Microwave ablation of hepatic tumors abutting the diaphragm is safe and effective.

OBJECTIVE: The purpose of this study was to evaluate the incidence of clinically significant diaphragmatic injuries and local tumor progression after microwave ablation of hepatic tumors abutting the diaphragm. MATERIALS AND METHODS: This retrospective study included 55 peripheral hepatic tumors abutting the diaphragm treated by microwave ablation versus a control group of 15 centrally located tumors. Treated tumors were further subdivided according to the use of artificial ascites (fluid vs no fluid) and whether instilled fluid achieved displacement of the liver surface away from the diaphragm (displaced vs nondisplaced). Measurements of tumor size, distance to the diaphragm, ablation zone size, displacement distance, length of the ablation zone along the liver capsule, diaphragm thickness, diaphragmatic hernia, and local tumor progression were made on pre- and postablation CT and MRI. The electronic medical record was reviewed for patient self-reported pain scores and other symptoms. Data were analyzed by use of the Kruskal-Wallis and Fisher exact tests. RESULTS: There were no cases of diaphragmatic hernia in peripheral or central tumors. Postablation diaphragm thickness was higher in peripheral hepatic tumors than in control tumors. Peripheral tumors had an overall higher incidence of postprocedure shoulder pain (18% vs 0%) and local tumor progression (5.5% vs 0%) compared with control tumors, but these differences did not achieve statistical significance (p = 0.2 and p = 1, respectively). CONCLUSION: Our study shows that microwave ablation of peridiaphragmatic hepatic tumors is safe, without incidence of diaphragmatic hernia, and can be performed with a low rate of local tumor progression.

Antenatal maternally-administered phosphodiesterase type 5 inhibitors normalize eNOS expression in the fetal lamb model of congenital diaphragmatic hernia.

PURPOSE: Pulmonary hypertension (pHTN), a main determinant of survival in congenital diaphragmatic hernia (CDH), results from in utero vascular remodeling. Phosphodiesterase type 5 (PDE5) inhibitors have never been used antenatally to treat pHTN. The purpose of this study is to determine if antenatal PDE5 inhibitors can prevent pHTN in the fetal lamb model of CDH. METHODS: CDH was created in pregnant ewes. Postoperatively, pregnant ewes received oral placebo or tadalafil, a PDE5 inhibitor, until delivery. Near term gestation, lambs underwent resuscitations, and lung tissue was snap frozen for protein analysis. RESULTS: Mean cGMP levels were 0.53±0.11 in placebo-treated fetal lambs and 1.73±0.21 in tadalafil-treated fetal lambs (p=0.002). Normalized expression of eNOS was 82%±12% in Normal-Placebo, 61%±5% in CDH-Placebo, 116%±6% in Normal-Tadalafil, and 86%±8% in CDH-Tadalafil lambs. Normalized expression of ß-sGC was 105%±15% in Normal-Placebo, 82%±3% in CDH-Placebo, 158%±16% in Normal-Tadalafil, and 86%±8% in CDH-Tadalafil lambs. Endothelial NOS and ß-sGC were significantly decreased in CDH (p=0.0007 and 0.01 for eNOS and ß-sGC, respectively), and tadalafil significantly increased eNOS expression (p=0.0002). CONCLUSIONS: PDE5 inhibitors can cross the placental barrier. ß-sGC and eNOS are downregulated in fetal lambs with CDH. Antenatal PDE5 inhibitors normalize eNOS and may prevent in utero vascular remodeling in CDH.

Complications of esophagectomy.

Esophagectomy remains the gold standard curative therapy for the treatment of esophageal cancer. Despite 125 years of evolution, esophagectomy remains a demanding procedure associated with a 5% to 10% mortality and a 50% morbidity rate. Knowledge of the multitude of techniques possible for performing this complex procedure, as well as the host of associated complications, is vital for the practitioner aspiring to treat this challenging disease.

Long term respiratory outcomes of congenital diaphragmatic hernia, esophageal atresia, and cardiovascular anomalies.

Intrathoracic congenital malformations may be associated with long-term pulmonary morbidity. This certainly is the case for congenital diaphragmatic hernia, esophageal atresia and cardiac and aortic arch abnormalities. These conditions have variable degrees of impaired development of both the airways and lung vasculature, with a postnatal impact on lung function and bronchial reactivity. Pulmonary complications are themselves frequently associated to non-pulmonary morbidities, including gastrointestinal and orthopaedic complications. These are best recognized in a structured multidisciplinary follow-up clinic so that they can be actively managed.

