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Biomedical subjects

J D Christensen

Publications and source records attributed to J D Christensen.

At least 55 records · Page 3Linked to original sources
PubMed1990

Influence of interleukin-1 beta on the secretion of oxytocin and vasopressin from the isolated rat neurohypophysis.

The effect of the cytokine interleukin-1 beta on the secretion of oxytocin and vasopressin from electrically stimulated rat neurohypophysis was examined in vitro. The release of oxytocin and vasopressin was concentration-dependently increased by interleukin-1 beta in the concentration range from 4.4 pM to 440 pM. The effect of interleukin-1 beta on oxytocin secretion was less intense as compared to vasopressin. After 440 pM interleukin-1 beta the electrically evoked release of oxytocin was increased about 22% and had not reached its maximum. The vasopressin response was maximal after 44 pM interleukin-1 beta, the response being increased 43% compared to control. No trace of interleukin-1 beta was found in the posterior pituitary (less than 350 pmol/lobe, radioimmunoassay). The results indicate that interleukin-1 beta might be involved the regulation of oxytocin and vasopressin at the pituitary level.

Animals↗
PubMed1989

Interleukin-1 beta stimulates the release of vasopressin from rat neurohypophysis.

The release of vasopressin from the isolated superfused rat neurohypophysis was measured. The electrically evoked release of vasopressin after phasic submaximal stimulation was increased on exposure to the cytokine, interleukin-1 beta (44 pM). The release returned to its control level when the peptide was withdrawn. The results indicates a permissive role of interleukin-1 beta in the release of vasopressin.

Animals↗
PubMed1989

Biphasic effect of a kappa-opioid receptor agonist on plasma oxytocin levels in rats.

The effect of the kappa-opioid receptor agonist, bremazocine, on plasma oxytocin levels in rats was measured by a sensitive radioimmunoassay. Initially, a decrease in plasma oxytocin levels was seen 30 min after injection. This was in accordance with the bremazocine inhibition of oxytocin release after submaximal electrical stimulation seen in isolated neurointermediate lobes. The initial decrease in plasma oxytocin reversed, and 4 h after injection of bremazocine a 20-fold increase in the oxytocin level was seen. The rise in plasma oxytocin was paralleled by a rise in plasma sodium. The biphasic time course of the plasma oxytocin response can be explained by a combination of an inhibition of oxytocin release from the neurohypophysis and an increased water excretion leading to an elevation in plasma sodium, which may be responsible for the late rise in plasma oxytocin. Down-regulation of the opioid receptors may also contribute to the delayed rise in plasma oxytocin.

Analgesics↗
PubMed1989

Prostaglandin E1 and prostaglandin F2 alpha in exudate in nickel allergy.

Ten nickel-allergic patients and 5 healthy control subjects participated in a study of the kinetics of the flux and concentration of migrated leukocytes and extracellular PGE1 and PGF2 alpha during a 48 h period, using a skin chamber technique. The patients were provided with two skin chambers, one with and one without nickel challenge. A higher flux of leukocytes, PGE1 and PGF2 alpha was observed during the second day of allergen exposure, while the concentrations probably due to dilution were unchanged or diminished, indicating an unspecific role of the prostaglandins during the contact allergic reaction. No correlations were found within the groups between the migration of leukocytes and the prostaglandin content.

Adult↗
PubMed1988

Role of gastrin-releasing peptide in pepsinogen secretion from the isolated perfused rat stomach.

We studied the effects of the neuropeptide gastrin-releasing peptide on pepsinogen secretion using an isolated perfused rat stomach with intact vagal innervation. Following electrical stimulation of the vagus nerves, the pepsin output to the luminal effluent increased from 94 +/- 7 to 182 +/- 24 units pepsin/min and the release of immunoreactive gastrin-releasing peptide to the venous effluent increased from 0.059 +/- 0.014 to 0.138 +/- 0.028 pmol/min. Infusion of gastrin-releasing peptide at 10(-8) M significantly increased pepsin output (from 87 +/- 17 to 129 +/- 22 units pepsin/min) and simultaneous infusion of gastrin-releasing peptide and carbachol at 10(-8) and 10(-6) M, respectively, resulted in an increase to almost 4 times the basal values. Atropine reduced but did not abolish the pepsin response to vagal stimulation and to infusion of gastrin-releasing peptide. Our results suggest that gastrin-releasing peptide participates in the vagal control of pepsinogen secretion.

Animals↗
PubMed1988

Lactoferrin, myeloperoxidase, lysozyme and eosinophil cationic protein in exudate in delayed type hypersensitivity.

