Alcoholism↗
PubMed1978

Purinergic innervation of the guinea-pig urinary bladder.

1 A number of criteria for considering adenosine 5'-triphosphate (ATP) as a neurotransmitter in the guinea-pig urinary bladder have been examined. In addition, the effect of tachyphylaxis to ATP on the response to non-adrenergic, non-cholinergic nerve stimulation has been re-examined.2 Quinacrine fluorescence histochemistry revealed a population of nerve fibres, ganglion cells, and nerve bundles in the bladder which were not seen in either the iris or vas deferens, where adrenergic and cholinergic nerves predominate. The distribution and morphology of the quinacrine-positive nerves in the bladder were different from those observed with catecholamine fluorescence and cholinesterase histochemistry, and were unaffected by chemical sympathectomy.3 Release of ATP from the bladder during stimulation of intramural excitatory nerves, in the presence of atropine and guanethidine increased to 3-12 times prestimulation levels. Tetrodotoxin abolished both the contractile response and the increase in ATP release resulting from intramural nerve stimulation. There was no increase in ATP release during contraction resulting from direct muscle stimulation following nerve paralysis with tetrodotoxin.4 Sympathectomy with 6-hydroxydopamine did not affect release of ATP in response to intramural nerve stimulation.5 Release of ATP was dependent on the concentration of calcium ion in the medium.6 Contractions in response to non-adrenergic, non-cholinergic intramural nerve stimulation were closely mimicked by ATP, but not by acetylcholine or histamine.7 Adenosine and dipyridamole reduced the contractions to both ATP and non-cholinergic nerve stimulation.8 2-2'-Pyridylisatogen was not a specific blocker of either ATP or intramural nerve stimulation in the guinea-pig bladder. 2-Substituted imidazolines initiated spontaneous activity making it impossible to assess any blocking action that they may have had.9 Prostaglandins (E(1), E(2) and F(2alpha)) gave weak, slow contractions and an increase in spontaneous activity. Both the response to ATP and non-adrenergic, non-cholinergic nerve stimulation were greatly potentiated in the presence of prostaglandins.10 In the presence of indomethacin the response to non-adrenergic, non-cholinergic nerve stimulation was virtually abolished following desensitization to ATP.

Acetylcholine↗
PubMed1978

Evidence for purinergic innervation of the anococcygeus muscle.

1 Fluorescence histochemical localization of quinacrine (which binds to adenosine 5'-triphosphate (ATP)) revealed nerve fibres running singly and in bundles in both rat and rabbit anococcygeus muscle. Single neurone cell bodies and ganglia containing between 2 and 50 cells were also observed.2 Catecholamine fluorescence studies revealed a dense adrenergic ground plexus, but no adrenergic ganglion cells were detected. No acetylcholinesterase-positive nerve fibres or ganglion cells were seen in the rat.3 When the tone was raised with guanethidine, a relaxation in response to field stimulation was revealed, which was unaffected by atropine but blocked by tetrodotoxin.4 Release of ATP increased 3 to 6 times above background during stimulation of these non-adrenergic, non-cholinergic, inhibitory nerves.5 Neither quinacrine staining nor the release of ATP during inhibitory nerve stimulation was affected by 6-hydroxydopamine treatment, which abolished catecholamine fluorescence.6 Exogenous ATP produced relaxation in high tone preparations of the rabbit anococcygeus muscle. ATP produced either contraction or a small relaxation followed by a contraction of the rat anococcygeus muscle, but treatment with low concentrations of the prostaglandin synthesis inhibitor indomethacin, converted the contraction to a relaxation.7 These data are consistent with the view that the anococcygeus muscle is innervated by purinergic inhibitory nerves.

Adenosine Triphosphate↗
PubMed1977

Effect of chlordiazepoxide on the partial reinforcement extinction effect.

Rats were trained to run in a straight alley under conditions of partial or continuous reinforcement. Extinction was slower after partial reinforcement. Chlordiazepoxide, administered during acquisition only, had no effect on acquisition but abolished the partial reinforcement extinction effect. The results support the hypothesis that chlordiazepoxide acts by attenuating the effects of averisive stimuli.

Animals↗
PubMedDate not supplied

Prognostic factors in minor salivary gland cancer.

BACKGROUND: Minor salivary gland cancer occurs infrequently and presents a diagnostic and therapeutic challenge. The purpose of this study was to determine prognostic factors for this disease. METHODS: The medical records of 95 patients diagnosed and treated at the University of Alabama at Birmingham over a 35-year period were reviewed. Information concerning patient, disease, and treatment characteristics was compiled for each case. Multivariate analysis was conducted using a rank regression procedure. RESULTS: State I or II cancer (p = .022), the absence of cervical lymph node metastases (p = .001), and surgical margins which were free of cancer (p < .001) were predictive of increased 4-year disease-free survival by multivariate analysis. CONCLUSION: Our findings emphasize the need for detection of early-stage disease combined with complete surgical extirpation of the cancer, which provide the patient with the best chance for locoregional control and long-term survival.

Adenocarcinoma↗
PubMedDate not supplied

Neurocompensatory responses to balloon-catheter-induced injury of the rat carotid artery.

Percutaneous transluminal angioplasty relieves discrete arterial stenosis but causes extensive vascular injury. There is denudation of the endothelium and variable medial disruption, but the effect on adventitial structures has not been studied in detail. We have investigated the innervation of the left and right carotid arteries after unilateral balloon-catheter-induced injury. Immunohistochemical examination of the arteries 1 day after Fogarty-catheter-induced injury of the left common carotid artery revealed a reduction in the density of protein gene product 9.5 (PGP)-, substance P (SP)- and calcitonin-gene-related peptide (CGRP)-containing nerves close to the medial smooth muscle of the injured vessel. At the same time, on the side contralateral to the injury, there was a substantial increase in the density of PGP-, SP- and CGRP-containing nerves innervating the carotid artery and vasa vasorum compared to controls. Immunoassay data from these vessels showed a selective increase in SP and CGRP contents of the contralateral carotid artery (SP, controls 0.02 +/- 0.01, operated 0.59 +/- 0.32 pmol/cm; CGRP, controls 0.03 +/- 0.01, operated 0.14 +/- 0.03 pmol/cm, n = 6, p < 0.05). Neuropeptide Y levels were unchanged. Twenty-eight days after surgery, at which time a neointima was present, peptide levels were no different from controls, and the innervation of both the left and right carotid arteries and vasa vasorum was indistinguishable from the controls. In conclusion, balloon-catheter-induced injury includes damage to the perivascular nerves and induces a transient increase in the density of sensory neuropeptide-containing nerves innervating the contralateral, uninjured side. This novel observation may reflect neurocompensatory responses to vascular injury.

Animals↗