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To determine the mechanism(s) underlying enhanced oxidative stress in kidneys of salt-sensitive hypertension, neonatal Wistar rats were given vehicle or capsaicin (CAP, 50 mg/kg sc) on the first and second days of life. After being weaned, male rats were assigned into four groups and treated for 2 wk with the following: vehicle + a normal sodium diet (NS, 0.4%, CON-NS), vehicle + a high-sodium diet (HS, 4%, CON-HS), CAP + NS (CAP-NS), and CAP + HS (CAP-HS). Systolic blood pressure was significantly increased in CAP-HS but not CAP-NS or CON-HS rats. Plasma and urinary 8-iso-prostaglandin F(2alpha) levels increased by approximately 40% in CON-HS and CAP-HS rats compared with their respective controls fed a NS diet (P < 0.05), and these parameters were higher in CAP-HS compared with CON-HS rats. Superoxide (O(2)(-)*) levels in the renal cortex and medulla increased by approximately 45% in CAP-HS compared with CON-HS, CON-NS, and CAP-NS rats (P < 0.05). Enhanced O(2)(-)* levels in the cortex and medulla in CAP-HS rats were prevented by preincubation of renal tissues with apocynin, a selective NAD(P)H oxidase inhibitor. Protein expression of NAD(P)H oxidase subunits, including p47(phox) and gp91(phox) in the renal cortex and medulla, was significantly increased in CAP-HS compared with CON-HS, CON-NS, and CAP-NS rats. In contrast, protein expression and activities of Cu/Zn SOD and Mn SOD were significantly increased in the renal medulla in both CAP-HS and CON-HS but in the cortex in CAP-HS rats only. Creatinine clearance decreased by approximately 45% in CAP-HS rats compared with CON-HS, CON-NS, and CAP-NS rats (P < 0.05). O(2)(-)* levels in the renal cortex of CAP-HS rats negatively correlated with creatinine clearance (r = -0.76; P < 0.001). Therefore, regardless of enhanced SOD activity to suppress oxidative stress, increased oxidative stress in the kidney of CAP-treated rats fed a HS diet is likely the result of increased expression and activities of NAD(P)H oxidase, which may contribute to decreased renal function and increased blood pressure in these rats. Our results suggest that sensory nerves may play a compensatory role in attenuating renal oxidative stress during HS intake.
The effects of two different stressors, heat shock (HS; 44 degrees C, 20 min) and ethanol (1.2 M, 60 min), on ion content and membrane potential were investigated in C6 rat glioma cells. Both treatments were previously shown to induce the HS response [26]. Intracellular pH (pH(i)), sodium ion concentration ([NA+]i), potassium ion concentration ([K+]i) and membrane potential were determined by means of continuous 31P and 23Na nuclear magnetic resonance (NMR), continuous fluorescence spectroscopy and 86Rb uptake. Lactate extrusion was determined in addition with respect to pH(i) regulation. The aim of this study was a detailed picture of HS and ethanol-induced ion changes in a single cell type, because stress-induced changes in the intracellular ionic balance may be important factors for determining proliferation, stress response and apoptosis. HS lowered the pH(i) from 7.38 +/- 0.04 to about 7.05 +/- 0.04. [Na+]i decreased during HS to 50% of the control and recovered to normal level 95 min after HS treatment. During HS, [K+]i remained constant but increased after HS. The membrane potential hyperpolarized from -83 mV to -125 mV and returned to initial values during HS treatment. Lactate extrusion increased 3-fold after HS. Ethanol (1.2 M) lowered the pH(i) from pH 7.38 +/- 0.04 to pH 7.0 +/- 0.04, but in contrast to heat strongly increased [Na]i. It hyperpolarized the membrane potential from -83 to -125 mV. Ethanol also increased lactate extrusion similar to HS. Also in contrast to the effect of HS, the potassium concentration decreased during ethanol treatment. The Na(+)-H+ exchanger monensin was used to overcome the apparent inhibition of the cellular Na(+)-H+ exchanger by HS. At normal pH(e) (7.4) monensin increased [Na+]i and pH(i) considerably. A subsequent HS reduced [Na+]i only minimally. Acidification of the cells by low pH(e) (6.2) prior to HS did not abolish the HS-induced drop of pH(i), indicating that the Na(+)-H+ exchanger was also inhibited at low pH(i). At low pH(e), monensin transports H+ into the cell. A subsequent HS decreased pH(i) only little, showing the importance of inhibition of the Na(+)-H+ exchanger for the HS-induced pH(i) decrease. 100 microM amiloride reduced pH(i) and [Na+]i in a similar way as HS, but did not change pH(i) and [Na+]i much during a HS. These results indicate that some of the HS-induced ionic changes are mediated by inhibition of the Na(+)-H+ exchanger, activation of Na(+)-K(+)-ATPase and changes of membrane conductance for ions.
