The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H2S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H2S donor, the effect of H2S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 μmol/l) dose and timedependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 μmol/l), a ATP-sensitive K+ channels (KATP) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine γ-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 μmol/l), increased sympathetic outflow. The results show that exogenous H2S in the carotid sinus inhibits sympathetic outflow. The effect of H2S is attributed to opening KATP channels and closing the L-calcium channels., Qi Guo, Yuming Wu, Hongmei Xue, Lin Xiao, Shneg Jin, Ru Wang., and Obsahuje bibliografii
Limited information is available about selection of the threshold for arterial blood pressure in critically ill patients, particularly in sepsis when normal organ blood flow autoregulation may be altered. The present experimental study investigated whether increasing perfusion pressure using norepinephrine in normotensive hyperdynamic porcine bacteremia affects intestinal macro- and microcirculation. Nine pigs received continuous i.v. administration of Pseudomonas aeruginosa (PSAE) to develop hyperdynamic, normotensive (mean arterial pressure [MAP] 65 mm Hg) sepsis. Norepinephrine was used to achieve 10-15 % increase in MAP. Mesenteric arterial blood flow (Qgut), ileal mucosal microvascular perfusion (LDFgut) and ileal-end-tidal PCO2 gap (PCO2 gap) were measured before norepinephrine, after 60 min of norepinephrine infusion and 60 min after norepinephrine infusion had been discontinued. During a 12 h period of PSAE infusion all pigs developed hyperdynamic circulation with significantly decreased MAP. Although the mesenteric blood flow remained unchanged, infusion of PSAE resulted in a gradual fall of ileal microvascular perfusion, which was associated with progressively rising PCO2 gap. Norepinephrine which induced a 10-15 % increase in perfusion pressure (i.e. titrated to attain near baseline values of MAP) affected neither Qgut nor the intestinal blood flow distribution (Qgut/CO). Similarly, norepinephrine did not change either LDFgut or PCO2 gap. In this hyperdynamic, normotensive porcine bacteremia, norepinephrine-induced increase in perfusion pressure exhibited neither beneficial nor deleterious effects on intestinal macrocirculatory blood flow and ileal mucosal microcirculation. The lack of changes suggests that the gut perfusion was within its autoregulatory range.
Pergolide, terguride and N,N'-spacer-linked oligomers of both have been tested for their ability to interact with 5 hydroxytryptamine(HT)2A receptors of rat tail artery. Pergolide was a potent partial agonist (pEC50 7.5, Emax 55 %) and antagonized 5-HT-induced contractions (pKP 7.2). Pergolide dimer 3 with a p-xylene spacer between the indole nitrogens (N-1) displayed somewhat lower agonist potency than pergolide (pEC50 7.0, Emax 55 %, pKP 6.6). The contractile responses to pergolide and dimer 3 were antagonized by the 5-HT2A receptor antagonist ketanserin (pA2 9.4, 9.1). In contrast to pergolide dimer 3, pergolide dimers 5 and 9 with an alkyl and an aralkyl spacer between the piperidine nitrogens (N-6) lacked agonism and displayed low affinity at 5-HT2A receptors (pA2 < 5.5). Terguride behaved as an insurmountable antagonist of 5-HT (pA2 8.4). Oligomers of terguride showed 5 to 50-fold lower affinity. It is concluded that pergolide and terguride show a high affinity for 5-HT2A receptors, but dimerization (oligomerization) of both drugs fails to increase affinity.
