Title: Livro Biofísica Básica – Ibrahim Felippe Heneine, Author: Faculdade Integrada Brasil Amazônia, Name: Livro Biofísica Básica – Ibrahim Felippe Heneine. Home · The two constituent parts of this work has been compiled by utilizing the main source which is Ibrahim Pecevi Efendis’ prominent work entitled Tarih-i Pecevi.

Author: Kagakinos Kazrakinos
Country: Solomon Islands
Language: English (Spanish)
Genre: Education
Published (Last): 21 July 2016
Pages: 166
PDF File Size: 15.38 Mb
ePub File Size: 6.30 Mb
ISBN: 158-1-94574-549-4
Downloads: 5991
Price: Free* [*Free Regsitration Required]
Uploader: Bralar

After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well.

This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome.

Hypothermic and normothermic patients had similar SB levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and SB and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases ibtahim activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.

The first 3 days after CA are considered the critical phase of PCAS, when patients develop progressive organ damage and increased inflammation [ 1 ]. Generation of ROS, especially superoxide biofisida, increases dramatically after reperfusion and depends on xanthine oxidoreductase XOR and other pathways [ 45 ].

Post-CA hypoxia leads not only to oxidative stress but also to marked metabolic acidosis. Anaerobic glycolysis decreases the glucose concentration within the tissues, while increasing lactate formation. Concomitantly, a compensatory mechanism to restore pH increases the levels of calcium, sodium, and other electrolytes, such as potassium and magnesium [ 7 ]. Elevated blood lactate levels are found in patients with poor outcome after CA, since these levels are associated with the time to achieve ROSC [ 8 ].

Mild biofiaica hypothermia MTH has been the only clinical treatment applied to reduce post-CA injury, and clinical basicaa animal model studies have supported the ibrwhim of MTH for improving brain recovery [ 9 — 11 ]. MTH also prevents damage to other tissues, including the myocardium, liver, and kidney [ 12 ]. Damage protection by MTH is reinforced by studies demonstrating reduced oxidative damage after treatment [ 11 — 13 ].

Hypothermia may also be involved in preventing acidosis and lactate clearance, thereby restoring normal metabolism [ ibbrahim15 ].

The hospital has beds and 59 ICU beds and treats approximately 25, patients per year. The study was approved by the institutional ethics committee, and written informed consent was obtained from the relatives of all participants. Patients were assigned to MTH according to the availability of the room equipped for this purpose. The full medical history of each patient was evaluated. Long-term survival was followed for 3 years after CA by telephone contact with the patient or family members. Body temperature was measured continuously by an esophageal temperature probe.

Clinical data analysis included blood pressure, internal body temperature, heart rate, and respiratory rate. Laboratory data were assessed in venous blood by the hospital biochemistry staff and included pH, glucose, lactate, and electrolyte levels. High-sensitivity C-reactive protein hs-CRPhematocrit, and hemoglobin gasica were analyzed daily by the hospital biochemistry staff.

Venous blood was drawn from the central venous biofislca for analysis of oxidative stress and neuronal injury biomarkers. Biofisjca were lysed and diluted 1: All assays were performed in triplicate. The results were normalized for total protein content by the Bradford method, using bovine serum albumin as standard [ 23 ].


Pairwise comparisons of estimated means by Bonferroni post hoc were used. Two-tailed Spearman’s correlation was used lbrahim examine the relationship between variables, and the GNU Image Manipulation Program, version 2. Baseline characteristics of patients are shown in Table 1. Age baisca sex did not differ significantly between normothermic and hypothermic patients.

Biofísica básica – Ibrahim Felippe Heneine – Google Books

ROSC also did not differ between groups, indicating that participants had similar baseline characteristics in both groups Table 1. Baseline characteristics of 42 comatose in- and out-of-hospital cardiac arrest patients. A total of 42 patients were included in the study. Blood hs-CRP levels, biofidica biomarker of inflammation, were not significantly altered by hypothermia treatment.

Livro Biofísica Básica – Ibrahim Felippe Heneine

Other important biomarkers of outcome after CA were evaluated, including blood levels of calcium, sodium, glucose, and lactate. The levels of lactate, calcium, sodium, and pH were not altered in hypothermic patients. Serum SB levels, a biomarker of brain injury, did not differ significantly in hypothermic patients.

MTH clearly reduced the oxidative damage parameters evaluated in the present study. Plasma carbonyl levels, a biomarker of protein oxidative damage, decreased significantly in patients treated with hypothermia at all time points after CA.

Likewise, hypothermic patients had decreased serum MDA levels, a biomarker of lipid oxidative damage, at all time points after CA Figure 1. XO activity did not differ significantly between hypothermic and normothermic patients. Schematic representation of the correlation analysis of xanthine oxidase XO activity.

Lines indicate positive solid lines and negative dotted lines correlations. The activities of antioxidant enzymes related to the detoxification of ROS were significantly altered by hypothermia treatment.

