CONTRACTION OF GLYCERINATED MITOCHONDRIA INDUCED BY ADENOSINE TRIPHOSPHATE AND DIVALENT CATIONS.
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Adenosine Triphosphate↗
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The effects of ischemia and reperfusion on mucosal respiratory function, adenosine triphosphate, electrolyte, and water content in the ascending colon of ponies.
OBJECTIVE: The purpose of this study was to examine the effects of ischemia and reperfusion on the biochemical integrity of equine colonic mucosa to assess the relative roles of ischemic- and reperfusion-induced damage. STUDY DESIGN: Two hours of no-flow ischemia experimentally induced by 720 degrees counterclockwise ascending colon volvulus followed by 2 hours reperfusion after derotation. ANIMALS: Ten ponies. METHODS: Ascending colon biopsies were obtained every hour for measurement of mucosal adenosine triphosphate (ATP), water, sodium, and potassium content. Additional samples were homogenized for assay of mitochondrial respiratory function. RESULTS: ATP content diminished 92% after ischemia and recovered to only 44% of control levels (P < .001 versus controls) after 2 hours reperfusion. Reperfusion increased mucosal water and decreased sodium and potassium content for the duration of the experiment. Both NADH-(pyruvate) and FADH-linked (succinate) respiration decreased after ischemia and did not recover during reperfusion indicating electron transport chain dysfunction. CONCLUSIONS: Two hours ischemia induced severe metabolic dysfunction in equine colon mucosa which persisted throughout reperfusion. Unequivocal evidence of injury specific to reperfusion was not observed in this study suggesting that much of the damage observed during reperfusion may be a continuation of injury induced during the ischemic period and not specific to reperfusion per se. CLINICAL RELEVANCE: This study suggests that greater efforts to metabolically support ischemically injured mucosa may be an important aspect of obtaining improved survival of horses affected by ascending colon volvulus (ACV).
Adenosine Triphosphate↗
Real-time detection and quantification of adenosine triphosphate sulfurylase activity by a bioluminometric approach.
A real-time, sensitive, and simple assay for detection and quantification of adenosine triphosphate sulfurylase (ATP:sulfate adenylytransferase, EC 2.7.7.4) activity has been developed. The method is based on detection of ATP generated in the ATP sulfurylase reaction between APS and PPi by the firefly luciferase system. For the Saccharomyces cerevisiae ATP sulfurylase, the concentrations of APS and PPi at the half-maximal rate were found to be about 0.5 and 7 microM, respectively. The assay is sensitive and yields linear response between 0.1 microU and 50 mU. The method can be used for monitoring and quantification of recombinant ATP sulfurylase activity in Escherichia coli lysate, as well as for detection of the activity during different purification procedures.
Adenosine Phosphosulfate↗
Heme oxygenase-1-derived carbon monoxide stimulates adenosine triphosphate generation in human hepatocyte.
Heme oxygenases cleave the pro-oxidant heme molecule into carbon monoxide, ferrous iron, and biliverdin, which is subsequently converted to bilirubin. Increasing the enzymatic activities of heme oxygenase by expression of its inducible isoform, heme oxygenase-1, protects hepatocyte from apoptosis. In the present study, we investigated the mechanisms involving in heme oxygenase-1-mediated cytoprotection. Heme oxygenase-1 could induce the expression of anti-apoptotic protein-Bcl-xL in human hepatocyte. This effect is associated with the activation of p38 MAPK signaling pathway. Carbon monoxide derived from heme oxygenase activities significantly increased adenosine triphosphate levels in hepatocyte that was essential for potentiation of the activation of p38 MAPK signaling. Our demonstration of the importance of the energy status to maximize an anti-apoptotic response provides a new insight into HO-mediated cytoprotection.
Adenosine Triphosphate↗
Changes in blood viscosity following nifedipine administration and its relation to the contents of adenosine triphosphate and 2,3-diphosphoglyceric acid in red blood cells in patients with angina pectoris.
