Anemia and transfusions in geriatric patients: a time for evaluation.

Anemia is common in the elderly, especially in very old patients who are often frail and may be institutionalized. Senescence, the ageing process, puts the elderly at risk of developing anemia for multiple reasons, but anemia may not be attributed to senescence unless a thorough diagnostic workup has excluded other etiologies. Nutritional deficiencies are common and need to be identified and treated appropriately. Inflammatory diseases and renal failure are also frequent etiological factors and tend to be chronic. Myelodysplastic syndromes increase in frequency with age and may be difficult to diagnose and only a minority of cases respond to appropriate treatment. Anemia is associated with poor outcome and symptomatic treatment with transfusions frequently has to be considered. Red blood cell transfusion has a high therapeutic index and is likely to be effective only if anemia is symptomatic or particularly severe, as a consequence, its use has been restricted to this group. Much of the evidence on usage is limited to younger adults and specific clinical situations. Geriatricians have to deal with a large number of patients with significant anemia but with an absence of well constructed guidelines for the frail and the very old. The object of the present article is to raise awareness that anemia in the geriatric group is multi-factorial and that the patients are more than merely older than those included in most studies, that the results of ongoing trials should be appropriately interpreted and will be important in guiding future practice.

Possible involvement of L-arginine-nitric oxide pathway in the modulation of stress-induced analgesia.

The possible participation of NO in the pain modulation and stress analgesia was studied in Wistar adult rats. Cerebral citruline as a stoichiometric coproduct of NO from L-arginine increased from the mean value 5.6 +/- 0.4 nM/mg.Pt. to 8.9 +/- 0.5 nM/mg.Pt. in acute immobilization stress. Intraperitoneal administration of L-arginine caused only in high doses (50 mg/kg body weight) a small transient decrease of tail-flick latencies to the thermoalgesic stimulus, without significant changes of the stress analgesia induced by the restraint stress. In the pretreated animals with L-NAME a progressive increase of latency time was obtained and the increased latencies induced by acute immobilization appeared significantly potentiated. These results offer new indirect evidence in favour of the modulatory role of NO in the thermoalgesic sensitivity and stress induced analgesia.

[Glutathione, a biochemical indicator for different types of cellular stress. The change in the GSH level in the brain of rats with hypoxia]. / Glutationul, indicator biochimic pentru diferite tipuri de stress celular. Modificarea nivelului GSH-ului în creierul de sobolani cu hipoxie.

By the ligation of left vertebral artery in some white, adult WISTAR rats, of 150-200 g, anaesthetized with ether, a cerebral hypoxia of 10 minutes was induced. After beheading, there was determined the level of SH-neproteic groups and glutathione (GSH) in the whole heparinized blood and there was observed an important decrease with -15.88% and -16.80% respectively, in comparison with the normal lot (100%), kept under the some laboratory conditions. The GSH level in the neural cytosol is also significantly decreased with -8.66% in rats with hypoxia. The GSH depletion in the induced hypoxia, by our experiment, might be due to the reaction between nitric oxide (NO.) radical and intracellular GSH (blood and neuronal cytosol), considering the literature in this field, and S-nitrosoglutathion (S-NO-GSH) bioactive intermediary is formed and it protects the hypoxied brain against the NO.-dependent cytotoxicity, in the initial phase of hypoxia. The decrease of GSH and SH-neproteic groups level is considered a biochemical marker of the growth of the free radicals level to O2 (NO., O2., OH., H2O2, 1O2), that appear in the hypoxic and/or ischemic stress, but also a major sign in the rol of "scavenger" and antioxidant of the radicals at the cerebral and sanguine level, in the above mentioned conditions.

Possible involvement of the L-arginine-nitric oxide pathway in the modulation of stress-induced analgesia.

The possible participation of nitric oxide (NO) in pain modulation and stress analgesia was studied in adult Wistar rats. Cerebral citruline as a coproduct of NO from L-arginine increased from the mean value 5.6 +/- 0.4 nM/mg.Pt. to 8.9 +/- 0.5 nM/mg.Pt. in acute restraint stress. In high doses (50 mg/kg body weight), intraperitoneal administration of L-arginine caused a small and transient decrease of the tail-flick latencies to the thermal stimulus, without significant changes of the stress analgesia induced by restraint stress. In animals pretreated with N-nitro-L-arginine methyl ester (NAME) a progressive increase of the latency time was obtained and the increased latencies induced by acute immobilization appeared significantly potentiated. These results offer new indirect evidence in favour of the modulatory role of NO in thermoalgesic sensitivity and stress-induced analgesia.