Surprisingly, PON1 activity, an antioxidant enzyme present in high-density lipoproteins, showed an inverse profile as compared to all other antioxidant enzymes under analysis. The activities of erythrocyte antioxidant enzymes were strongly correlated. The present study evaluated the effects of MTH on oxidative damage and antioxidant profile in post-CA patients. The results suggest that MTH reduces oxidative damage and increases the activity of most of the analyzed antioxidant enzymes.

Oxidative stress has been implicated as a crucial factor in organ damage and hemodynamic dysfunction during PCAS, and, in this setting, MTH may be a suitable treatment option to reduce oxidative stress. Interestingly, after rewarming, d-ROM levels returned to control-group levels, different from the results reported in the present study, where MDA and carbonyl levels remained lower in the hypothermic group even after rewarming.

It is a different methodological approach compared to carbonyl and MDA levels, specific markers of the oxidation of amino acids residues and lipids, respectively. In a porcine model of CA, MTH also reduced serum reactive oxygen metabolite levels compared to animals under controlled normothermia [ 12 ].

To the best of our knowledge, no previous study has reported on protein carbonyl as a marker of oxidative damage after CA. These results support the hypothesis that oxidative damage is reduced by MTH.

Further ibeahim are needed to elucidate the effect of temperature on XOR regulation. Hypoxic acidosis plays a relevant role in XOR regulation [ 31 ], but its exact mechanism of action has yet to be described.

During post-CA acidosis, blood calcium, sodium, and other electrolytes are increased as a compensatory mechanism for high lactate levels [ 7 ].

Interestingly, the present results show that XO activity was positively correlated with lactate and inversely correlated with pH, calcium, and sodium, suggesting that Basoca regulation might have been related to acidosis in our patients. Although XO activity did not correlate with oxidative damage biomarkers in the present study, it was positively correlated with SB levels. Despite our initial vasica that XO activity would correlate with MDA and bilfisica levels, it is possible that the different profiles found in XO activity as compared to the markedly low carbonyl and MDA levels in the hypothermic group may explain this lack of correlation.


MTH decreased the plasma biological antioxidant potential BAP during treatment in post-CA patients, returning to control levels after rewarming [ 13 ]. The BAP provides a global measurement of many enzymatic and nonenzymatic antioxidants together, indistinctly. Data from basjca studies do not support our results; however, instead of using the BAP test, we used specific methods for each antioxidant enzyme. Moreover, there was no correlation between serum PON1 activity and erythrocyte enzymes.

After MTH was recommended by international resuscitation guidelines [ 3435 ], many studies began to point out that the reduction of neuronal damage by MTH is based on the control of body temperature rather than on hypothermia per se.

Livro Biofísica Básica – Ibrahim Felippe Heneine – PDF Free Download

However, other studies have pointed out the benefits of MTH by comparing hypothermic to controlled normothermic temperature management. Interestingly, the levels of the marker of neuronal injury, neuron-specific enolase, were not altered by hypothermia [ 12 ].

Although SB is considered a better marker of poor neurological outcome as compared to neuron-specific enolase [ 37 ], in the present study, SB levels were not altered by MTH as well. Hs-CRP levels, widely used as marker of inflammation, were not altered by hypothermia. Its levels are inside the range expected for CA patients submitted to MTH [ 38 ]; however, no previous studies comparing hs-CRP levels in normothermia versus hypothermia patients were found.

Decreased glucose and elevated lactate levels are well known after CA due to anaerobic glycolysis [ 7 ].

Although it is known that hypothermia increases glucose concentration, parsimony is required to evaluate glucose data in post-CA patients, since glucose levels are actively controlled in the Bqsica.

High lactate levels and impaired lactate clearance are frequently associated with poor outcome after CA [ 1639 ]. Lactate levels play an important role in the metabolic acidosis consequent of CA, and the acidosis may be attenuated by increased calcium and sodium levels [ 7 ].

In the present study, pH, lactate, calcium, and sodium were not altered by MTH, suggesting hypothermia may not contribute to the attenuation of post-CA acidosis. The main limitation of this study is the lack of a control group of patients who did not undergo CA, making it difficult to discuss the influence of CA alone on oxidative stress parameters.

The study is also limited by the lack of pre-CA biochemical and biodisica data, which could not be obtained due to the large number of out-of-hospital CA patients. Another limitation relates to differences in medication, since hypothermic patients received specific medication during MTH. Due to the high complexity of and time required for sample collection, the small number of patients, especially in the hypothermic group, is an important limitation.

Moreover, hypothermia and acidosis may alter XO activity after CA. Altogether, the present ibrahik support our initial hypothesis by providing strong evidence that hypothermia can reduce oxidative stress in post-CA patients.

The authors alone are responsible for the content and writing of this paper. Hackenhaar conducted the research, analyzed the data, and wrote the paper; Fernanda S. Guerra and Carlos A. Vieira, and Mara S. Benfato designed and supervised the study.

National Center for Biotechnology Information baxica, U. Oxid Med Cell Longev. Published online May 1. Medeiros12 Fernanda M. Heemann12 Camile S. Behling12 Jordana S. Putti12 Camila D.

Subscribe US Now