The effect of oral administration of nifedipine (Adalat) on whole blood viscosity in patients with angina pectoris was investigated. Whole blood viscosity at a low shear rate of 37.5 s-1 was significantly reduced from 7.90 +/- 0.18 cP to 7.30 +/- 0.27 cP (1 cP = 1 mPa x s) after nifedipine administration (p less than 0.01), though the value at the high shear rate of 375 s-1, Casson yield stress value and Casson viscosity hardly decreased. Content of adenosine triphosphate (ATP) and 2,3-diphosphoglyceric acid (2,3-DPG) in the erythrocytes affecting blood viscosity, especially low shear rate viscosity, showed little change, and the hematocrit value was little varied either. Nifedipine, a Ca antagonist, has been known to inhibit Ca entry into the cells. These findings suggest that nifedipine reduces whole blood viscosity, especially low shear rate value, due to inhibition of Ca entry into the red blood cells, without increasing metabolic changes of ATP or 2,3-DPG in the erythrocytes, though measurement of Ca content in erythrocyte was unsolved.
2,3-Diphosphoglycerate↗
The effects of ibuprofen and diclofenac on the chemotaxis and adenosine triphosphate level of polymorphonuclear cells in vitro.
Investigations were carried out to determine the effect of ibuprofen and diclofenac on the chemotaxis of human polymorphonuclear cells. The experiments were done with the drugs alone as well as in the presence of leukotriene B4 (LTB4). A modified quantitative bioluminescence assay was used to measure chemotaxis, which allowed the calculation of differences in the spontaneous migration in contrast to the effects of the drugs, and simultaneously, also, the evaluation of whether the inhibition or augmentation of the chemotaxis was due to influences on the adenosine triphosphate (ATP) level of the cells. It was found that high concentrations (10 mM) of either ibuprofen or diclofenac destroy the intracellular ATP of polymorphonuclear cells (PMN). Therefore, the reported inhibition of the chemotaxis by ibuprofen at a concentration of 10 mM cannot be understood as a part of the chemotactic process. In the range of 1 microM and 0.1 mM ibuprofen and diclofenac did not statistically affect the intracellular ATP level of PMN cells but at the same time a distinct inhibition of the chemotactic response of PMN cells was observed. This effect occurred even in the presence of a potent chemoattractant (leukotriene B4). Ibuprofen (0.1 mM) reduced chemotaxis to 67% and the same concentration of diclofenac reduced it to 56% of the values of LTB4 alone.
Adenosine Triphosphate↗
Adenosine-triphosphate in trauma-related and elective hypothermia.
BACKGROUND: In trauma patients, hypothermia is a frequent event. According to the literature, the majority of trauma patients are presenting a core temperature of less than 34 degrees C at admission. In contrast to the benefit of hypothermia in elective surgery, clinical experience with hypothermia in trauma patients has identified hypothermia to be one major cause of severe posttraumatic complications. It was hypothesized that this diverse effect of hypothermia is related to depletion of high-energy phosphates like adenosine triphosphate (ATP) in trauma patients. To verify this hypothesis, the relation of ATP plasma levels and hypothermia was examined in a clinical study. METHODS: Three different groups of patients were under study. The first group (group A, normothermic control group) included patients (n = 15) undergoing elective surgery of the lower limb with a mean operation time of 113 minutes. The second study group (group B, hypothermic control) was composed of patients (n = 15) who were subjected to elective coronary artery bypass operation under hypothermia (31 degrees C for 48 minutes, mean total operation time being 205 minutes). The third study group (group C) included trauma patients (n = 23, mean Injury Severity Score [ISS] of 24.7). At the time of admission, 10 patients presented a core temperature more than or equal to 34 degrees C (group C1, mean ISS, 25.2; mean T(A), 34.5 degrees C), 13 patients presented a T(A) less than 34 degrees C (group C2, mean ISS, 26.0; mean T(A), 32.9 degrees C). In both groups of surgical patients, the ATP plasma level was measured preoperatively, at 2, 4, and 24 hours postoperatively. For trauma patients, this measurement was performed at admission and 24 hours later. Within the same schedule, body core temperature was recorded and the clinical course was documented as well. RESULTS: Elective limb surgery in normothermic patients resulted only in a transient decrease in ATP plasma levels (preoperative, 87.8 micromol/dL; 4 hours postoperative, 52.0 micromol/dL). At 24 hours, the ATP plasma level (62.6 +/- 10.0 micromol/dL) has increased toward baseline level. Elective hypothermia in patients subjected to coronary bypass also resulted only in a transient decrease