Effect of special Hungarian probiotic kefir on faecal microflora

AIM:To investigate the effect of a four-week consump-tion of a special Hungarian probiotic agent(Biofir~ )onthe faecal microflora in human healthy subjects.METHODS:The effect of Biofir~ with 10~6/cm~3 initialgerms on the faecal microflora was studied in 120healthy volunteers(71 females,49 males).The tradition-al Russian type kefir was used as control.The variousgerm groups and pH values were determined in wk 2,4and 6.RESULTS:The number of all microbes increased duringthe 4-week probiotic treatment.The number of microbesincreased 4.3-fold in the control group and 6.8-fold inBiofir-treated group.The probiotic kefir caused multipli-cation of the probiotic flora,meanwhile the undesiredbacteria multiplied in the control group.No significantchange of pH values of the faeces was found in bothgroups.CONCLUSION:The Hungarian probiotic kefir (Biofir~ )iscapable of promoting multiplication of probiotic bacterialflora in the large bowel.     

Systemic and regional hemorheological consequences of warm and cold hind limb ischemia-reperfusion in a canine model

We have studied systemic and regional changes in hemorheological parameters after complete acute limb ischemia and reperfusion (I/R) in 24 mongrel dogs. Unilateral cooled and non-cooled vascular ischemia (3 h)-reperfusion (4 h), and sham-operations were performed. Blood samples were collected from the excluded region, during reperfusion and for 5 days. Whole blood and plasma viscosity (WBV, PV), relative cell transit time (RCTT) of erythrocytes, fibrinogen level and hematological parameters were determined. In I/R groups WBV of excluded blood was significantly higher compared to the base (p < 0.05), and RCTT increased during the reperfusion. On 2nd-3rd days RCTT increased significantly in both I/R groups. In each group PV and fibrinogen showed continuous increase during the postoperative period, prominently in cooled I/R group, and furthermore WBV corrected for hematocrit (40%) was the highest in cooled I/R group. These suggest that surgical acute limb I/R may cause hemorheological changes, which are more serious after cooling. (Grants: OTKA-T032571, 6003/1/2001/ETT.)     

Altered structure and reduced distensibility of arteries in Dahl salt-sensitive rats

OBJECTIVES: The role of salt sensitivity in arterial stiffening and the structural basis of reduced arterial distensibility were investigated in Dahl salt-sensitive (DS) rats. METHODS: Three-month-old male DS rats received a normal (0.7% NaCl) or a high-sodium (2% NaCl) diet for 3 months. Dahl salt-resistant (DR) rats were controls. Pressure-volume (distensibility) relationships were measured in in-vitro-perfused segments of right carotid and iliac arteries, in the presence and absence of extracellular calcium. The left carotid and iliac arteries were perfusion-fixed at 100 mmHg for morphometric measurements. RESULTS: The average monthly tail systolic blood pressure (SBP) of DS rats on normal and high-sodium diets were increased compared to that of DR rats. Compared to controls, carotid and iliac artery pressure-volume curves of DS rats on normal and high-sodium diets were shifted toward the pressure axis, without a change in elastic moduli. In DS rats, reduced distensibility of the carotid artery was accompanied by increased lumen diameter and increased thickness of media and elastic lamellae, the wall to lumen ratio being unchanged; wall thickness was increased and lumen diameter unchanged in the iliac artery. The high-sodium diet had no effect on either distensibility or dimensions of carotid and iliac arteries in DS or DR rats. CONCLUSION: Geometry (increased or unchanged lumen and increased wall thickness), rather than increased stiffness of wall components, appears to be the cause of reduced distensibility of arteries in DS rats. Structural and functional adaptation to salt sensitivity may occur on what is considered a 'normal' sodium diet.     

Development of structural vascular changes in salt-fed rats

The hypothesis that long-term administration of a physiologically relevant high salt diet to rats leads to the development of structural vascular changes that predispose to hypertension was tested. Adult male Sprague-Dawley rats were fed 2% NaCl diet for 3 or 6 months; rats fed 0.7% NaCl diet were controls. Then, the systemic circulation of the rats was perfusion-fixed at 100 mm Hg. The junction of the mesentery and small intestine, the renal cortex, and segments of left carotid artery, thoracic aorta, and second order mesenteric arteries were embedded in paraffin or epoxy for morphometric measurements. The average monthly tail systolic blood pressure (BP) of salt-fed rats at 3 and 6 months were unchanged. The following morphometric changes in salt-fed rats were observed: 1) dilatation of the carotid artery at 3 months (P <.05); 2) dilatation and reduced wall-to-lumen ratio of the second order mesenteric artery (P <.01); 3) increased wall-to-lumen ratio of small mesenteric resistance arteries (P <.01); 4) reduced wall-to-lumen ratio of renal cortical resistance arteries at 6 months (P <. 05); and 5) unchanged structure of aorta. The long-term administration of a high salt diet leads to structural vascular changes in normotensive rats. There are important regional and segmental variations in the long-term adaptation of arteries to a high salt diet.     

Suppressed Ca2+/CaM/CaMKII-dependent KATP channel activity in primary afferent neurons mediates hyperalgesia after axotomy

Painful axotomy decreases K_ATP channel current (IK_ATP) in primary afferent neurons. Because cytosolic Ca²⁺ signaling is depressed in injured dorsal root ganglia (DRG) neurons, we investigated whether Ca²⁺–calmodulin (CaM)–Ca²⁺/CaM-dependent kinase II (CaMKII) regulates IK_ATP in large DRG neurons. Immunohistochemistry identified the presence of K_ATP channel subunits SUR1, SUR2, and Kir6.2 but not Kir6.1, and pCaMKII in neurofilament 200–positive DRG somata. Single-channel recordings from cell-attached patches revealed that basal and evoked IK_ATP by ionomycin, a Ca²⁺ ionophore, is activated by CaMKII. In axotomized neurons from rats made hyperalgesic by spinal nerve ligation (SNL), basal K_ATP channel activity was decreased, and sensitivity to ionomycin was abolished. Basal and Ca²⁺-evoked K_ATP channel activity correlated inversely with the degree of hyperalgesia induced by SNL in the rats from which the neurons were isolated. Inhibition of IK_ATP by glybenclamide, a selective K_ATP channel inhibitor, depolarized resting membrane potential (RMP) recorded in perforated whole-cell patches and enhanced neurotransmitter release measured by amperometry. The selective K_ATP channel opener diazoxide hyperpolarized the RMP and attenuated neurotransmitter release. Axotomized neurons from rats made hyperalgesic by SNL lost sensitivity to the myristoylated form of autocamtide-2-related inhibitory peptide (AIPm), a pseudosubstrate blocker of CaMKII, whereas axotomized neurons from SNL animals that failed to develop hyperalgesia showed normal IK_ATP inhibition by AIPm. AIPm also depolarized RMP in control neurons via K_ATP channel inhibition. Unitary current conductance and sensitivity of K_ATP channels to cytosolic ATP and ligands were preserved even after painful nerve injury, thus providing opportunities for selective therapeutic targeting against neuropathic pain.