Heparan sulfate (HS) is the anionic polysaccharide side chain of HS proteoglycans (HSPGs) present in basement membranes, in extracellular matrix, and on cell surfaces. Recently, agrin was identified as a major HSPG present in the glomerular basement membrane (GBM). An increased permeability of the GBM for proteins after digestion of HS by heparitinase or after antibody binding to HS demonstrated the importance of HS for the permselective properties of the GBM. With recently developed antibodies directed against the GBM HSPG (agrin) core protein and the HS side chain, we demonstrated a decrease in HS staining in the GBM in different human proteinuric glomerulopathies, such as systemic lupus erythematosus (SLE), minimal change disease, membranous glomerulonephritis, and diabetic nephropathy, whereas the staining of the agrin core protein remained unaltered. This suggested changes in the HS side chains of HSPG in proteinuric glomerular diseases. To gain more insight into the mechanisms responsible for this observation, we studied GBM HS(PG) expression in experimental models of proteinuria. Similar HS changes were found in murine lupus nephritis, adriamycin nephropathy, and active Heymann nephritis. In these models, an inverse correlation was found between HS staining in the GBM and proteinuria. From these investigations, four new and different mechanisms have emerged. First, in lupus nephritis, HS was found to be masked by nucleosomes complexed to antinuclear autoantibodies. This masking was due to the binding of cationic moieties on the N-terminal parts of the core histones to anionic determinants in HS. Second, in adriamycin nephropathy, glomerular HS was depolymerized by reactive oxygen species (ROS), mainly hydroxyl radicals, which could be prevented by scavengers both in vitro (exposure of HS to ROS) and in vivo. Third, in vivo renal perfusion of purified elastase led to a decrease of HS in the GBM caused by proteolytic cleavage of the agrin core protein near the attachment sites of HS by the HS-bound enzyme. Fourth, in streptozotocin-induced diabetic nephropathy and during culture of glomerular cells under high glucose conditions, evidence was obtained that hyperglycemia led to a down-regulation of HS synthesis, accompanied by a reduction in the degree of HS sulfation.
To determine the role of endothelin-1 (ET-1) and its receptors in salt-sensitive hypertension induced by sensory nerve degeneration, selective ET(A) antagonist (ABT-627) and ET(B) antagonist (A-192621) were used. Newborn Wistar rats were given vehicle or 50 mg/kg capsaicin subcutaneously on the first and second days of life. After the weaning period, male rats were divided into eight groups, and subjected to the following treatments for 2 weeks: control + normal salt diet (Con+NS, 0.5%), control + high salt diet (Con+HS, 4%), control + high salt diet + ABT-627 (Con+HS+ABT-627), control + high salt diet + A-192621 (Con+HS+A-192621), capsaicin + normal salt diet (Cap+NS), capsaicin + high salt diet (Cap+HS), capsaicin + high salt diet + ABT-627 (Cap+HS+ABT-627), capsaicin + high salt diet + A-192621 (Cap+HS+A-192621). Both ABT-627 (5 mg/kg/d) and A-192621 (30 mg/kg/d) were given by oral gavage twice a day. Mean arterial pressure (MAP, mm Hg) was higher in Con+HS+A-192621 (141 +/-11) than in Con+NS (94 +/- 10), Con+HS (95 +/- 5), and Con+HS+ABT-627 (97 +/- 6) (P<0.05). MAP was also higher in Cap+HS (152 +/- 6) and Cap+HS+A-192621 (180 +/- 7) than in Cap+NS (99 +/- 3) and Cap+HS+ABT-627 (104 +/- 5) (P<0.05), and it was higher in Cap+HS+A-192621 than in Cap+HS (P<0.05). Enzyme immunometric assay showed that ET-1 plasma concentration (pg/mL) was higher in Con+HS+A-192621 (7.59 +/- 0.78) than in Con+NS (2.68 +/- 0.56), Con+HS (2.50 +/- 0.92), and Con+HS+ABT-627 (3.54 +/- 0.79) (P<0.05). ET-1 plasma concentration was also higher in Cap+HS (8.95 +/-.16), Cap+HS+ABT-627 (9.82 +/- 1.22) and Cap+HS+A-192621 (10.97 +/- 0.57) than in Cap+NS (3.06 +/- 0.73) (P<0.05). We conclude that blockade of the ET(A) receptor prevents the development of salt sensitive hypertension induced by sensory nerve degeneration, indicating that activation of the ET(A) receptor by increased plasma ET-1 level contributes to elevation of blood pressure in this model. In contrast, blockade of the ET(B) receptor leads to an increase in blood pressure in both normal and sensory nerve degenerated rats fed a high salt diet. These results suggest that ET(B) plays an antihypertensive role in response to high salt intake under both normal and sensory nerve degenerated conditions.