in ATP plasma levels. During the operation period, including hypothermia, the ATP plasma level was comparable (50.4 micromol/dL) to group A and also returned back toward normal values at 24 hours (58.2 micromol/dL). All trauma patients revealed a significant low ATP plasma level at admission compared with both control groups. Looking at subdivided groups the most significant drop in ATP plasma level (28.5 micromol/dL) was noted in patients presenting an initial core temperature less than 34 degrees C and ISS more than 30. Even 24 hours later, the ATP level of this subgroup was significantly diminished, despite a rise up to 44.4 micromol/dL. In contrast, only a moderate drop in ATP plasma concentration (59.2 micromol/dL) was noted in the group of T(A) more than or equal to 34 degrees C and ISS less than 20. This group revealed almost normal values (68.3 micromol/dL) 24 hours after trauma. In addition to hypothermia, the metabolic state, reflected by the plasma lactate levels, significantly influenced the ATP plasma levels, as high lactate levels were paralleled by low ATP levels. Also, the overall outcome was related to injury severity and hypothermia. CONCLUSION: Hypothermia in elective surgery, established by active cooling, preserves the ATP storage and maintains an aerobic metabolism, which both contribute to the beneficial effect of hypothermia in ischemia/reperfusion in cardiovascular surgery. However, in trauma patients hypothermia is caused by insufficient heat production due to utilization of ATP under anaerobic metabolic conditions. Low ATP plasma levels combined with hypothermia seem to be a predisposition for post-traumatic complications like organ failure.
Adenosine Triphosphate↗
Adenosine triphosphate synthesis, mitochondrial number and activity, and pyruvate uptake in oocytes after gonadotropin injections.
OBJECTIVE: To determine the effects of gonadotropin injection on the energy generation of mature oocytes. DESIGN: Randomized prospective study. SETTING: Gamete and stem cell biotechnology laboratory at Seoul National University in Korea. ANIMAL(S): Twelve- to 15-week-old golden hamsters (Mesocricetus auratus). INTERVENTION(S): Injections of pregnant mare serum gonadotropin (PMSG; 5 or 15 IU), of hCG (5 or 15 IU), or of PMSG and hCG (15 IU of each; PMSG + hCG group) were administered to female hamsters. MAIN OUTCOME MEASURE(S): Adenosine triphosphate (ATP) synthesis, mitochondrial population number and activity, and pyruvate uptake were measured. RESULT(S): Significant (P<.05) differences were found in the ATP levels; compared with the control (no injection), a dramatic increase was detected after injections of 15 IU of hCG or of 15 IU of PMSG and 15 IU of hCG. In the same treatments, the mitochondrial population (mitochondrial DNA copy number) significantly increased, whereas mitochondrial activity measured by the ratio of activated to less-activated mitochondria did not change. A significant increase in pyruvate uptake was detected after the injections of 15 IU of PMSG and 15 IU of hCG. CONCLUSION(S): The change in ATP synthesis activity was a major cause for the adverse effect of gonadotropins on oocyte development in the hamster. The injections of 15 IU of hCG, or of 15 IU of PMSG and 15 IU of hCG, dramatically increased the ATP level, the mitochondrial population number, and pyruvate uptake.
Adenosine Triphosphate↗
The role of adenosine triphosphate, chalones, and specific proteins in controlling tumor growth fraction.
During growth of Ehrlich ascites tumor cells in vivo, the proportion of cells in the S phase of the proliferative cell cycle decreases in a manner analogous to the decreasing growth fraction often associated with the growth of solid tumors. An examination of biochemical parameters that might regulate the growth fraction of Ehrlich ascites tumors by causing accumulation of cells in G1-G0 shows that (a) the tumor progresses from an aerobic to an anerobic state as it approaches the plateau phase of growth, as indicated by lactate dehydrogenase content, but cellular adenosine triphosphate content remains constant; (b) tumor-specific growth inhibitors (chalones) are not detectable in cell-free ascites fluid from plateau-phase tumors; (c) electrophoretically identifiable soluble proteins isolated from tumor cells that have been exposed to labeled amino acids in vivo are qualitatively identical during early and late tumor growth; and (d) ornithine decarboxylase activity increases in a bimodal fashion in the first 10 hr after transplantation of 10(7) cells and then declines rapidly during the first few days of growth. The second (and larger) of the two ornithine decarboxylase increases coincides with the surge of cells from G1-G0 into S phase, suggesting that this enzyme, or the polyamines that it synthesizes, may play a role in controlling the growth fraction of this cell population.
