PubMed Health⌕ Search

Biomedical subjects

R Crowe

Publications and source records attributed to R Crowe.

At least 55 records · Page 3Linked to original sources
PubMed1982

Regional differences in the density of perivascular nerves and varicosities, noradrenaline content and responses to nerve stimulation in the rabbit ear artery.

Quantitative image analysis of fluorescent nerve following histochemical localization of monoamines in stretch preparations of the rabbit ear artery (REA) reveals marked differences in the density of innervation between the proximal and distal regions. The innervation in the proximal region is about twice as dense as that in the distal region and there are approximately 10,500 and 6,500 varicosities per mm2 vessel area in these two regions, respectively. These varicosities have approximately the same mean diameter throughout the length of the vessel. The noradrenaline contents per gram wet weight of tissue in the proximal and distal regions are 1.93 and 0.94 microgram, respectively. It is estimated that noradrenaline contents per mm2 nerve plexus area are 0.30 and 0.08 ng and that the nerve endings consist 2.8 x 10(-14) and 1.2 x 10(-14) g per varicosity in the proximal and distal REA, respectively. Sympathetic nerve stimulation in vitro with frequencies up to 8 Hz elicits larger and faster contractions in the proximal REA and the threshold frequency is less than in the distal region. This study also indicates that care should be taken to use the same region when using the REA for pharmacological and physiological studies.

Adrenergic Fibers↗
PubMed1981

Comparative studies of quinacrine-positive neurones in the myenteric plexus of stomach and intestine of guinea-pig, rabbit and rat.

The number of quinacrine-fluorescent nerve cell bodies and the percentage of the ganglion area occupied by this fluorescence within stretch preparations of the myenteric plexus of the stomach and ileum of the guinea-pig, rabbit and rat were assessed. The number of quinacrine-positive cell bodies per cm2 of plexus varied between 1045 in the rabbit ileum to 2633 in the rat stomach, whilst the percentage of the ganglionic area occupied by fluorescence was approximately 10%. The distribution of quinacrine-fluorescent nerve fibres and cell bodies in the myenteric plexus was compared to the distribution of nerves revealed by catecholamine fluorescence and by staining for acetylcholinesterase in the stomach and ileum of all three species. Quinacrine fluorescence appears to be selective for non-adrenergic, non-cholinergic nerves; the possibility that it binds to high levels of ATP is discussed.

Acetylcholinesterase↗
PubMed1981

Perinatal development of quinacrine-positive neurons in the rabbit gastrointestinal tract.

Nerve showing positive reaction to quinacrine are described in rabbit ileum and stomach during perinatal development and compared to the distribution of nerves revealed by catecholamine fluorescence and by staining for acetylcholinesterase Acetylcholinesterase- and quinacrine-positive neurons were observed on the twenty-third day of gestation in both the ileum and stomach, but catecholamine fluorescence was not detected in nerves until the twenty-fifth and twenty-sixth days of gestation in the stomach and ileum respectively. The possibility that quinacrine is binding to high accumulations of ATP is discussed.

Acetylcholinesterase↗
PubMed1981

Adrenergic innervation in autonomic failure.

In 10 patients with chronic autonomic failure, the sympathetic perivascular nerve plexuses from quadriceps muscle biopsies were studied by catecholamine fluorescence and electronmicroscopy. There was almost complete absence of catecholamine fluorescence and fewer than normal numbers of small granular (noradrenergic) vesicles in all nerves studied. The most marked depletion of noradrenergic vesicles was seen in two of the patients with pure autonomic failure, but more studies are needed for a full quantitative comparison of pure autonomic failure and autonomic failure with multiple system atrophy (Shy-Drager syndrome).

Aged↗
PubMed1980

Mitral valve prolapse in anxiety neurosis (panic disorder).

Our purpose was to determine the incidence of mitral valve prolapse in patients with anxiety neurosis or panic disorder, with symptoms including recurrent anxiety attacks, dyspnea, palpitations, chest pain, dizziness, and paresthesias. Twenty-one patients and 20 age- and sex-matched normal controls were studied. Objective cardiac abnormalities were significantly (p < 0.05) more frequent in the patient group as compared to the control group; these comprised echocardiographic prolapse, ST-T abnormalities on resting ECG, premature ventricular contractions on exercise ECG, and the combination of echo prolapse with clicks/murmurs of exercise-induced PVC. We conclude that patients with anxiety neurosis or panic disorder may also have evidence of an organic abnormality--the mitral prolapse syndrome.

Adult↗
PubMed1979

Non-adrenergic, non-cholinergic (purinergic?) inhibitory innervation of the rabbit rectococcygeus muscle.

A powerful non-adrenergic, non-cholinergic inhibitory innervation of the rabbit rectococcygeus was unmasked by atropine in preparations in which tone had been raised either by carbachol or prostaglandin E2-Flourescent histochemical localization of quinacrine (which binds ATP) revealed ganglia and associated nerve bundles which were neither adrenergic nor cholinergic both on the surface and within the rectococcygeus muscle. Treatment of the rabbit with 6-hydroxydopamine abolished catecholamine fluorescence without affecting quinacrine-stained neural elements. Release of ATP from the rectococcygeus increased 2-4 times above background levels during stimulation of intramural inhibitory nerves. In preparations in which the tone was raised, ATP caused an inhibitory response comparable to that produced by non-adrenergic, non-cholinergic nerve stimulation. Indomethacin reduced the increase in tone and spontaneous activity following washout of ATP in low tone preparations, and potentiated the relaxations produced by ATP in high tone preparations. These results suggest that the rabbit rectococcygeus, as well as receiving a cholinergic excitatory innervation and an adrenergic inhibitory innervation, is also innervated by purinergic inhibitory nerves.

Acetylcholinesterase↗
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↗