Abstract Objective: To analyze the inflammation resulting from myocardial revascularization techniques with and without cardiopulmonary bypass, based on ultrasensitive C-reactive protein (US-CRP) behavior. Methods: A prospective non-randomized clinical study with 136 patients was performed. Sixty-nine patients were enrolled for Group 1 (on-pump coronary artery bypass - ONCAB) and 67 patients were assigned to Group 2 (off-pump coronary artery bypass - OPCAB). All study participants had blood samples collected for analysis of glucose, triglycerides, creatinine, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and creatinephosphokinase (CPK) in the preoperative period. The samples of creatinephosphokinase MB (CKMB), troponin I (TnI) and US-CRP were collected in the preoperative period and at 6, 12, 24, 36, 48 and 72 hours after surgery. We also analyzed the preoperative biological variables of each patient (age, smoking, diabetes mellitus, left coronary trunk lesion, body mass index, previous myocardial infarction, myocardial fibrosis). All angiographically documented patients with >70% proximal multiarterial stenosis and ischemia, documented by stress test or classification of stable angina (class II or III), according to the Canadian Cardiovascular Society, were included. Reoperations, combined surgeries, recent acute myocardial infarction, recent inflammatory disease, deep venous thrombosis or recent pulmonary thromboembolism, acute kidney injury or chronic kidney injury were not included. Results: Correlation values between the US-CRP curve and the ONCAB group, the treatment effect and the analyzed biological variables did not present expressive results. Laboratory variables were evaluated and did not correlate with the applied treatment (P>0.05). Conclusion: The changes in the US-CRP at each moment evaluated from the postoperative period did not show any significance in relation to the surgical technique applied.

RESUMO Tumores do mediastino podem crescer lentamente e atingir proporções gigantes sem apresentar sintomas, tornando a remoção cirúrgica problemática. As dimensões exacerbadas da neoplasia dificultam as manobras cirúrgicas, com risco de hemorragia incontrolável e comprometimento de estruturas adjacentes, levando à utilização de medidas de exceção, como a derivação circulatória veno-venosa, a embolização pré-operatória e a circulação extracorpórea total. Diante disto, descrevemos a técnica de laminação tumoral, que permite a ressecção total ou quase total de tumores considerados, muitas vezes, irressecáveis, tendo por base os resultados alcançados em quatro pacientes portadores de neoplasias gigantes do mediastino.

ABSTRACT Mediastinum tumors may grow slowly and reach giant proportions without symptoms, hindering surgical removal. Tumor big dimensions difficult surgical maneuvers, with risk of uncontrollable bleeding and prejudice to surrounding structures. It may be necessary the use of exceptional measures such as venous-venous circulatory deviation, pre-operatory embolization and total extracorporeal circulation. We describe the technique of tumor lamination that allows for complete or almost complete resection of such tumors that in many occasions are not resectable. The description is based on the results of four patients treated with mediastinum giant tumors.

OBJETIVO: Avaliar o efeito do pantoprazol na recuperação funcional de corações isolados de ratos submetidos à isquemia e reperfusão com e sem pré-condicionamento isquêmico. MÉTODOS: Em quatro grupos de oito ratos Wistar, após anestesia os corações foram removidos e perfundidos com Krebs-Henseleit (95% O2, 5% CO2, 37ºC). Os corações de GI, GII, GIII e GIV foram submetidos a 20' de isquemia e 30'de reperfusão. Em GII e GIV realizou-se pré condicionamento com 5' de isquemia e 5' de reperfusão antes dos 20' de isquemia. Em GIII e GIV, pantoprazol 100mcg foram injetados imediatamente antes dos 20' de isquemia. Frequência cardíaca (FC), Fluxo Coronariano (FCo), Pressão Sistólica (PS), + dP/dt e -dP/dt foram registrados em (T0) e (t30). Estatística: Kruskal-Wallis (P <0,05). RESULTADOS: Não houve diferenças (P> 0,05) entre grupos nos valores de FC e de CFo. Diferenças (P <0,05) ocorreram entre GI e GII, GIII e GIV, com PS t30 reduzida para 32% GI, 65% GII, 65% GIII e 73% GIV. Em t30 + dP/dtmax 34% GI, 61% GII, 63% GIII e 72% GIV. A -dP/dtmax t30 GI 28%, GII 63%, GIII 75% e GIV 75%. Não houve diferença estatística (P< 0,05) nos valores de PS, +dP/dtmax e -dP/dtmax entre os GII, GIII e GIV. CONCLUSÕES: A administração do pantoprazol antes da indução da isquemia protegeu significativamente a recuperação funcional miocárdica com resultados de SP, +dP/ dtmax e -dP/dtmax semelhantes aos do pré-condicionamento isquêmico contra lesão de isquemia-reperfusão