Adenosine Triphosphate↗
Juvenile-onset Parkinsonism as a result of the first mutation in the adenosine triphosphate orientation domain of PINK1.
BACKGROUND: Mutations in the PTEN-induced putative kinase 1 (PINK1) gene at 1p36 have been involved in autosomal recessive early-onset parkinsonism. OBJECTIVE: To describe the clinical and genetic features of the largest kindred reported to date with early-onset parkinsonism associated with the PINK1 gene. DESIGN: Clinical and genetic study. SETTING: Collaborative study. Patients Eight patients from Sudan with particularly early onset (ages 9-17 years) and phenotypes varying from dopa-responsive dystonia-like to typical early-onset parkinsonism. MAIN OUTCOME MEASURES: The PINK1 genotype and Parkinson disease status of all available family members. RESULTS: The disease was caused by a novel mutation, p.A217D, located in the highly conserved adenosine triphosphate orientation site of the PINK1 kinase domain. CONCLUSION: This study extends the phenotypic and molecular spectrum of the PINK1 gene and the geographic origin of patients with PINK1 gene mutations.
Adenosine Triphosphate↗
Diseases of adenosine triphosphate synthesis in children.
There is an expanding understanding of primary genetic oxidative-phosphorylation disorders and the recognition of new multi-system clinical phenotypes in the energy metabolism diseases. Although initially recognized in association with mitochondrial DNA mutations, there is progress in the more laborious identification of nuclear DNA encoded genes relevant to mitochondrial structure and function. More pathogenic mitochondrial DNA and nuclear DNA mutations have been identified. Diagnosis of these disorders is often difficult and relies on a concurrence of findings, including recognition of a variety of clinical signs and symptoms, biochemical marker screening, electron transport chain enzyme measurements, and mitochondrial DNA or nuclear DNA mutation assay of genes relevant to mitochondrial structure, function or adenosine triphosphate metabolic pathways. Clinical diagnostic assessment now can be augmented by physiologic imaging techniques, including nuclear magnetic resonance spectroscopy and positron emission tomography. These capabilities should be increasingly helpful for studies of clinical progression and therapeutic intervention. Biologic studies, in families and patients, are beginning to address the factors of mitochondrial replication and segregation that underlie cellular/tissue heteroplasmy and clinical variability. Most epigenetic factors affecting organ-specific and phenotypic variability, however, remain to be elaborated.
Adenosine Triphosphate↗
Regulation of platelet aggregation and adenosine triphosphate release in vitro by 17beta-estradiol and medroxyprogesterone acetate in postmenopausal women.
Clinical studies have suggested that hormone replacement therapy (HRT) may reduce the risk of coronary heart disease in postmenopausal women. Although progestins are commonly added to HRT preparations for uteroprotection, the perceived beneficial cardiovascular effects of HRT are thought to be mediated predominantly by the estrogen component. Platelets play a critical role in the pathogenesis of atherosclerosis and cardiovascular disease and, hence, it is possible that the cardiovascular effects of estrogens are mediated, at least in part, through inhibition of illicit platelet activation. The aim of this study was to examine the effects of sex steroids on adenosine diphosphate (ADP)-induced platelet aggregation and adenosine triphosphate (ATP) release in vitro in postmenopausal women. In addition, the effects of antiestrogens 14-hydroxy tamoxifen (4-OHT) and ICI 182780] and antiprogestins (RU 486 and ZK 98299) were also investigated. Preincubation of platelet-rich plasma (PRP) with antiestrogens or antiprogestins did not alter subsequent platelet aggregation or ATP release in response to ADP. However, preincubation with 17beta-estradiol (E2) significantly inhibited ADP-mediated platelet aggregation by a mean (+/-SEM) of 37%+/-6% (p = 0.02) and ATP release by 82%+/-6% (p = 0.03), an effect that was reversed by the addition of ICI 182780 or 4-OHT but not RU 486 and ZK 98299. Although the progestin medroxyprogesterone acetate (MPA) also significantly inhibited platelet aggregation (by 28%+/-5%, p = 0.02) and ATP release (by 63%+/-9%, p = 0.02), this inhibition was not reversed by the addition of antiprogestins or antiestrogens. These data show that sex steroids can modulate platelet function in vitro. Furthermore, as platelets are devoid of nuclear components, these findings indicate that estrogens may regulate platelet function through binding to a non-nuclear receptor with ligand-binding properties similar or identical to the wild-type receptor. By contrast, MPA appears to exert its effect through a mechanism that does not involve binding to the "classical" progesterone receptor.
