Antidiuretic and nephrotoxic effects of putrescine in rats.

Putrescine, intraperitoneally injected either into intact or into hypophysectomized rats, caused a reduction in urine volume at doses of 200\u2013300 mg/kg. At doses of 100 mg/kg or more, there was also a significant loss of potassium. The highest dose (300 mg/kg) caused haemoglobinuria, proteinuria, increased natriuresis, increased urinary osmolarity, reduced aldosteronaemia, ectasis of glomerular capillaries and tubular damage. The underlying mechanisms(s) are probably mostly linked to the strong cationic charge of putrescine and to its binding to fixed anions of tubular-cell membrane

Effect of gamma-hydroxybutyrate in two rat models of focal cerebral damage

Gamma-Hydroxybutyrate (GHB) and its lactone, gamma-butyrolactone (GBL) have been previously shown to produce a protective effect in animal models of cerebral ischaemia/hypoxia, as well as in human conditions of head injury-induced coma. The aim of the present research was to study the effect of GHB in experimental conditions of focal cerebral damage, either induced by ischaemia or excitotoxicity. Under general anaesthesia, rats were injected into the right striatum with either endothelin-1 (ET-1, 0.43 nmol) or kainic acid (7.5 nmol) in a volume of 1 mul. Sham-lesioned rats received 1 mul of the solvent. Both ET-1- and kainic acid-lesioned rats were randomly assigned to one of the following intraperitoneal (i.p.) treatments: (i) and (ii) GHB, 100 or 300 mg kg(-1) 2 h after the lesion, followed by 50 or 100 mg kg(-1), respectively, every 12 h; (iii) saline, 2 ml kg(-1), same schedule. Sham animals were treated with saline, 2 ml kg(-1), same schedule. Treatments lasted for 10 days. The higher dose of GHB produced a significant protection against the ET-1-induced impairments in sensory-motor orientation and coordinated limb use (evaluated 24 and 42 days after the lesion) and in place learning and memory (Morris test, performed 19 and 39 days after the lesion). The same dose regimen reduced the circling behaviour induced by apomorphine in kainate-lesioned rats (10 days after the lesion), and limited or prevented at all the histological damage produced either by ET-1 or by kainic acid (evaluated 43 or 10 days after the lesion, respectively). These results show that GHB limits both histological and functional consequences of a focal ischaemic or excitotoxic insult of the brain, in rats, even if the treatment is started 2 h after the lesion

Supplemental Material, DS2_CPCJ_10.1177_1055665618770795 - Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate

<p>Supplemental Material, DS2_CPCJ_10.1177_1055665618770795 for Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate by Susanna Botticelli, Thomas Klit Pedersen, Annelise Küseler, Sven Erik Nørholt, and Paolo M. Cattaneo in The Cleft Palate-Craniofacial Journal</p

Supplemental Material, DS3_CPCJ_10.1177_1055665618770795 - Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate

<p>Supplemental Material, DS3_CPCJ_10.1177_1055665618770795 for Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate by Susanna Botticelli, Thomas Klit Pedersen, Annelise Küseler, Sven Erik Nørholt, and Paolo M. Cattaneo in The Cleft Palate-Craniofacial Journal</p

Supplemental Material, DS1_CPCJ_10.1177_1055665618770795 - Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate

<p>Supplemental Material, DS1_CPCJ_10.1177_1055665618770795 for Novel 3-D Analysis for the Assessment of Cleft Dimensions on Digital Models of Infants With Unilateral Cleft Lip and Palate by Susanna Botticelli, Thomas Klit Pedersen, Annelise Küseler, Sven Erik Nørholt, and Paolo M. Cattaneo in The Cleft Palate-Craniofacial Journal</p

Neuroprotective effect of gamma-hydroxybutyrate in transient global cerebral ischemia in the rat

The effect of gamma-hydroxybutyrate on the histological and behavioral consequences of transient brain ischemia was studied in the four vessel occlusion rat model. In saline-treated animals, 30 min ischemia caused a massive loss of neurons in the hippocampal CA1 subfield (normal neurons: 14%, 5%, 23% and 30% on the 3rd, 10th 15th and 65th day after ischemia, respectively). gamma-Hydroxybutyrate - 300 mg/kg intraperitoneally (i.p.) 30 min before or 10 min after arteries occlusion, followed by 100 mg/kg i.p. twice daily for the following 10 days - afforded a highly significant protection (normal neurons on the 3rd, 10th, 15th and 65th day after ischemia: 88% and 91%, 80% and 80%, 91% and 90%, 72% and 71% in rats receiving the first dose before or after arteries occlusion, respectively). The ischemia-induced sensory-motor impairment was significantly attenuated in rats receiving the first dose of gamma-hydroxybutyrate before arteries occlusion. Finally, the ischemia-induced impairment in spatial learning and memory, evaluated starting 27 days after the ischemic episode, was significantly attenuated by gamma-hydroxybutyrate, either injected first at 30 min before or 10 min after arteries occlusion. Lower doses of gamma-hydroxybutyrate had no significant effect. In conclusion, these results indicate that gamma-hydroxybutyrate provides significant protection against both histological and behavioral consequences of transient global cerebral ischemia in rats. (C) 2000 Elsevier Science B.V. All rights reserved