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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of delusional major depression associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) are described. Delusional depression and SIADH may both result from alterations of brain catecholamine neurotransmitters, and may coexist more commonly than previously thought. Implications for clinical practice and future research are discussed.
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PMID:Delusional depression and inappropriate antidiuretic hormone secretion. 664 2

The effect of 1 and 5 micrograms AVP injections on open field and photoactivity chamber behavior of D.I. and normal Long-Evans animals was studied. Administration of 5 micrograms AVP (SC) resulted in a statistically significant depression of both open field and photochamber activity in the D.I. rat, but had a less pronounced effect on normal animals. However, 1 microgram AVP resulted in only minor alterations of activity in both D.I. and normal animals. In terms of learned behavior, D.I. and normal animals displayed similar within-session habituation when comparisons were made following the same treatment conditions. Thus, this study supports the hypothesis that vasopressin may influence memory tasks by modulation of related states of emotionality, motivation, and/or attention rather than by direct involvement in the retrieval and/or consolidation of information.
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PMID:Effect of vasopressin on open field and activity behavior of the vasopressin-deficient (Brattleboro) rat. 665 16

Extracellular recordings from antidromically-identified neurosecretory cells in the rat supraoptic nucleus (SON) indicate that electrical stimulation (1 Hz, 50 microseconds, 200 microA) in the subfornical organ (SFO) alters the excitability of 89% (n = 31) of phasically-active (putative vasopressin-secreting) and 94% (n = 16) of continuously-active (putative oxytocin-secreting) neurons; 45% of cells display a long latency (mean 80.2 +/- 20.5 ms, S.D.) prolonged (150-350 ms) increase in excitability; 26% of cells demonstrate a similar excitation, preceded by a brief decrease in firing at a latency of 30.5 +/- 13.1 ms; 15% of cells display only a depression in their activity, lasting up to 150 ms. Ninety percent of non-neurosecretory (i.e. non-antidromic) neurons (n = 19) within or above th SON also display orthodromic excitatory or inhibitory responses to SFO stimulation; however, these cells usually respond with shorter latencies, and none demonstrate the prolonged excitation seen among neurosecretory cells. With SON stimulation, antidromic activation observed from 6 of 18 SFO neurons (latency range of 12-27 ms) confirms a projection from SFO to the SON area. These data suggest a predominantly facilitatory influence of SFO neurons on the excitability of both vasopressinergic and oxytocinergic neurosecretory cells in the rat, thereby supporting a role for the SFO in body water balance.
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PMID:Subfornical organ--supraoptic nucleus connections: an electrophysiologic study in the rat. 673 27

A modification of neuroleptanalgesia by substituting fentanyl with buprenorphine is presented. Both anaesthesia techniques could be applied alternatively. We did not recognize any significant difference between the two groups concerning haemodynamics, the secretion of the so called stress hormones (antidiuretic hormone, cortisol) as well as the postoperative respiratory depression. The long lasting analgesia, which could be achieved by buprenorphine, can be advantageous in certain surgical interventions. The lack of a potent antagonist for buprenorphine in addition to its longer half-life for--not being of advantage in any anaesthesia--is discussed.
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PMID:[Modified neuroleptanalgesia with buprenorphine]. 681 64

Infusion of noradrenaline at rates between 32-160 nmol.min-1 for 30 min into one lateral cerebral ventricle of conscious sheep caused a diuresis which was accompanied by negative solute-free water reabsorption and which lasted for 90-120 min. The range of noradrenaline infusion rates used reflects differences between individual animals in the rate of infusion necessry to cause diuresis. Intracerebroventricular (ICV) infusion of noradrenaline at half the diuretic rate caused no significant changes in urine flow. The diuresis induced by ICV noradrenaline infusion was prevented by concurrent ICV administration of the alpha-adrenergic antagonist, phentolamine, but was not prevented by concurrent ICV administration of the beta antagonist, propranolol, or by concurrent intravenous infusion of phentolamine. Intravenous infusion of noradrenaline at rates that were diuretic by ICV infusion caused a diuresis of approximately 30 min duration which coincided with the period of intravenous noradrenaline infusion. This diuresis was prevented by concurrent intravenous infusion of phentolamine. These results were interpreted as indicating that the higher rates of ICV infusion of noradrenaline caused the prolonged water diuresis by acting at a site in the brain and, thereby, inhibiting the release of endogenous vasopressin. ICV infusion of noradrenaline at all rates was followed by a reduction in mean arterial blood pressure and pulse pressure with variable changes in heart rate and by depression of the rates of renal clearance of PAH, potassium and total solute.
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PMID:Diuretic effect of intraventricular and intravenous infusions of noradrenaline in conscious sheep. 690 39