Adenosine Triphosphate↗
Adenosine triphosphate deficiency: a genre of optic neuropathy.
PURPOSE: To offer clinical evidence that deficiency of vitamin B12 may adversely affect the neuronal function of patients who also have the 14,484 mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy (LHON). METHODS: A case of a 27-year-old man with vitamin B12 deficiency and the 14,484 mitochondrial DNA mutation is presented and the literature on causes of some metabolic optic neuropathies reviewed. RESULTS: Visual loss and neurologic symptoms of vitamin B12 deficiency occurred together, at a time when the level of vitamin B12 was subnormal. Vision and other sensory functions began to improve within 2 months of vitamin therapy, and normal vision eventually was restored. CONCLUSIONS: The relatively prompt improvement and the eventual complete recovery of vision following vitamin replacement therapy suggest that the subnormal level of vitamin B12 precipitated visual loss. Given the clinical similarities of subnormal vitamin B12, LHON, and nutritional/tobacco amblyopia, deficiency of adenosine triphosphate might be a unifying etiology for several types of optic neuropathy. This energy hypothesis provides a theoretical basis for the enigmatic phenomena of centrocecal scotomata and recovery of visual function after prolonged blindness.
Adenosine Triphosphate↗
Adeno-associated virus Rep78/Rep68 promotes localized melting of the rep binding element in the absence of adenosine triphosphate.
We have applied fluorescence anisotropy and molecular beacon fluorescence methods to study the interactions between the Adeno-associated virus Rep78/Rep68 protein and the 23-bp Rep binding element (RBE). Rep78/Rep68 stably interacted with both the single- and double-stranded conformations of the RBE, but the interaction mechanisms of single- and double-stranded DNA appeared to be fundamentally different. The stoichiometry of Rep78 association with both the separate top and bottom strands of the RBE was 1:1, and the relative dissociation constant (K(D)) values of these associations were calculated to be 2.3x10(-8) and 3.2x10(-8) M, respectively. In contrast, the stoichiometry of Rep78 association with the double-stranded RBE was 2:1, and the dissociation constant was determined to be 4.2x10(-15) M(2). Moreover, Rep78/Rep68 interaction with the 23-bp duplex RBE appeared to cause localized melting of the double-stranded DNA substrate in the absence of adenosine triphosphate (ATP). This melting activity showed slower kinetics than binding and may contribute to the initiation of ATP-dependent Rep78 helicase activity.
Adenosine Triphosphate↗
Management of detrusor dysfunction in the elderly: changes in acetylcholine and adenosine triphosphate release during aging.
Numerous studies have detailed age-related changes in the structure and function of the bladder that may contribute to the high prevalence of overactive bladder (OAB) in the elderly population, but the relation of these changes to OAB symptoms remains unclear. Physiologic and neurochemical studies have been conducted in human detrusor strips obtained from people of different ages, focusing on potential changes in cholinergic and purinergic neurotransmission, as well as the release and actions of acetylcholine (ACh) from nonneuronal bladder cells. Results from physiologic and microdialysis experiments indicate that purinergic transmission increases with age, whereas cholinergic transmission decreases. These effects are most likely because of decreased release of ACh and increased release of adenosine triphosphate (ATP) from postganglionic parasympathetic axons innervating the bladder. Immunohistochemical experiments showed that choline acetyltransferase in the human detrusor is contained not only in parasympathetic axons, but also in cells of the urothelium. The release of nonneuronal ACh increases with age and detrusor stretch. The age-related increase in purinergic transmission in the detrusor and other data indicating that responses to ATP are increased in detrusor overactivity suggest that purinergic receptor antagonists may provide a useful complement to muscarinic receptor antagonists in the treatment of older patients with OAB. Nonneuronal ACh release may play a key role in the storage phase of the micturition reflex, and this may explain, at least in part, the effectiveness of antimuscarinic agents for the treatment of OAB.