A skin window technique was used to study the morphology of leucocytes in upper dermis and exudate during nickel challenge in patients with contact allergy to nickel. Contact allergic patients and healthy volunteers tested with a skin widow without addition of nickel to the chamber medium served as controls. The morphology of the leucocytes in dermis was studied in biopsies taken 8, 24, or 48 h after skin window application, and in a parallel test the morphology of the exudate was examined by sequential collection of the chamber medium during a 48 h period. The infiltrate in dermis of contact allergic patients with nickel challenge in the chamber medium showed a time-dependent increase of mononuclear cells, eosinophils and basophils and a concomitant decrease of polymorphonuclear granulocytes, characteristic of a combined specific and unspecific inflammation. The morphology of the exudate in contact allergic patients exposed to nickel showed a dominance of polymorphonuclear granulocytes throughout the study period, while mononuclear cells, eosinophils and basophils were detected at a much lower quantity and with a considerable delay. Further, we studied the kinetics of the leucocyte granule proteins: lactoferrin, myeloperoxidase, lysozyme and eosinophil cationic protein in exudate fluid in a parallel test. A significant higher flux was found for all during the second day of allergen exposure compared to contact allergic patients without allergen challenge as well as normal volunteers. The increased protein fluxes were not accompanied by an increased flux of polymorphonuclear granulocytes in the exudate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

The influence of morphine and naloxone on plasma oxytocin concentration in the rat.

Subcutaneous injections of morphine decrease the plasma oxytocin level significantly in both normohydrated rats and rats dehydrated for 24 hrs. This effect of morphine is naloxone-reversible. Injections of naloxone increase the plasma oxytocin level in a time dependent manner, when the oxytocin system is stimulated by dehydration, but have no effect on basal oxytocin level. This observation indicates liberation of an endogenous opioid, during stimulation of the neurohypophysis, leading to inhibition of the oxytocin secretion. A discrepancy in the time course between the plasma oxytocin enhancing effect and the morphine reversing effect of naloxone is observed. On the basis of this observation two different opioid receptors are suggested to be involved in the effect of naloxone on the neurohypophysis.

Animals↗
PubMed1987

GABA receptor stimulation increases the release of vasopressin and oxytocin in vitro.

The release of oxytocin and vasopressin from rat neurointermediate lobes was determined in vitro. The electrically evoked release of posterior pituitary hormones was markedly potentiated by the GABA receptor agonist, isogauvacin, an effect which was abolished by the GABAA receptor antagonist bicuculline. Spontaneous hormone outflow was not affected by the substances tested. The results suggest the existence of a GABA receptor on the terminal fibres in the pituitary, facilitating the release of oxytocin and vasopressin.

Animals↗
PubMed1985

Morphine antidiuresis in conscious rats: contribution of vasopressin and blood pressure.

Intracerebroventricular injections of morphine (5-20 micrograms) produced a dose dependent antidiuresis in the conscious hydrated rat. Naloxone pretreatment completely abolished this antidiuretic effect, but pretreatment with a specific antidiuretic vasopressin antagonist did not change the morphine antidiuresis. The vasopressin concentration in the first voided urine after antidiuresis from morphine treated rats was found to be in the same range as the vasopressin concentration in urine from saline treated rats. Injections of 20 micrograms morphine intracerebroventricularly in conscious hydrated rats gave a short decrease in heart rate but not in mean arterial blood pressure. This indicates, that either liberation of vasopressin nor a fall in systemic blood pressure contribute to the morphine antidiuresis.

Animals↗
PubMed1985

Refractory condylomata acuminata: a controlled clinical trial of carbon dioxide laser versus conventional surgical treatment.

Uncontrolled trials indicate that treatment of condylomata acuminata with the carbon dioxide laser is effective and probably superior to conventional surgical treatment. We performed a controlled study of refractory condylomata acuminata to clarify whether this is the case. In this randomised trial 21 patients were treated with the carbon dioxide laser and 22 by conventional surgery after having been treated with podophyllin for an average of 33 and 35 weeks respectively. Five and seven patients respectively had previously required additional treatment, such as an operation. The treatment schedule was equally effective for both groups of patients. No difference between the two groups was seen in numbers of recurrences, postoperative pain, healing time, and rate of scar formation (p greater than 0.1-0.2). Treatment of recalcitrant condylomata acuminata with the carbon dioxide laser did not offer any advantages over traditional surgery, including electrocautery.

Adult↗
PubMed1984

Human leukocyte cyclic AMP and cyclic GMP levels during chemotaxis in delayed type hypersensitivity.

Ten nickel-allergic patients and six healthy control subjects participated in a study of the morphology, kinetics and evolution of the cAMP and cGMP concentrations of migrated leukocytes, using an improved skin chamber technique. Also studied was the effect of nickel exposure in the chamber medium during development of an eczematous reaction in the nickel-allergic patients. Nickel exposure had a specific effect on the morphology, from the 24th hour to the end of the 48 h observation period, with a significant increase in the percentages of basophils, eosinophils and lymphocytes and a decrease of neutrophils. A significantly increased leukocyte migration rate (LMR) was observed from the 27th to 39th hour in six of the allergic patients exposed to nickel. There were no specific permanent changes in cAMP and cGMP concentrations during nickel exposure. The control chambers of the allergic patients and healthy controls had identical leukocyte morphology, LMR and leukocyte concentrations of cAMP and cGMP. However, no correlations were found between LMR, cAMP and cGMP in the eczema patients throughout the observation period.

Adult↗