Importance of anesthesia for the genesis of neurogenic pulmonary edema in spinal cord injury

There are reports describing both provocation and inhibition of neurogenic pulmonary edema by anesthetic drugs. Therefore, we compared the effect of two types of anesthesia on the formation of neurogenic pulmonary edema in rats with balloon-induced acute spinal cord injury. Animals with sham procedure (group 1) were anesthesized by intraperitoneal sodium pentobarbital. In the experimental groups, rats were submitted to acute spinal cord lesion by insufflations of a balloon in the epidural space at T8 for 1 min (group 3 under i.p. sodium pentobarbital and group 2 under i.p. xylazine-ketamine anesthesia). In rats with pentobarbital anesthesia, systolic blood pressure doubled the baseline value during compression, whereas this effect was less pronounced in the ketamine-xylazine group. The pulmonary index (100 x wet lung weight/body weight) was 0.395 (+/-0.018) in sham-operated rats, rose to 0.499 (+/-0.060) in group 2, and was maximum under pentobarbital anesthesia (0.639+/-0.14; p=0.0018). Histologic examination of the spinal cord showed parenchymal ruptures and acute hemorrhage. Comparison of the pulmonary index with histologic slides of lung parenchyma revealed that relevant intra-alveolar edema occurred only for index values above 0.55. On electron microscopy, endothelial alterations, and damage of the alveolar lining cells were found. Our study indicates that neurogenic pulmonary edema caused by spinal cord injury is less pronounced in rats under xylazine-ketamine anesthesia, when compared with pentobarbital.     

Neurodevelopmental outcome after prenatal exposure to opiates

To study the developmental effects of prenatal exposure to opiates, a prospective follow up study of 34 drug-exposed (opiates and nicotine) and 42 reference infants (nicotine exposure only) was conducted from January 1992 to September 1995. At the time of delivery, 12 of 34 mothers used opiates without medical control. Twenty-two mothers participated in a methadone maintenance programme. At 1 year, the average Griffiths Developmental Quotient (DQ) was lower in the drug-exposed group (mean: 100.5 vs. references 107.9; P < 0.001). This difference was mainly due to lower subscales “locomotor” (mean 100.8 vs. 111.4; P < 0.05) and “intellectual performance” (mean 100.8 vs. 108.5; P < 0.05) in the drug-exposed group. Severe developmental retardation mean DQ (−2 SD) was diagnosed in 2 drug-exposed infants. Mild developmental retardation (mean DQ: 1 SD– > 2 SD) was found in 7 drug-exposed and in 3 reference infants (P < 0.05). Neurological abnormalities were found more frequently in the drug-exposed group (11 vs. 3 infants; P < 0.01). Among the opiate-exposed infants, the subscales “hearing and speech” and “intellectual performance” were lower in the uncontrolled drug-using than in the methadone group. The 17 fostered infants showed no difference in developmental outcome compared with the 10 infants living with their biological parents (mean DQ: 100.0 versus 101.3). Conclusions At 1 year infants prenatally exposed to opiates are at risk for mild psychomotor developmental impairment. Received: 1 August 1997 / Accepted in revised form: 15 January 1998     

Changes of nucleolar organizer regions in granulopoietic precursors during the course of chronic myeloid leukemia

The aim of the present study was to analyze the nucleolar organizer region (AgNOR) pattern of granulopoietic precursors in chronic myeloid leukemia (CML) at diagnosis and during the course of the disease. Clusters of AgNORs and isolated dots were counted separately in 24 cases of CML at diagnosis, in 19 cases during the relapse of the chronic phase after treatment, and in 16 cases of blast crisis. For comparison, 20 cases of normal bone marrow were studied. Each cell type had its own characteristic AgNOR pattern, as has been described for normal bone marrow. There was no significant difference in the number of AgNORs between cells in the peripheral blood and bone marrow. Compared with normal granulopoiesis, myeloblasts in CML at diagnosis had lower numbers of clusters, which decreased further during relapse of chronic phase and in blast crisis. Promyelocytes and myelocytes showed significantly fewer dots. The number of AgNOR clusters correlates inversely with the duration of the cell cycle. Therefore, these findings are consistent with the progressive loss in proliferative activity of immature precursors described during the course of CML. As the number of dots indicates cellular maturation, their lower number in promyelocytes and myelocytes in CML favors the concept of a discordant maturation process described in this desease. The separate counting of clusters and dots provides a useful, simple, and cheap method of describing cytokinetic changes during the course of this myeloproliferative