OBJECTIVE: To evaluate pantoprazole effect in the functional recovery of isolated hearts of rats, submitted to ischemia and reperfusion with and without ischemic preconditioning. METHODS: In four groups of eight Wistar breed rats, the hearts were removed after anesthesia and perfused with Krebs-Henseleit solution (95% O2, 5% CO2, 37ºC). GI, GII, GIII and GIV hearts were submitted to ischemia (20 min) and reperfusion (30 min). In GII and GIV, preconditioning was performed with 5 min of ischemia and 5 min of reperfusion before 20 min of the ischemia period induction. In GIII and GIV pantoprazole 100 mg was done before a 20 min-period of ischemia induction. Heart Rate (HR), Coronary Flow (CoF), Systolic Pressure (SP), +dP/dt and -dP/dt were registered before (t0) and after reperfusion (t30). Kruskal-Wallis (P<0.05) test was used. RESULTS: There were no differences (P>0.05) between groups among HR and CoF values. Differences occurred between groups, I and II, III and IV at t30 with SP reduced for 32% mean value in GI, 65% GII, 65% GIII, and 73% GIV; The t30 + dP/dtmax were 34% in GI, 61% GII, 63% GIII and 72% GIV. The t30 -dP/dtmax were GI 28%, GII 63%, GIII 75 % and GIV 75%; (P<0.05). There were no significant differences in the SP, +dP/dtmax, and -dP/dtmax between Groups II, III and IV results. CONCLUSIONS: The administration of pantoprazole before induction of ischemia significantly protected the myocardial functional recovery with the results of SP, + dP / dtmax and dP/dtmax similar to the ischemic preconditioning against ischemia-reperfusion

OBJETIVO: Analisar efeitos do omeprazol na proteção da recuperação funcional de corações isolados de ratos submetidos à lesão de isquemia-reperfusão. MÉTODOS: Foram estudados 12 ratos Wistar, peso corpóreo médio de 280g. Após anestesia com injeção intra-abdominal de 10mg de cetamina e 2mg de xilazina, os corações foram removidos e mantidos em perfusão com solução Krebs-Henseleit (95%O2 e 5% CO2, 37ºC, 110-120mmHg de pressão de perfusão e pressão diastólica de 8 mmHg) em sistema Langendorff, modificado, descartável, modelo FCSFA-ServCor (Comex Ltda.). Os seis corações do Grupo I (GI) e os seis do Grupo II (GII) foram submetidos a 20 minutos de isquemia e 30 minutos de reperfusão. Nos corações do Grupo II, imediatamente antes da isquemia, foram administrados via perfusão coronária 200mcg de omeprazol. Foram controlados frequência cardíaca (FC), fluxo coronário (FCo), pressão sistólica (PS), +dP/dt e -dP/dt, após estabilização (t0) e no final da reperfusão (t30). Empregou-se método não paramétrico de Kruskal-Wallis (P<0,05) para análise estatística dos dados. RESULTADOS: Não ocorreram diferenças (P>0,05) entre os valores de FCo e FC nos dois grupos. No final do período de reperfusão (t30), foram significantes (P<0,05) as variações da PS reduzida para 28,0±3,6% do valor inicial (t0) no Grupo I e para 79.0±5,9% no Grupo II; a +dP/dtmax declinou para 31,0±5,6% no GI, mantendo-se em 99,4±11,2% (P<0,05) no GII e a -dP/dtmax declinou para 26,0±7,3% no GI, mantendo-se em 82,0±2, 2% no GII (P<0,05). CONCLUSÃO: A administração do omeprazol antes da indução da isquemia coronária protegeu significantemente a recuperação funcional do miocárdio.