Hydrogen sulfide (HS-) impairs the oxidation of butyrate in colonocytes and is found in excess in feces of patients with ulcerative colitis. The possible pathogenic role of HS- in ulcerative colitis was further investigated. To investigate the metabolic effect of free and bound fecal HS-, isolated rat colonocytes were incubated in the presence of butyrate without and with the addition of (1) HS- in water, (2) sterile filtrates of fecal homogenates supplemented and incubated with HS- and known sources of fecal HS- production, and (3) HS- incubated with fecal agents known to bind HS-. Oxidation rates were obtained by quantifying the production of CO2. Total and free HS-, as well as the fecal ability to bind HS-, were determined in health and ulcerative colitis. Compared to the production of CO2 by colonocytes incubated with 2 mmol/liter of butyrate, the further addition of 1.25 and 2.5 mmol/liter of HS- in water reduced the production of CO2 by 57.6+/-10.0 and 98.9+/-1.4%, respectively. However, when adding fecal filtrate of homogenate supplemented with HS- corresponding to 1.25 and 2.5 mmol/liter of HS- in water, the reduction of CO2 production was only 30.7+/-12.0 and 53.2+/-14.0%, respectively. Neither the fecal level of total or free HS- nor the remarkable fecal ability to bind HS- differed in health or quiescent and active ulcerative colitis. Bound HS- had no or little effect on CO2 production. Addition of fecal filtrate of nonsupplemented homogenate to colonocytes significantly reduced the oxidation of butyrate to CO2 about 25%, which could not be ascribed to fecal HS-. In conclusion, fecal HS- has little effect on butyrate oxidation in colonocytes and does not seem to play a pathogenic role for UC by impairing colonic epithelial metabolism. Other fecal agents seem to be more potent metabolic inhibitors than fecal HS-. The role of colonic contents in the pathogenesis of ulcerative colitis remains circumstantial.
We recently demonstrated that Campylobacter jejuni produces a capsular polysaccharide (CPS) that is the major antigenic component of the classical Penner serotyping system distinguishing Campylobacter into >60 groups. Although the wide variety of C. jejuni serotypes are suggestive of structural differences in CPS, the genetic mechanisms of such differences are unknown. In this study we sequenced biosynthetic cps regions, ranging in size from 15 to 34 kb, from selected C. jejuni strains of HS:1, HS:19, HS:23, HS:36, HS:23/36 and HS:41 serotypes. Comparison of the determined cps sequences of the HS:1, HS:19 and HS:41 strains with the sequenced strain, NCTC11168 (HS:2), provides evidence for multiple mechanisms of structural variation including exchange of capsular genes and entire clusters by horizontal transfer, gene duplication, deletion, fusion and contingency gene variation. In contrast, the HS:23, HS:36 and HS:23/36 cps sequences were highly conserved. We report the first detailed structural analysis of 81-176 (HS:23/36) and G1 (HS:1) and refine the previous structural interpretations of the HS:19, HS:23, HS:36 and HS:41 serostrains. For the first time, we demonstrate the commonality and function of a second heptose biosynthetic pathway for Campylobacter CPS independent of the pathway for lipooligosaccharide (LOS) biosynthesis and identify a novel heptosyltransferase utilized by this alternate pathway. Furthermore, we show the retention of two functional heptose isomerases in Campylobacter and the sharing of a phosphatase for both LOS and CPS heptose biosynthesis.
