Pozne morfološke promene u pulpi zuba molara Wistar pacova sa aloksanskim diabetesom

The aim of this study was examination of late changes in the dental pulp of rats with experimental diabetes. The experiment involved 36 male albino rats, initially 35 days old and 89.45±9.95 g body wight. The animals were separated into 6 equal groups. The first (T1), third (T2) and fifth (T3) groups of animals were given a single dose of alloxan tetrahydrate approximately 80 mg/ kg body weight. Just before the application, the substance was dissolved in physiological saline, and each animal was given 1 ml in the tail vein. The second (C1), fourth (C2), and sixth (C3) group of animals were used as appropriate control groups and received 1 ml of physiological saline injection. Body weights were measured and glycemia was checked weekly. The animals in groups T1 and C1 were sacrificed on the 63rd day, groups T2 and C2 on the 95th day and groups T3 and C3 on the 125th day by decapitation. The block of mandibular molars was taken for histological examination. The results of histological examinations showed stasis, in microcirculation, as well as in large blood vessels of the pulp, and necrosis of the pulp tissue in animals after 63 days of experimental diabetes. Pulps of the animals killed after 95 days showed, besides massive pulp necrosis, abscess forms localized in the mesial horn of the pulp. This evidence was not present in every animal from group T2. Pulps of the animals sacrificed after 125 days showed hydropic degeneration of the pulp with massive and diffuse presence of vacuoles in odontoblasts.Cilj ovog rada je bio ispitivanje poznih promena na pulpi zuba pacova sa eksperimentalnim dijabetom. Eksperiment je izveden na 36 muških albino pacova, starih 35 dana, telesne mase 89.45 ± 9.95 g. Životinje su bile podeljene u 6 grupa. Prva (T1), treća (T2) i peta (T3) grupa životinja primila je jednokratnu dozu aloksan tetrahidrata, približno oko 80 mg/kg mase tela. Neposredno pre aplikacije, supstanca je rastvorena u fiziološkom rastvoru i svakoj životinji je dat 1 ml rastvora u repnu venu. Druga (C1) četvrta (C2) i šesta (C3) grupa životinja bile su kontrolne grupe i dobijale su 1 ml čistog fiziološkog rastvora. Jednom nedeljno merena je telesna masa i glikemija. Životinje grupe T1 i C1 su žrtvovane 63-eg dana, životinje grupe T2 i C2 95-og dana a životinje grupe T3 i C3 125-og dana eksperimenta dekapitacijom. Za histološka ispitivanja uzeti su isečci mandibularnih molara. Rezultati histoloških ispitivanja pokazuju stazu kako u mikrocirkulaciji tako i u velikim krvnim sudovima pulpe kao i nekrozu tkiva pulpe kod životinja žrtvovanih 63-ćeg dana eksperimentalnog dijabeta. Kod nekih životinja žrtvovanih 95-og dana pored masivne nekroze pulpe, u uočavaju se abscesi lokalizovani na mezijalnom rogu. Pulpe životinja žrtvovanih 125-og dana ukazuju na hidropsnu degeneraciju pulpe sa masovnom i difuznom pojavom vakuola u odontoblastima

L-arginine reduces tubular cell injury in acute post-ischaemic renal failure

Background. The pathophysiology of renal ischaemia, resulting in tubular cell injury and leading to acute renal failure (ARF), remains unclear. An ever-increasing number of investigations focus on a possible role of nitric oxide (NO) in regulating circulation during ARF. In this context, we investigated the influence of chronic stimulation or inhibition of NO synthesis, or both, on haemodynamic parameters, histology and plasma renin activity (PRA) after ischaemia-reperfusion injury of rat kidneys. Methods, Experiments were performed on adult, male Wistar rats. Before induction of ARF, a group of animals was treated with a NO synthesis inhibitor (L-NAME) and another group was treated with a precursor of NO synthesis (L-arginine). The animals received those substances for 4 weeks. Control groups received the same amount of tap water for 4 or 8 weeks and were divided into groups with ARF (4 weeks-ARF group and 8 weeks-ARF group) and a sham-operated group. Another group of rats was treated first with L-NAME and then with L-arginine in their drinking water, for 4 weeks for each of these two substances. All parameters were evaluated 24 h after the induction of ischaemic ARF or the sham operation. Results, Our results show that such long-term stimulation of NO release by L-arginine improved renal haemodynamics in the ischaemic form of ARF. Renal blood Bow (RBF) increased by 96% in the L-arginine-treated rats with ARF compared with the group with ARF alone. Inhibition of NO synthesis worsens renal haemodynamics after ARF. However, this aggravation can be reversed by L-arginine. The rate of water reabsorption was reduced in all groups with ARF, but this reduction was least in the group treated with L-arginine. The rate of Na+ reabsorption was reduced in all groups 24 h after renal ischaemia, but a significant decrease was observed after the inhibition of NO synthesis. Histological examination of the kidney specimens showed that morphological changes were least in the rats treated with L-arginine, when compared with all other groups with ARF. Nevertheless, the lesions were most prominent in the L-NAME + ARF group. In this group, the areas of corticomedullar necrosis were more widespread in comparison with other groups, especially the L-arginine group where only swelling of the proximal tubular cells was observed. Treatment with L-NAME was not accompanied by any significant alteration in the plasma concentration of angiotensin I (ANG I), while in the group treated with L-arginine ANG I had a tendency to decrease. Conclusions. Acute post-ischaemic renal failure may be alleviated by administering the NO substrate (L-arginine). NO acts cytoprotectively on tubular epithelial cells in ischaemia-reperfusion injury of rat kidney. Evidence of this comes from both histopathological findings and increased tubular water and sodium reabsorption. However, inhibition of NO synthesis (provoked by L-NAME) worsens renal haemodynamics and aggravates morphological changes after ARF. These aggravations can, however, be reversed by L-arginine

Regional hemodynamics after chronic nitric oxide inhibition in spontaneously hypertensive rats

Background: Inhibition of nitric oxide (NO) synthase by L-arginine analogs is associated with elevation of blood pressure in rats. Because endothelium-dependent vasomotion in different vascular beds is not homogenous, the aim of this study was to characterize and compare regional hemodynamic responses in carotid, femoral, and renal vascular beds after chronic NO inhibition in spontaneously hypertensive rats. The possible role of circulating endothelin and renin angiotensin systems in mediating the effects of chronic NO inhibition was also studied. Methods: Systemic and regional hemodynamics, left ventricular mass, plasma renin activity, and plasma endothelin-l were determined in control and N-omega-nitro-L-arginine methyl ester (L-NAME)-treated (10 mg/kg/day, 4 weeks) spontaneously hypertensive rats. Results: L-NAME treatment increased arterial pressure and total peripheral and regional vascular resistance and decreased cardiac output, stroke volume, and regional blood flow. An in-crease in blood flow ratio and a decrease in vascular resistance ratio between carotid and renal as well as femoral and renal vascular beds in rats treated with L-NAME was found. Blood flow and vascular resistance ratios between femoral and carotid vascular beds remained unchanged. L-NAME increased plasma renin activity and left ventricular weight/body weight ratio, whereas plasma endothelin-l was not modified. Conclusions: The results of this study showed that the renal circulation seemed to be more sensitive to the effects of chronic NO inhibition than carotid and femoral vascular beds. Simultaneous activation of the renin angiotensin system may further potentiate cardiovascular effects of chronic NO inhibition. No evidence that circulating endothelin-l plays a role in this model of hypertension was found. KEY INDEXING TERMS: Nitric oxide; Regional hemodynamics; Plasma renin activity; Endothelin; Spontaneously hypertensive rats