[Protective effects of tetrandrine against congenital diaphragmatic hernia in rats].

OBJECTIVE: To study the protective effect of the prenatal use of tetrandrine (TET) against congenital diaphragmatic hernia (CDH) in rats and possible mechanisms. METHODS: Pregnant female Sprague-Dawley rats were randomly divided into 3 groups: control, nitrofen and TET treatment. The later two groups were administered with nitrofen by gavage on day 9.5 of gestation. On day 18.5 of gestation, TET (30 mg/kg) was given by gavage (once a day, for three days) in the TET treatment group. On day 21 of gestation, parts of pregnant rats were delivered by cesarean section and amniotic fluid was collected. The fetal rats were examined for a diaphragmatic hernia. Lung histologic evaluations with microscope and immunohistochemistry staining of TNF-α were performed. TNF-α in amniotic fluid was detected using ELISA. The remaining pregnant rats were allowed to deliver spontaneously at term. The survival of pup rats was observed until 24 hrs of age. RESULTS: In the nitrofen group, significant lung hypoplasia was presented not only in fetuses with CDH but also in those without CDH. Stronger expression of TNF-α was observed in fetal lungs and amniotic fluid in the nitrofen group, even when CDH was absent. The TET treatment group showed improved lung development compared with the nitrofen group. The incidence of large diaphragmatic hernia in the TET treatment group was lower than that in the nitrofen group (P<0.05), and the expression of TNF-α in fetal lungs and amniotic fluid in the TET treatment group was also lower than in the nitrofen group (P<0.01). The 24-hr survival rate of pup rats in the TET group was higher than that in the nitrofen group (P<0.01). CONCLUSIONS: Prenatal use of TET can improve nitrofen-induced pulmonary hypoplasia, decrease the incidence of large diaphragmatic hernia and increase the survival rate of pup rats, possibly through a reduction in the production of TNF-α in fetal lungs and amniotic fluid in rats with CDH.

Prenatal administration of retinoic acid upregulates connective tissue growth factor in the nitrofen CDH model.

PURPOSE: Recent studies have suggested that retinoids may be involved in the molecular mechanisms of pulmonary hypoplasia (PH) in congenital diaphragmatic hernia (CDH). Connective tissue growth factor (CTGF) plays a key role in foetal lung development and remodelling during later gestation. CTGF knockout mice exhibit PH with similar characteristics to the human and nitrofen-induced PH. Prenatal administration of retinoic acid (RA) has been shown to stimulate alveologenesis in nitrofen-induced PH. In vitro studies have revealed that RA can induce CTGF gene expression. We hypothesized that pulmonary gene expression of CTGF is downregulated during the later stages of lung development, and that prenatal administration of RA upregulates CTGF in the nitrofen CDH model. METHODS: Pregnant rats were exposed to either olive oil or nitrofen on day 9 (D9) of gestation. RA was given intraperitoneally on D18, D19 and D20. Foetuses were harvested on D21 and divided into control, CDH, control + RA and CDH + RA group. Pulmonary CTGF gene and protein expression levels were determined using RT-PCR and immunohistochemistry. RESULTS: On D21, CTGF relative mRNA expression levels were significantly downregulated in CDH group compared to controls. After RA treatment, expression levels of CTGF were significantly upregulated in CDH + RA and control + RA compared to the CDH group. Immunohistochemical studies confirmed these results. CONCLUSION: Downregulation of pulmonary CTGF gene and protein expression during later stages of lung development may interfere with normal alveologenesis in the nitrofen CDH model. Upregulation of CTGF pulmonary gene expression after prenatal RA treatment may promote lung growth by promoting alveologenesis in the nitrofen-induced CDH model.

Late administration of antenatal vitamin A promotes pulmonary structural maturation and improves ventilation in the lamb model of congenital diaphragmatic hernia.