Alzheimerova choroba (ACH) se řadí mezi závažná neurodegenerativní onemocnění provázená oxidačním stresem. Produkty radikálových reakcí mohou difundovat z primárních míst a být detekovány v cerebrospinální tekutině (CSF) či krvi. Tyto produkty představují potenciální biochemické markery pro diagnostiku ACH. Nejvíce pozornosti je zaměřeno na analýzu CSF, protože odráží patologické změny v mozkové tkáni u ACH. V CSF byly potvrzeny zvýšené hladiny oxidačních produktů lipidů i proteinů. Hladiny vitaminů jsou snížené, nicméně existují i práce, které nenašly rozdíly oproti kontrolám. Některé studie se zaměřily na detekci produktů oxidačního stresu v krvi u ACH, ale výsledky nejsou konzistentní. Část prací ukazuje na nárůst oxidačních produktů a snížené hladiny antioxidantů v plazmě. Nicméně jiné práce tyto výsledky nepotvrdily. Z hlediska hledání diagnostického biomarkeru pro ACH má význam se zaměřit na specifické produkty peroxidace lipidů, tzv. lipofuscinoidní pigmenty (LFP), v erytrocytech. Na základě fluorescenčních analýz LFP je možné najít specifický produkt v krvi u ACH., Alzheimer´s disease (AD) is a serious neurodegenerative disorder accompanied by oxidative stress. Products of free radical reactions diffuse from primary sites and can be detected in cerebrospinal fluid (CSF) and blood. Such products represent potential biochemical markers for diagnosis of AD. Most studies are focused on CSF since its composition reflects pathological changes in the brain in AD. Increased levels of lipid and protein oxidative products have been found in CSF. Levels of vitamins were reduced in CSF. However, there are studies which show no difference between AD and controls. There is research on free radical products in blood in AD but results are not consistent. Several studies show increased oxidative products and reduced antioxidant in plasma. Nevertheless, others did not confirm it. Considering the investigation of a diagnostic biomarker for AD, specific end-products of lipid peroxidation, so called lipofuscin-like pigments (LFP), in erythrocytes represent an important possibility. A specific product in blood in AD can be found by means of fluorescence analyses of LFP., Skoumalová A., and Literatura 35
Perigraft serom je poměrně vzácná komplikace, která může vzniknout po implantaci cévní protézy z dakronu nebo expandovaného polytetrafluoretylenu (ePTFE). Předkládáme kazuistiku 54letého pacienta s perigraft seromem okolo axillofemorálního bypassu (ePTFE protézou). Konečným řešením byla explantace této extraanatomické rekonstrukce a implantace aortobiilického bypassu s použitím cévní protézy z jiného materiálu. Článek diskutuje terapeutické možnosti této komplikace na základě publikovaných prací. Žádná guidelines ani jiná doporučení neexistují. Závěrem, přístup k léčbě perigraft seromu zůstává striktně individuální. Náhrada cévní protézy s použitím implantátu z jiného materiálu se zdá být nejlepší možností řešení pro recidivující perigraft seromy tam, kde jiné méně invazivní postupy selhaly., Perigraft seroma is quite a rare complication that may occur after implantation of Dacron or expanded polytetrafluoroethylene (ePTFE) vascular grafts. We report a case of a 54-year-old patient with perigraft seroma around an axillofemoral bypass (ePTFE graft). Definitive treatment involved the explantation of this extraanatomic bypass with perigraft seroma and the implantation of an aortobiiliac bypass using vascular prosthesis made of a different material. Based on published studies, therapeutic options for this complication are discussed. No guidelines or recommendations are available. In conclusion, the approach to perigraft seroma treatment remains strictly individual. Vascular graft replacement using grafts made of different material seems to be the best option in the case of recurring perigraft seroma, where less invasive procedures were not successful., and A. Gazi, R. Staffa, T. Novotný, Z. Kriz, M. Hermanová
For a rank-$1$ matrix $A= {\bold a \bold b}^t$, we define the perimeter of $A$ as the number of nonzero entries in both $\bold a$ and $\bold b$. We characterize the linear operators which preserve the rank and perimeter of rank-$1$ matrices over semifields. That is, a linear operator $T$ preserves the rank and perimeter of rank-$1$ matrices over semifields if and only if it has the form $T(A)=U A V$, or $T(A)=U A^t V$ with some invertible matrices U and V.
The most dramatic changes in pulmonary circulation occur at the time of birth. We hypothesized that some of the effects of perinatal hypoxia on pulmonary vessels are permanent. We studied the consequences of perinatal exposure to hypoxia (12 % O2 one week before and one week after birth) in isolated lungs of adult male rats (~12 weeks old) perfused with homologous blood. Perfusion pressure-flow relationship was tilted towards lower pressures in the perinatally hypoxic as compared to the control, perinatally normoxic rats. A non-linear, distensible vessel model analysis revealed that this was due to increased vascular distensibility in perinatally hypoxic rats (4.1±0.6 %/mm Hg vs. 2.3±0.4 %/mm Hg in controls, P = 0.03). Vascular occlusion techniques showed that lungs of the perinatally hypoxic rats had lower pressures at both the pre-capillary and post-capillary level. To assess its role, basal vascular tone was eliminated by a high dose of sodium nitroprusside (20 µM). This reduced perfusion pressures only in the lungs of rats born in hypoxia, indicating that perinatal hypoxia leads to a permanent increase in the basal tone of the pulmonary vessels. Pulmonary vasoconstrictor reactivity to angiotensin II (0.1-0.5 µg) was reduced in rats with the history of perinatal hypoxia. These data show that perinatal hypoxia has permanent effects on the pulmonary circulation that may be beneficial and perhaps serve to offset the previously described adverse consequences., V. Hampl, J. Bíbová, J. Herget., and Obsahuje bibliografii
We tested the effect of perinatal (one week prenatal and one week postnatal) normobaric hypoxia on the immune response of rats in their 9th week of life. We found that perinatally hypoxic rats produced less serum antibodies after sequential immunization with ovalbumin and sheep red blood cells. Also phagocytosis of HEMA microparticles by neutrophil leukocytes from perinatally hypoxic rats was depressed as well as the oxidative burst of their peritoneal macrophages and neutrophils. These results demonstrate that perinatal hypoxia has an important effect on the immune system of the rat.