Acetylcholine↗
31P magnetic resonance spectroscopy detection of response-predictive adenosine triphosphate decrease in irradiated radiation-induced fibrosarcoma-1 tumors.
RATIONALE AND OBJECTIVES: In previous phosphorus-31 (31P) magnetic resonance (MR) spectroscopy studies of radiation-induced fibrosarcoma (RIF-1), tumor model single-dose x-ray irradiation was applied at subcurative doses. A more effective x-ray does was used in this study, allowing correlation of treatment efficacy with the early changes observed in the 31P MR spectra of RIF-1 tumors. METHODS: Subcutaneous RIF-1 tumors of 60 mice were examined by 31P MR spectroscopy shortly before a single localized x-ray dose of 40 Gy and at eight times (2, 12, 24, 48, 72, 120, 168, and 216 hours) thereafter. RESULTS: Early increases in the relative concentration of inorganic phosphate and decreases in adenosine triphosphate (ATP), most notably at 2 and 12 hours (each P < 0.00001), were observed that lasted up to 48 hours after irradiation. Phosphomonoester and tumor pH showed decreases that reversed even earlier. Reduction of ATP measured at 48 hours after irradiation was, however, correlated with percent tumor shrinkage observed during the subsequent weeks (r = -0.59; P < 0.00001). CONCLUSIONS: Sustained loss of RIF-1 tumor ATP is predictive of treatment efficacy. Temporary depression of high-energy phosphate in favor of inorganic phosphate does not necessarily lead to cell death.
Adenosine Triphosphate↗
Heparin from intestine and lung source administered in large dose to dogs with acute myocardial ischemia. Similar and dissimilar effects on electrocardiograms and adenosine triphosphate.
Intestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p less than 0.00005), and 76% in number (t = 11.6 p less than 0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p less than 0.008), and 35% in number (t = 3.2 p less than 0.01). The difference between IMH and BLH in ischemic myocardium was a significant adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH-treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.
Acute Disease↗
The adenosine-triphosphate-sensitive potassium-channel opener pinacidil is effective in blood cardioplegia.
BACKGROUND: This study was designed to evaluate the adenosine-triphosphate-sensitive potassium channel opener pinacidil as a blood cardioplegic agent. METHODS: Using a blood-perfused, parabiotic, Langendorff rabbit model, hearts underwent 30 minutes of normothermic ischemia protected with blood cardioplegia (St. Thomas' solution [n = 8] or Krebs-Henseleit solution with pinacidil [50 micromol/L, n = 81) and 30 minutes of reperfusion. Percent recovery of developed pressure, mechanical arrest, electrical arrest, reperfusion ventricular fibrillation, percent tissue water, and myocardial oxygen consumption were compared. RESULTS: The percent recovery of developed pressure was not different between the groups (52.3 +/- 5.9 and 52.8 +/- 6.9 for hyperkalemic and pinacidil cardioplegia, respectively). Pinacidil cardioplegia was associated with prolonged electrical and mechanical activity (14.4 +/- 8.7 and 6.1 +/- 3.9 minutes), compared with hyperkalemic cardioplegia (1.1 +/- 0.6 and 1.1 +/- 0.6 minutes, respectively; p < 0.05). Pinacidil cardioplegia was associated with a higher reperfusion myocardial oxygen consumption (0.6 +/- 0.1 versus 0.2 +/- 0.0 mL/100 g myocardium/beat; p < 0.05) and a higher percent of tissue water (79.6% +/- 0.7% versus 78.6% +/- 1.2%; p < 0.05). CONCLUSIONS: Systolic recovery was not different between groups, demonstrating comparable effectiveness of pinacidil and hyperkalemic warm blood cardioplegia.
Animals↗