PURPOSE: The lungs in congenital diaphragmatic hernia (CDH) are hypoplastic and immature making respiratory support one of the most challenging aspects of caring for these neonates. Vitamin A is essential for normal lung growth and development. It also promotes alveolarization. The aim of this study is to investigate the effects of antenatal vitamin A on lung growth and alveolarization and ventilation in the lamb model of CDH. METHODS: This study was approved by the Animal Care Committee of the State University of New York at Buffalo, and conforms to the National Institute of Health guidelines. Diaphragmatic defects were created at 79-81 days gestation. Group 1 lambs (CDH, n = 5) were untreated. In group 2 (CDH + vitamin A, n = 6) and group 3 lambs (control + vitamin A, n = 3) right jugular venous catheters were inserted at 118-120 days and retinyl palmitate (vitamin A) was administered until 135 days. The control group (n = 5) consisted of twin littermates. Lambs were delivered at 136-139 days and ventilated for 2 h according to a set protocol. The left lungs were harvested and fixed for histology. RESULTS: Lung compliance was significantly higher in CDH + vitamin A (median 0.27, range 0.1-0.48 ml/cmH(2)O/kg) versus CDH lambs (median 0.07, range 0.07-0.18 ml/cmH(2)O/kg), P < 0.05. At 1 h CDH + vitamin A lambs experienced significantly lower PaCO(2) (median 115, range 35-194 mmHg vs. median 192, range 168-234 mmHg) and higher arterial pH (median 7.0, range 6.74-7.35 vs. median 6.73, range 6.5-6.81) than CDH lambs, P < 0.05. The lung weight to body weight ratio of CDH + vitamin A lambs was significantly less than that of CDH lambs (P < 0.05). Histology showed small thick walled air-spaces and no true alveoli in CDH lambs. In contrast, true alveoli and thinning of the inter-alveolar septums were seen in CDH + vitamin A lambs. CONCLUSION: This is the first study to demonstrate an improvement in lung function and structural maturation when antenatal vitamin A is given in a surgical model of CDH.

Prenatal retinoic acid treatment upregulates late gestation lung protein 1 in the nitrofen-induced hypoplastic lung in late gestation.

PURPOSE: Pulmonary hypoplasia (PH), the leading cause of mortality in congenital diaphragmatic hernia (CDH), is associated with arrested alveolarization. Late gestation lung protein 1 (LGL1) plays a crucial role in the regulation of alveolarization. Inhibition of LGL1 impairs alveolar maturation in fetal rat lungs. LGL1 heterozygotus knockout mice display delayed lung maturation. It is well known that prenatal administration of retinoic acid (RA) stimulates alveologenesis in nitrofen-induced PH. In vitro studies have reported that RA is a key modulator of LGL1 during alveologenesis. We hypothesized, that pulmonary gene expression of LGL1 is downregulated in the late stage of lung development, and that prenatal administration of RA upregulates pulmonary LGL1 expression in the nitrofen CDH model. METHODS: Pregnant rats were exposed to nitrofen on day 9 (D9) of gestation. RA was given intraperitoneally on D18, D19 and D20. Fetal lungs were dissected on D21 and divided into control, control + RA, CDH and CDH + RA group. Expression levels of LGL1 were determined using RT-PCR and immunohistochemistry. RESULTS: On D21, LGL1 relative mRNA expression levels were significantly downregulated in CDH group compared to controls. After RA treatment, gene expression levels of LGL1 were significantly upregulated in CDH + RA and control + RA compared to CDH group. Immunohistochemical studies confirmed these results. CONCLUSION: Downregulation of pulmonary LGL1 gene expression in the late stage of lung development may interfere with normal alveologenesis. Upregulation of LGL1 pulmonary gene expression after RA treatment may promote lung growth by stimulating alveologenesis in the nitrofen CDH model.

Downregulation of Midkine gene expression and its response to retinoic acid treatment in the nitrofen-induced hypoplastic lung.