A replication-defective recombinant retrovirus containing the human papilloma virus E6/E7 genes (LXSN-16 E6E7) was used to immortalize stromal cells from human marrow. The E6/E7 gene products interfere with the function of tumor-suppressor proteins p53 and Rb, respectively, thereby preventing cell cycle arrest without causing significant transformation. Twenty-seven immortalized clones designated HS-1 to HS-27 were isolated, four of which are characterized in this report. Two cell lines, HS-5 and HS-21, appear to be fibroblastoid and secrete significant levels of granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage-CSF (GM-CSF), macrophage-CSF (M-CSF), Kit ligand (KL), macrophage-inhibitory protein-1 alpha, interleukin-6 (IL-6), IL-8, and IL-11. However, only HS-5 supports proliferation of hematopoietic progenitor cells when cocultured in serum-deprived media with no exogenous factors. Conditioned media (CM) from HS-5 promotes growth of myeloid colonies to significantly greater extent than a cocktail of recombinant factors containing 10 ng/mL of IL-1, IL-3, IL-6, G-CSF, GM-CSF, and KL and 3 U of erythropoietin (Epo). Two additional clones, HS-23 and HS-27, resemble "blanket" cells, with an epithelioid morphology, and are much larger, broader, and flatter when compared with HS-5 and HS-21. These lines secrete low levels of growth factors and do not support proliferation of isolated progenitor cells in cocultures. CM from HS-23 and HS-27 also fail to support growth of myeloid colonies. Both HS-23 and HS-27 express relatively high levels of VCAM-1, yet HS-27 is the only line that supports the formation of "cobblestone" areas by isolated CD34+38lo cells. We hypothesize that HS-5, HS-21, HS-23, and HS-27 represent functionally distinct components of the marrow microenvironment.
The synthesis of dopamine, from L-beta-3,4-dihydroxyphenylalanine (L-DOPA), in renal tissue of rats on either a normal sodium (NS) or high sodium (HS) diet for 1 week or 6 weeks was examined. Aromatic L-amino acid decarboxylase (AAAD) activity determined in kidney homogenates in "1 week HS" (Vmax = 11.5 +/- 1.6 nmol/mg protein/hr) and "6 weeks HS" rats (Vmax = 10.6 +/- 1.5 nmol/mg protein/hr) was greater (P < 0.02) than that in "NS" rats (Vmax = 7.7 +/- 0.8 nmol/mg protein/hr). Km (microM) values in "NS", in "1 week HS" and "6 weeks HS" rats were similar. The formation of dopamine in kidney slices loaded with 100 microM L-DOPA depended exponentially on the concentration of sodium in the medium (0-160 mM). In kidney slices obtained from "1 week HS" rats the decarboxylation of added L-DOPA was significantly greater (P < 0.01) than that observed in kidney slices obtained from "NS" and "6 weeks HS" rats; the rate constant of formation of dopamine as a function of sodium concentration in the incubation medium was, however, similar in "NS" rats to that in "1 week HS" and "6 weeks HS" rats. Ouabain produced a concentration dependent decrease in the synthesis of dopamine in all three experimental groups; the magnitude of the inhibitory effect of 1.0 mM ouabain was greater in "1 week HS" rats (77% reduction; P < 0.01) than in "NS" rats (59% reduction; P < 0.01) and in "6 weeks HS" rats (23% reduction; P = 0.08). Activation of protein kinase C by phorbol 12,13-dibutyrate (PDBu) and the calcium ionophore A23187 produced a concentration-dependent reduction in the formation of dopamine in rat kidney slices, but not in kidney homogenates; the magnitude of the inhibitory effect was greater in "1 week HS" rats than in "NS" and "6 weeks HS" rats. Submaximal concentrations of PDBu (10 nM) were synergistic with the inhibitory effect of A23187 on the formation of dopamine: again, this effect was more marked in "1 week HS" rats than in "NS" and "6 weeks HS" rats. The effects of PDBu and PDBu plus A23187, but not those of A23187 alone, were antagonized in a concentration-dependent manner by d-sphingosine, a protein kinase C inhibitor. It is concluded that the increased activity of AAAD in renal tissues of rats submitted to HS intake is accompanied in "1 week HS" but not in "6 weeks HS" rats by enhanced inhibition of dopamine formation during protein kinase C activation.
