Chronic renal failure in equine due to ascending pyelonephritis predisposed by cauda equina syndrome: case report / Insuficiência renal crônica em equino devido à pielonefrite ascendente predisposta por síndrome da cauda equina: relato de caso

Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gêneroStreptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)

Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gênero Streptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)

Activation of locus coeruleus heme oxygenase-carbon monoxide pathway promoted an anxiolytic-like effect in rats

The heme oxygenase-carbon monoxide pathway has been shown to play an important role in many physiological processes and is capable of altering nociception modulation in the nervous system by stimulating soluble guanylate cyclase (sGC). In the central nervous system, the locus coeruleus (LC) is known to be a region that expresses the heme oxygenase enzyme (HO), which catalyzes the metabolism of heme to carbon monoxide (CO). Additionally, several lines of evidence have suggested that the LC can be involved in the modulation of emotional states such as fear and anxiety. The purpose of this investigation was to evaluate the activation of the heme oxygenase-carbon monoxide pathway in the LC in the modulation of anxiety by using the elevated plus maze test (EPM) and light-dark box test (LDB) in rats. Experiments were performed on adult male Wistar rats weighing 250-300 g (n=182). The results showed that the intra-LC microinjection of heme-lysinate (600 nmol), a substrate for the enzyme HO, increased the number of entries into the open arms and the percentage of time spent in open arms in the elevated plus maze test, indicating a decrease in anxiety. Additionally, in the LDB test, intra-LC administration of heme-lysinate promoted an increase on time spent in the light compartment of the box. The intracerebroventricular microinjection of guanylate cyclase, an sGC inhibitor followed by the intra-LC microinjection of the heme-lysinate blocked the anxiolytic-like reaction on the EPM test and LDB test. It can therefore be concluded that CO in the LC produced by the HO pathway and acting via cGMP plays an anxiolytic-like role in the LC of rats.

Acute stress-induced antinociception is cGMP-dependent but heme oxygenase-independent

Endogenous carbon monoxide (CO), which is produced by the enzyme heme oxygenase (HO), participates as a neuromodulator in physiological processes such as thermoregulation and nociception by stimulating the formation of 3′,5′-cyclic guanosine monophosphate (cGMP). In particular, the acute physical restraint-induced fever of rats can be blocked by inhibiting the enzyme HO. A previous study reported that the HO-CO-cGMP pathway plays a key phasic antinociceptive role in modulating noninflammatory acute pain. Thus, this study evaluated the involvement of the HO-CO-cGMP pathway in antinociception induced by acute stress in male Wistar rats (250-300 g; n=8/group) using the analgesia index (AI) in the tail flick test. The results showed that antinociception induced by acute stress was not dependent on the HO-CO-cGMP pathway, as neither treatment with the HO inhibitor ZnDBPG nor heme-lysinate altered the AI. However, antinociception was dependent on cGMP activity because pretreatment with the guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (ODQ) blocked the increase in the AI induced by acute stress.

Gender-related differences in the effects of nitric oxide donors on neuroleptic-induced catalepsy in mice

It has been suggested that nigrostriatal dopaminergic transmission is modulated by nitric oxide (NO). Since there is evidence that gonadal hormones can affect extrapyramidal motor behavior in mammals, we investigated the effects of isosorbide dinitrate (ISD), linsidomine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP), three pharmacologically different NO donors, on neuroleptic-induced catalepsy in 60- to 80-day-old male and female albino mice. Catalepsy was induced with haloperidol (1 mg/kg, ip) and measured at 30-min intervals by means of a bar test. Drugs (or appropriate vehicle) were injected ip 30 min before haloperidol, with each animal being used only once. ISD (5, 20 and 50 mg/kg) caused a dose-dependent inhibition of catalepsy in male mice (maximal effect 120 min after haloperidol: 64 percent inhibition). In the females only at the highest dose of ISD was an attenuation of catalepsy observed, which was mild and short lasting. SIN-1 (10 and 50 mg/kg) did not significantly affect catalepsy in female mice, while a significant attenuation was observed in males at the dose of 50 mg/kg (maximal inhibition: 60 percent). SNAP (20 mg/kg) significantly attenuated catalepsy in males 120 min after haloperidol (44 percent inhibition), but had no significant effect on females. These results basically agree with literature data showing that NO facilitates central dopaminergic transmission, although the mechanisms are not fully understood. They also reveal the existence of gender-related differences in this nitrergic modulation in mice, with females being less affected than males