PURPOSE: Nitrofen-induced congenital diaphragmatic hernia (CDH) model has been widely used to investigate the pathogenesis of pulmonary hypoplasia (PH) in CDH. Recent studies have suggested that retinoids may be involved in the molecular mechanisms of PH in CDH. Prenatal treatment with retinoic acid (RA) has been reported to improve the growth of hypoplastic lung in the nitrofen CDH model. Midkine (MK), a RA-responsive growth factor, plays key roles in various organogenesis including lung development. In fetal lung, MK mRNA expression has its peak at E13.5-E16.5 and is markedly decreased during mid-to-late gestation, indicating its important role in early lung morphogenesis. We designed this study to investigate the hypothesis that the pulmonary MK gene expression is downregulated in the early lung morphogenesis in the nitrofen-induced PH, and to evaluate the effect of prenatal RA treatment on pulmonary MK gene expression in the nitrofen-induced CDH model. METHODS: Pregnant rats were exposed to either olive oil or nitrofen on day 9 of gestation (D9). Fetal lungs were harvested on D15, D18, and D21 and divided into control, nitrofen with or without CDH [CDH(+) or CDH(-)]. In addition, RA was given on days D18, D19, and D20 and fetal lungs were harvested on D21, and then divided into control + RA and nitrofen + RA. The pulmonary gene expression levels of MK were evaluated by real-time RT-PCR and statistically analyzed. Immunohistochemistry was also performed to examine protein expression/distribution of MK in fetal lung. RESULTS: The relative mRNA expression levels of MK were significantly downregulated in nitrofen group compared to controls at D15 ((§)p < 0.01), whereas there were no significant differences at D18 and D21. MK gene expression levels were significantly upregulated in nitrofen + RA (0.71 ± 0.17) compared to the control (0.35 ± 0.16), CDH(-) (0.24 ± 0.15), CDH(+) (0.39 ± 0.19) and control + RA (0.47 ± 0.13) (*p < 0.05). Immunoreactivity of MK was also markedly decreased in nitrofen lungs compared to controls on D15, and increased in nitrofen + RA lungs compared to the other lungs on D21. CONCLUSION: Downregulation of MK gene on D15 may contribute to primary PH in the nitrofen CDH model by disrupting early lung morphogenesis. Upregulation of MK gene after RA treatment in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential to rescue PH in CDH through RA-responsive growth factor signaling.

Understanding abnormal retinoid signaling as a causative mechanism in congenital diaphragmatic hernia.

Congenital diaphragmatic hernia (CDH) is a frequently occurring source of severe neonatal respiratory distress. It has been hypothesized that abnormal retinoid signaling contributes to the etiology of this developmental anomaly. Here, we use rodent models toward specifically understanding the role of retinoid signaling in the developing diaphragm and how its perturbation is a common mechanism in drug-induced CDH. This includes monitoring of retinoic acid (RA) response element (RARE) activation with RARE-lacZ mice, RA supplementation studies, systematic analyses of the expression profile of key elements in the RA signaling pathway within the developing diaphragm, and the in utero delivery of a RA receptor (RAR) antagonist. These data demonstrate the timing of RARE perturbation by CDH-inducing teratogens and the efficacy of RA supplementation. Furthermore, a detailed profile of retinoid binding proteins, synthetic enzymes, and retinoid receptors within primordial diaphragm cells was obtained. The expression profile of RAR-alpha was particularly striking in regard to its overlap with the regions of primordial diaphragm affected in multiple CDH models. Blocking of RAR signaling with the pan-RAR antagonist BMS493 induced a very high degree of CDH, with a marked left-right sidedness that depended on the timing of drug delivery. Collectively, these data demonstrate that retinoid signaling is essential for normal diaphragm development, providing further support to the hypothesis that abnormalities related to the retinoid signaling pathway cause diaphragmatic defects. This study also yielded a novel experimental model that should prove particularly useful for further studies of CDH.

Effect of prenatal tetrandrine administration on transforming growth factor-beta1 level in the lung of nitrofen-induced congenital diaphragmatic hernia rat model.