BACKGROUND: Irritant contact dermatitis of the hands is very common in dental laboratory technicians due to frequent contact with various irritants. Barrier creams (HS) are often avoided because a tight grip of tools and small objects is necessary; furthermore dental objects must not be contaminated by HS. In this study the efficacy of HS applied during working hours was compared to skin care products (HP) applied only after work. METHOD: 2 popular commercial HS (HS-1, HS-2) and 2 moisturizers containing urea and beeswax respectively (HP-1, HP-2) were evaluated in 5 laboratories by a total of 192 technicians. Every technician used one HS (several applications during working hours) and one HP applied at home at least once daily for 4 weeks each with a wash-out period of 2 weeks in between. The sequence HS-HP, HP-HS was randomized for every laboratory in two single blind cross over designs for both combinations (HS-1 with HP-1, HS-2 with HP-2). The technicians scored the products on a scale of efficacy (worse, none, good, very good). The skin condition was evaluated by a dermatologist at the beginning of the study, after 4, 6 and 10 weeks on a scale for erythema, infiltration, vesicles, fissures and scaling to produce a sum score. Furthermore, transepidermal water loss (TEWL) was measured on the back of the hand and on the ventral aspect of the forearm at the beginnung and the end of the 4 weeks application period. The quotient of these two parameters was used for statistical evaluation (covariance analysis). RESULTS: The assessment of either "good" or "very good" was as follows: HS-1 58%; HS-2 67%; HP-1 77%; HP-2 98%. Both HP, particularly HP-2, were judged superior to either HS. This was confirmed by the improvement of the skin condition (HS-1 35%; HS-2 44%; HP-1 55%; HP-2 56%). Statistical significance of the differences in TEWL data was clearly demonstrated: HP-1 better than HS-1 (p = 0.007); HP-2 better than HS-2 (p = 0.03). The acceptance of the products was high. The majority was willing to continue its usage after the study (68 %-89 %). CONCLUSIONS: The results demonstrate that the use of after work moisturizers is highly beneficial and under the chosen study conditions even superior to barrier creams applied at work. This approach is more practical for many professions and may effectively reduce the frequency of irritant contact dermatitis.
Most patients with non-lesional temporal lobe epilepsy (NLTLE) will have the findings of hippocampal sclerosis (HS) on a high resolution MRI. However, a significant minority of patients with NLTLE and electroclinically well-lateralized temporal lobe seizures have no evidence of HS on MRI. Many of these patients have concordant hypometabolism on fluorodeoxyglucose-PET ([18F]FDG-PET). The pathophysiological basis of this latter group remains uncertain. We aimed to determine whether NLTLE without HS on MRI represents a variant of or a different clinicopathological syndrome from that of NLTLE with HS on MRI. The clinical, EEG, [18F]FDG-PET, histopathological and surgical outcomes of 30 consecutive NLTLE patients with well-lateralized EEG but without HS on MRI (HS-ve TLE) were compared with 30 consecutive age- and sex-matched NLTLE patients with well-lateralized EEG with HS on MRI (HS+ve TLE). Both the HS+ve TLE group and the HS-ve TLE patients had a high degree of [18F]FDG-PET concordant lateralization (26 out of 30 HS-ve TLE versus 27 out of 27 HS+ve TLE). HS-ve TLE patients had more widespread hypometabolism on [18F]FDG-PET by blinded visual analysis [odds ratio (OR = + infinity (2.51, -), P = 0.001]. The HS-ve TLE group less frequently had a history of febrile convulsions [OR = 0.077 (0.002-0.512), P = 0.002], more commonly had a delta rhythm at ictal onset [OR = 3.67 (0.97-20.47), P = 0.057], and less frequently had histopathological evidence of HS [OR = 0 (0-0.85), P = 0.031]. There was no significant difference in surgical outcome despite half of those without HS having a hippocampal-sparing procedure. Based on the findings outlined, HS-ve PET-positive TLE may be a surgically remediable syndrome distinct from HS+ve TLE, with a pathophysiological basis that primarily involves lateral temporal neocortical rather than mesial temporal structures.