OBJECTIVE: To evaluate the myocardium contractility alterations of isolated hearts of rats, submitted to ischemia and reperfusion with and without administration of the omeprazole. METHODS: Twelve Wistar breed rats with 270g mean body weight was studied. After anesthesia by intraperitoneal injection of ketamine 10mg and xylazine 2mg, their hearts were removed and perfused with Krebs-Henseleit solution (95% of O2 and 5% of CO2, 37ºC, 110-120 mmHg perfusion pressure, 8 mmHg ventricular diastolic pressure) in the São Francisco de Assis disposable Langendorff system model Comex Ltda, MG. The six hearts of Group I (GI) and of the Group II (GII) were submitted to 20 min ischemia and 30 min reperfusion. In GII hearts, intracoronary injection of omeprazole 200 mcg was done immediately before the ischemia period induction. The following parameters were registered after the stabilization period (t0), and after the reperfusion period (t30): heart rate (HR), coronary flow (CoF), systolic pressure (SP), +dP/dt and -dP/dt. The Kruskal-Wallis test (P<0.05) was applied to statistical analysis. RESULTS: There were no significant differences (P>0.05) between groups among HR and CoF values. Differences (P<0.05) occurred between groups, I e II after the reperfusion period (t30) regarding systolic pressure reduced for 28.0±3.6% in the control group GI and for 79.0±5.9% in GII; The +dP/dtmax declined to be only 31.0±5.6% in GI, preserving 99.4±11.2% values in GII (P<0.05). The t30 -dP/dtmax values were GI 26.0±7.3% and GII 82.0±2.2% (P<0.05). CONCLUSION: The omeprazole administration before ischemia induction significantly protected the myocardium function recovery.

OBJETIVO: Estudar os efeitos do benzodiazepínico midazolam no fluxo coronariano (Fco), freqüência cardíaca (FC) e contratilidade miocárdica de corações isolados de ratos submetidos ao precondicionamento isquêmico (PCI). MÉTODOS: Foram utilizados 30 ratos Wistar sem distinção de sexo. Após anestesia com éter etílico, os corações foram postos em perfusão (solução de Krebs-Henseleit, 95% de O2 e 5% de CO2, 37°C, 110-120mmHg), em sistema tipo Langendorff descartável. Foram constituídos cinco grupos de seis animais: GI- Controle; GII- Isquemia; GIII- PCI; GIV- Isquemia + 100mcg de midazolam ; GV- PCI + 100mcg de midazolam. Após estabilização (t0), e nos tempos t5, t10, t15, t20 e t25, foram registrados a FC, Fco, pressões sistólica (PS) e diastólica (PD) e dP/dt. A PD foi mantida em 5 ± 2 mmHg. Empregou-se método estatístico ANOVA e Teste de Tukey para p < 0,05. RESULTADOS: Não ocorreram variações significantes entre FCo e FC. Na dP/dt, ocorreram diferenças (p<0,05) entre os grupos I e II (respectivamente 94,7±23,0 e 62,3±12,1%). O precondicionamento (GIII), melhorou significantemente os resultados do grupo II (respectivamente 62,3±12,1 e 87,1±12,4 %). A queda da dP/dt no grupo II não foi impedida pelo midazolam (GIV) ( 62,3±12,1 e 60,5±15,8 %). No grupo III a dP/dT foi 87,1±12,4%, sendo que no grupo V, apenas 55,5±17,2% (p<0,05). CONCLUSÃO: O midazolan quando administrado antes da isquemia não impediu deterioração isquêmica do miocárdio. Quando administrado antes do precondicionamento aboliu seu efeito protetor.

PURPOSE: To study the effects of benzodiazepine midazolam in the coronary flow (Cflo), cardiac frequency (CF) and myocardial contractility in isolated hearts of rats subjected to ischemic preconditioning (IPC). METHODS: 30 Wistar rats were used, undistinguished by gender. After anesthesia with ethyl ether, the hearts were put into perfusion (Krebs-Henseleit solution, 95% O2 and 5% CO2, 37°C, 110-120mmHg), in disposable Langendorff type system. Five groups of six animals were constituted: GI- Control; GII- Ischemia; GIII- IPC; GIV- Ischemia + 100mcg of midazolam; GV- IPC + 100mcg of midazolam. After stabilization (t0), and on times t5, t10, t15, t20 and t25, CF, Cflo, systolic pressure (SP) and diastolic pressure (DP) and dP/dt were recorded. DP was maintained at 5 ± 2 mmHg. The statistical method ANOVA and Tukey Test were employed for p < 0.05. RESULTS: No significant variations have occurred between Cflo and CF. On Pd/td, differences have occurred (p<0.05) between groups I and II (respectively 94.7±23.0 and 62.3±12.1%). The preconditioning (GIII), improved significantly the results in the group II (respectively 62.3±12.1 and 87.1±12.4 %). The decrease in dP/dt in group II was not prevented by midazolam (GIV) (62.3±12,1 and 60.5±15.8 %). In group III, dP/dt was 87.1±12.4%, whereas in group V, only 55.5±17.2% (p<0.05) CONCLUSION: Midazolam, when administered before the ischemia, was unable to prevent the ischemic deterioration of the myocardium. When administered before the preconditioning, it has abolished its protective effect.