PURPOSE: Tetrandrine (Tet) is a bisbenzylisoquinoline alkaloid isolated from the root of Stephania tetrandra, which has been used in traditional Chinese medicine to treat patients with silicosis, asthma, and pulmonary hypertension, and others and can be used as a pulmonary therapeutic agent. We hypothesized that it can also improve the lung growth in congenital diaphragmatic hernia (CDH) for its multiple biological effects. There are increasing evidences that suggest transforming growth factor beta1(TGF-beta1) plays a crucial role in fetal lung growth and morphogenesis. The aim of this study was to evaluate the effect of prenatal administration of Tet and to investigate its possible mechanism on the expression of TGF-beta1 in the lung of nitrofen-induced CDH rat model. METHODS: A CDH model was induced in pregnant Sprague-Dawley rats by administration of nitrofen on day 9.5 of gestation (Ed9.5 term, day 22). Tetrandrine (30 mg/kg) was given through gavage (once a day, for 3 days) on Ed11.5. Accordingly, there were 3 groups as follows: control (n = 9), CDH (n = 9), and CDH + Tet (n = 9). All the fetuses were delivered by cesarean delivery on Ed16.5, 18.5, and 21.5, respectively, to check if diaphragmatic hernia existed on each fetus, then the lung tissue weight (LW) and body weight (BW) of each fetus were recorded. Histologic evaluations and TGF-beta1 immunohistochemistry staining in the lung sample were performed for image analysis. RESULTS: Diaphragmatic hernia was observed in 95 of the 112 rat fetuses in CDH and CDH + Tet groups on Ed18.5 and Ed21.5 (84.8%), the incidence between the 2 groups had no statistical significance (P = .642). Lung weight/body weight in the CDH group and the CDH + Tet group were lower than that in the control group (P < .01), and LW/BW in the CDH group was lower than that in the CDH + Tet group (P < .05). Observed under the light microscope and electron microscope, marked hypoplasia of the lungs in fetuses among the CDH groups was observed, in contrast to improvement of the lungs in CDH + Tet fetuses. Statistical differences in morphological parameters (percentage of alveoli area, counting bronchus) were found even on Ed16.5 when diaphragm had not closed (P < .01). The number of type II pneumocytes and lamellar bodies in each group had no significant difference (P > .05). The immunoreactivity of TGF-beta1 in CDH group and CDH + Tet group were markedly stronger than that in the control group (P < .01). In addition, TGF-beta1 expression in the CDH group was stronger than that in the CDH + Tet group (P < .01). CONCLUSION: Nitrofen can interfere with lung development early in the fetal rat development before and separate from diaphragm development, and increased expression of TGF-beta1 in the lung of CDH rat model may suppress lung growth and development. Prenatal treatment with Tet can improve the growth of the lung of the nitrofen-induced CDH fetuses and its mechanism seems to be involved in downregulating the expression of TGF-beta1. It is a likely new approach to treat CDH and its coexistent lung hypoplasia by maternal Tet administration.

Prediction of mortality and need for neonatal extracorporeal membrane oxygenation in fetuses with congenital diaphragmatic hernia: logistic regression analysis based on MRI fetal lung volume measurements.

OBJECTIVE: The purpose of this study was to use logistic regression analysis of prenatal MRI fetal lung volume measurements to calculate mortality and the need for extracorporeal membrane oxygenation (ECMO) therapy among fetuses with congenital diaphragmatic hernia (CDH). SUBJECTS AND METHODS: The fetal lung volume measurements of 65 fetuses with CDH were obtained between 32 and 34 weeks' gestation by means of MRI performed with multiplanar T2-weighted HASTE and true fast imaging with steady-state precession sequences. Logistic regression analysis was used to assess the prognostic value of the fetal lung volume measurements for prenatal prediction of fetal survival and need for neonatal ECMO. RESULTS: Fetal lung volume was a highly significant predictor of survival (p < 0.0001) and neonatal ECMO requirement (p = 0.0006). The mortality was 84% and the ECMO requirement 80% among fetuses with a lung volume of 5 mL. The mortality was 0.4% and the ECMO requirement 20% among patients with a fetal lung volume of 30 mL. CONCLUSION: Logistic regression analysis of MRI fetal lung volume measurements is highly valuable in predicting mortality among neonates with CDH, and it may help to estimate the need for neonatal ECMO. The method is feasible for facilitating parental guidance and may help in choosing postnatal therapeutic options, including ECMO therapy.

[Effects of folic acid fortification in the rates of malformations at birth in Chile]. / Efecto de la fortificación de la harina con ácido fólico sobre la evolución de las tasas de prevalencia al nacimiento de malformaciones congénitas en los hospitales chilenos del ECLAMC.

BACKGROUND: The effects of folic acid fortification on neural tube defects is well known. Other reports show a beneficial effect of the fortification on orofacial clefts, urinary malformations and defects caused by limb reduction. AIM: To determine the changes in prevalence of congenital malformations after the start of flour folic acid fortification in Chile. MATERIAL AND METHODS: The rates of 22 malformations occurring in the maternity of the University of Chile Clinical Hospital and other Chilean hospitals participating in the Latin American Collaborative Study of Congenital Malformations (ECLAMC) were compared before and after the start of flour folic acid fortification. RESULTS: After the start of folic acid fortification a significant reduction in the rates of anencephalia, spina bifida and diaphragmatic hernia, was observed. The rates of all other malformations remained stable or increased. The rates of all malformations at the University of Chile Clinical Hospital had a steady increase until 2005 and were significantly higher than in the rest of hospitals participating in ECLAMC. CONCLUSIONS: Folic acid fortification was associated with an expected reduction in rates of spina bifida and anencephalia and an unexpected reduction in the rates of diaphragmatic hernia.