OBJECTIVE: A unique model of hypertension developed in our laboratory shows that neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to salt load with a significant rise in blood pressure. Considering that capsaicin impairs the micturition reflex, increased retention of urine in the bladder of capsaicin-treated rats may lead to nephropathy and therefore to an increase in blood pressure. The present study was designed to test the hypothesis that abnormalities in renal function and blood pressure in this model are independent of urine retention, and are reversible when a high-salt diet is withdrawn. DESIGN AND METHODS: Newborn Wistar rats were given either 50 mg/kg capsaicin subcutaneously or vehicle on the first and second days of life. After weaning, one set of male rats was treated for 3 weeks with: capsaicin pretreatment plus high-sodium diet (4%, CAP-HS), capsaicin plus normal-sodium diet (0.5%, CAP-NS), control plus high-sodium diet (CON-HS), and control plus normal sodium diet (CON-NS). The other set of male rats was given the same treatment for 4 weeks except that the two high-salt-treated groups were switched to normal salt (CAP-HS-NS and CON-HS-NS) for the last week. Chronic bladder catheterization was carried out in all rats to maintain free flow of urine. Western blot was used for measurement of the capsaicin (vanilloid) receptor levels in dorsal root ganglia. Radioimmunoassay was used for measurement of plasma renin activity and plasma aldosterone levels. RESULTS: Capsaicin (vanilloid) receptor contents in dorsal root ganglia were markedly decreased in all capsaicin-treated groups. Plasma renin activity and plasma aldosterone levels were higher in CAP-HS rats than in CON-HS rats, but were not statistically different between CAP-HS-NS and CON-HS-NS rats. Urine Na excretion but not urine volume was decreased and water intake increased in CAP-HS compared with CON-HS, but these parameters were not statistically different between CAP-HS-NS and CON-HS-NS rats. Although systolic blood pressure and mean arterial pressure were higher in CAP-HS and CAP-HS-NS rats than in CON-HS and CON-HS-NS rats, they were higher in CAP-HS than in CAP-HS-NS rats. CONCLUSION: Despite elimination of urine retention, sensory denervation impairs renal function and leads to an increase in blood pressure in response to high salt intake. The abnormalities in renal function and blood pressure in sensory denervated rats are reversible, at least in part, when high salt intake is withdrawn. These data support the hypothesis that sensory innervation counterbalances the pro-hypertensive systems and serves as a modulator to control salt sensitivity and cardiovascular function.
BACKGROUND: Terminal warm blood cardioplegia, "Hot shot", is the method for providing an energy replenishment and/or early recovery of aerobic metabolism without electromechanical activity at initial reperfusion. The mechanism of beneficial effects of this Hot Shot is multifactorial. This study was designed to assess the effects of terminal warm blood cardioplegia by comparing with oxygenated terminal warm crystalloid cardioplegia. METHODS: In Group HS-B, n=8 (oxygenated blood; 37 degrees C, Ht: 20%, K+ 20 mEq/l, pH 7.237, PO2 219 mmHg) and in Group HS-C, n=8 (bloodless oxygenated (5% CO2+95%O2) crystalloid, 37 degrees C, K+ 20 mEq/l, pH 7.435, PO2 624 mmHg), terminal warm cardioplegia (20 ml/kg for 5 minutes) was studied in the isolated blood perfused neonatal lamb heart following 2 hr of cardioplegic ischemia. Another eight hearts served as control without any kind of terminal cardioplegia. After 60 min of reperfusion, LV function was measured. Coronary blood flow (CBF), oxygen content, and oxygen consumption (MVO2) were measured and the oxygen extraction ratio was calculated in Group HS-B and HS-C during terminal cardioplegia and/or reperfusion. Results are given as % recovery of preischemic values. RESULTS: HS-B as well as HS-C groups showed better functional recovery in maximum developed pressure (DP: 78.0+/-8.3 in HS-B vs 65.2+/-9.2%; p=0.018), maximum dp/dt (67.3+/-6.2 in HS-B, 65.3+/-7.4 in HS-C vs 55.8+/-5.0%; p=0.003, p=0.02), DP V10 (87.1+/-8.5 in HS-B vs 67.2+/-9.9%; p=0.0001), and peak dp/dt V10 (76.4+/-7.6 in HS-B, 69.8+/-8.1 in HS-C vs 58.6+/-6.9 %; p=0.0001) than the control group. Between the HS-B and HS-C groups, HS-B showed better functional recovery in terms of DP V10 (p=0.01). Oxygen delivery of terminal cardioplegia was almost four times higher in HS-B group (90.4+/-17.7 vs 18.7+/-1.1 mcl/ml), contrarily, HS-C group showed four times higher oxygen extraction ratio compared to HS-B group (0.78+/-0.06 vs 0.18+/-0.11), thus oxygen consumption during hot shot was maintained at the same level in both groups. CBF in the control group was lower than that in the other groups at 60 min of reperfusion. CONCLUSIONS: Reperfusion with both terminal warm cardioplegia including blood and oxygenated crystalloid cardioplegia resulted in better recovery of function and higher levels of CBF with slightly better function in terminal warm blood cardioplegia.