Vasopressin produced analgesia in mice as estimated by using abdominal constriction tests (ED50 8.5 micrograms/kg i.v.) or hot plate method (ED50 63 micrograms/kg i.v.). However, vasopressin (10 micrograms/kg i.v.) produced no depression of locomotor activity in mice. Vasotocin had slight analgesic action; oxytocin or norepinephrine had none and there was no direct correlation between pressor response and analgesia. The analgesic action was nonopiate in nature as it was uninfluenced by the narcotic antagonist naltrexone at 5 to 15 mg/kg, but it was reserved by a vasopressin antagonist. Intraventricular administration of vasopressin (1-10 micrograms/kg) to mice produced no significant analgesia, suggesting a primarily peripheral locus of analgesic action. Vasopressin may play a role as an endogeneous pain regulating substance.
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PMID:Characterization of vasopressin analgesia. 705 94

To analyze the relationship between the splanchnic and systemic effects of vasopressin and to measure its efficacy in lowering portal pressure relative to what can be accomplished by zero gradient shunting, intraoperative measurements of cardiac output and relevant pressures were made in 30 patients undergoing selective or total shunts. Vasopressin caused a significant increase in systemic vascular resistance and pulmonary capillary wedge pressure, but an insignificant overall reduction in cardiac index (CI). However, in ten patients the decrease in CI exceeded 20%, suggesting a subpopulation of especially susceptible individuals. High initial CI, age, pre-existent heart disease, and severity of cirrhosis did not predict greater vulnerability. Adding an infusion of nitroprusside regularly reverted CI to control levels, regardless of the extent of cardiac output depression. Vasopressin was 38% as effective as a subsequent shunt in reducing splanchnic venous pressure. The portal hypotensive action bore no relationship to CI, but the pressure decrease caused by vasopressin was predictive of the reduction that could be achieved by shunting. The effects of the two types of shunts on systemic hemodynamics were minor and remarkably similar.
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PMID:Vasopressin and splanchnic shunting. A quantitative comparison. 707 52

The effects on cerebral blood flow of alpha- or beta-adrenergic receptor stimulation of cerebral vessels were examined in 13 unanesthetized goats before and during hypercapnia produced by inhalation of 10% CO2 in air. This procedure increased the PCO2 from 34 to 52 and was accompanied by a fall in pH from 7.39 to 7.26. Electrical stimulation of the cervical sympathetic nerve and injections of norepinephrine and tyramine into the internal maxillary artery produced reductions in cerebral blood flow that were abolished or reduced in hypercapnia. The increase in cerebral blood flow in response to beta-adrenergic stimulation with isoproterenol was also reduced. Hypercapnia caused a similar depression of the constrictor and dilatory effects of the nonadrenergic drugs vasopressin and diazoxide. The results show a decreased response of cerebral vessels to adrenergic and nonadrenergic stimuli in hypercapnia. The findings do not suggest any difference between the refractoriness of cerebral vessels in hypercapnia and that described in other vascular beds.
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PMID:Reduction of cerebrovascular reactivity during hypercapnia. 708 68

The contraction of the potassium depolarized pulmonary artery of the guinea pig was diminished by the calcium antagonists nifedipine, gallopamil, diltiazem, verapamil and prenylamine. The drugs are listed here in order of activity. The uptake of 45Ca of the depolarized pulmonary artery was reduced by nifedipine, verapamil and prenylamine in this order of activity. The depression of the coronary flow of the isolated guinea pig heart, which was brought about by barium chloride, antigenic rabbit serum or vasopressin plus oxytocin was reduced by infusion of prenylamine. The positive inotropic effect of K-strophanthin on the isolated, electrically stimulated left atrium of the guinea pig heart was reduced by gallopamil, verapamil, prenylamine, diltiazem and nifedipine in this order of activity.
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PMID:Effects of calcium antagonists on coronary spasm and pulmonary artery contraction in comparison to their antagonistic action against K-strophanthin in isolated guinea pig atria. 710 Feb 59

Seven dogs prepared with carotid loops were used to evaluate the responsiveness of the cerebral osmoreceptors regulating plasma vasopressin concentration (pAVP). Intracarotid and intravenous infusions of hypo- and hypertonic solutions were used to alter cerebral plasma osmolality. Bilateral intracarotid infusion of hypertonic saline (0.90 mmol NaCl kg-1 . min-1 . artery-1) significantly elevated jugular vein plasma osmolality (pOsm) in the first minute (P less than 0.05). Systemic values, determined from saphenous vein samples, were increased after 6 min. After 4 min of infusion, systemic pAVP was significantly increased, attaining a constant level at 6 min. Subsequent experiments with infusions 6 min in duration demonstrated that hypertonic saline infused intracarotidly significantly increased pAVP in a dose-related fashion, whereas similar solutions administered intravenously did not alter pAVP. Hypotonic infusions (intravenous or intracarotid) did not change pAVP consistently. The lack of a depression in pAVP during hypotonic infusions is consistent with the argument that jugular pOsm must be elevated above a threshold to stimulate the release of vasopressin. Linear relationships were demonstrated for jugular pNa+ and pOsm to pAVP employing the threshold model. Cerebral osmoreceptors that regulate plasma vasopressin concentration respond linearly to increasing tonicity above a threshold stimulating the release of vasopressin.
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PMID:Osmotic control of plasma vasopressin in the dog. 712 42


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