[Glutathione, a biochemical indicator for different types of cellular oxidative stress. II. Ethanol poisoning]. / Glutationul, indicator biochimic pentru diferite tipuri de stress oxidativ celular. Nota II: Intoxicatia cu etanol.

Eight male volunteers, all alcohol addicts selected from the patients of the Padureni unit, deprived for a minimum of two weeks of alcohol, but with an at least 2-year history of alcohol addiction, received 0.5 ml absolute alcohol/kg body weight. Following dynamically the alteration of plasma reduced glutathione content, a significant increase (+8.27%) 30 minutes after alcohol ingestion and a decrease (-7.02%) before ingestion, as compared to plasma glutathione level in sex and age-matched clinically normal subject (100%) was noticed. The change in the --SH groups content in plasma after chronic alcohol ingestion leads to the occurrence of cell oxidative stress, as well as to a decreased resistance of hepatic cell and whole body as a result of the lipid peroxidation process and/or occurrence of detrimental reactive radical species, issuing from O2.

[Glutathione and the redox index in different types of cellular oxidative stress. I. Acrylonitrile (ACN) poisoning]. / Glutationul si indexul redox in diferite tipuri de stres oxidativ celular. I. Intoxicatia cu acrilonitril (ACN).

The professional poisoning with acrylonitrile of some subjects induced a significant decrease of reduced glutathione (81.30%), redox ratio reduced glutathione/oxidized glutathione (90.74%) and "Benzi-redox index" (55.84%) but an increase of oxidized glutathione level (112.6%) as compared to normal controls (100%). This proves the occurrence, in time, of the cellular oxidative stress and/or were obtained.

Researches on the influence of some pharmacological interferences of the metabolism of icosanoids on the glycemia in rats.

We studied the influence of cloprostenol (CIPG) 200 micrograms/Kg i.p. (a synthetic analogue of PGF2-alpha) and of imidazol 70 mg/Kg i.p. (a selective inhibitor of thromboxane synthetase) on fasting glycemia and on hypoglycemia induced by Actrapid insulin 0.5 UI/Kg i.p. to rats (male adults). The determinations of glycemia were made 60 minutes and 3 hours after the administration of the substances. The tests were made in groups of 20 animals which were not fed 14 hours before the experiment, but were not deprived of water. The results were interpreted statistically by means of the "t" test. The data obtained show that CIPG 200 micrograms/Kg i.p. is a significant hyperglycemic icosanoid (statistically p less than 0.01) both in the case of fasting glycemia and in the case of insulin hypoglycemia. The hyperglycemic effect was stronger at 60 min. Imidazol does not modify significantly either glycemia or insulin hypoglycemia, which pleads for a more reduced implication of thromboxanes in the regulation of glycemia in comparison to the prostaglandins.

[The involvement of adenosine and adenosine deaminase in experimental myocardial infarct]. / Implicatiile adenozinei si adenozindezaminazei în infarctul miocardic experimental.

By the ligature of the left coronary artery in the rat anesthetized with nembutal (10 mg/100 i.p.) a significant increase of the 5'-nucleotidase activity (Wooton method) was noticed 10 minutes after the left ventricle infarction (from an average value of 1038.5 +/- 187 mU/g tissue to 1537 +/- 225 mU/g fresh tissue). The adenosine desaminase levels spectrophotometrically determined by Denstedt technique, do not appear significantly modified 10 or 30 minutes after the left ventricle infarction. The chromatographically determined adenosine levels, by HPLC technique, decrease from the average value of 11.63 +/- 1.4 micrograms/mg PT to 8.60 +/- 1.0 micrograms/mg PT 30 minutes after infarction. The observed changes are explained by the conditions of hypoxia in the infarcted ventricle which lead to the raise in adenosine levels by activating the 5'-nucleotidase and their depression by a very fast metabolism of the same substance.