Tracheal occlusion: a review of obstructing fetal lungs to make them grow and mature.

Fetal lung growth and functional differentiation are affected strongly by the extent that pulmonary tissue is distended (expanded) by liquid that naturally fills developing future airspaces. Methods that prevent normal egress of this lung fluid through the trachea magnify mechanical stretching of lung parenchymal cells, thereby promoting lung development. Indeed, experimental observations demonstrate that in utero tracheal occlusion (TO) performed on fetuses during the late canalicular-early saccular stage potently stimulates pulmonary growth and maturation. In this review, we present the four principle non-human animal models of TO/obstruction and discuss them in relation to their utility in elucidating lung development, in remedying congenital diaphragmatic hernia (CDH) as well as in investigating the stretching effects on growth and remodeling of the fine vasculature.

Efecto de la fortificación de la harina con ácido fólico sobre la evolución de las tasas de prevalencia al nacimiento de malformaciones congénitas en los hospitales chilenos del ECLAMC / Effects of folic acid fortification in the rates of malformations at birth in Chile

Background: The effects of folic acid fortification on neural tube defects is well known. Other reports show a beneficial effect of the fortification on orofacial clefts, urinary malformations and defects caused by limb reduction. Aim: To determine the changes in prevalence of congenital malformations after the start of flour folic acid fortification in Chile. Material and methods: The rates of 22 malformations occurring in the maternity of the University of Chile Clinical Hospital and other Chilean hospitals participating in the Latin American Collaborative Study of Congenital Malformations (ECLAMC) were compared before and after the start of flour folic acid fortification. Results: After the start of folic acid fortification a significant reduction in the rates of anencephalia, spina bifida and diaphragmatic hernia, was observed. The rates of all other malformations remained stable or increased. The rates of all malformations at the University of Chile Clinical Hospital had a steady increase until 2005 and were significantly higher than in the rest of hospitals participating in ECLAMC. Conclusions: Folic acid fortification was associated with an expected reduction in rates of spina bifida and anencephalia and an unexpected reduction in the rates of diaphragmatic hernia.

Differential effects of vitamin A on fetal lung growth and diaphragmatic formation in nitrofen-induced rat model.

Congenital diaphragmatic hernia (CDH) is associated with high neonatal mortality and morbidity due to pulmonary hypoplasia and pulmonary hypertension. Antenatal interventions have been developed in an attempt to reduce the unacceptable mortality rate of CDH. The pathogenesis of pulmonary hypoplasia is not fully understood. It is not clear whether the increase of lung growth would be necessary for diaphragmatic closure. Vitamin A is important for various aspects of lung development. Therefore, the aim of this study was to examine whether antenatal treatment with vitamin A can increase lung growth and reduce the incidence of CDH in a nitrofen-treated rat model. The animals were randomly assigned to four groups: control, vitamin A, nitrofen, and nitrofen/vitamin A (NIP/Vit A). The incidence of CDH in the NIP/Vit A group (54%) was markedly lower than that in the nitrofen-treated group (85%). Although lung weight was decreased in the nitrofen-treated and NIP/vitamin A groups, the fetal lung weight-to-body weight ratio was slightly increased in the NIP/vitamin A group, compared to the nitrofen-treated group. The mRNA levels of lung surfactant proteins were decreased in the NIP/vitamin A group. We conclude that antenatal treatment with vitamin A reduced the incidence of CDH without lung maturation in the nitrofen-induced rat model.

Injection of subphrenic saline during radiofrequency ablation to minimize diaphragmatic injury.

An 82-year-old man with a history of colorectal cancer presented with metastatic disease to the liver (Couinaud segment 8). We describe the techniques that we employed to successfully perform radiofrequency ablation of a liver metastasis near the dome of the diaphragm utilizing subphrenic infusion of normal saline. The aim of this technique was to prevent thermal injury of the diaphragm.

[Treatment arterial hypertension by beta-adrenergic blockers in elderly patients with gastrointestinal disorders]. / Primenenie beta-adrenoblokatorov u pozhilykh bol'nykh s arterial'noi gipertoniei na fone zheludochno-kishechnykh rasstroistv.

Beta-adrenergic blocking agents are applied successfully in patients with arterial hypertension and ischemic heart disease not only in cardiology but also in gastroenterology.