Effects of isoproterenol on myocardial lipid metabolism in rat hearts perfused with and without exogenous substrates

Effects of isoproterenol on myocardial lipid metabolism were studied in perfused rat hearts by the Langendorff apparatus without recirculation. Fatty acids in phospholipid, free fatty acid and partial glyceride fractions did not alter during the initial 30-min perfusion. However, fatty acids in triglyceride fraction decreased along with the perfusion. Isoproterenol enhanced the decrease in triglyceride fatty acid in the presence of glucose, but not in the absence of glucose. When hearts were perfused for 30 min with exogenous myristirate in the presence of glucose, triglyceride fatty acid did not decrease in the control perfusion, and incorporation of myristiric acid into triglyceride fraction increased in the presence of isoproterenol. When hearts were perfused with myristirate in the absence of glucose, fatty acid in triglyceride fraction slightly decreased during the control 30-min perfusion, and marked bradycardia or ventricular arrest occurred within 10 min after the start of perfusion with solution containing isoproterenol. Triglyceride content 10 min after perfusion was not different from the control value. Mechanical performance of hearts with myristirate and isoproterenol improved when the amount of glucose in the perfusing solution was increased. The findings indicate that glucose may play an important role in the mechanical performance of the heart perfused with a solution containing isoproterenol.     

Two cases of coronary artery spasm induced by indocyanine green

There is no evidence in the literature that coronary artery spasm is induced by indocyanine green (ICG). In the present report, we describe 2 cases who developed chest pain with transient ST elevation on electrocardiograms after intravenous administration of ICG.     

Small ileal neurofibroma causing intussusception in a non-neurofibromatosis patient

Neurofibromas in the small intestine are usually accompanied by von Recklinghausen's disease (neurofibromatosis), and usually originate in the intramuscular plexus of Auerbach. We present here a solitary neurofibroma, which caused an ileocolic intussusception, originating in the submucosal plexus of Meissner in a non-neurofibromatosis patient. To our knowledge, there is no previous report of a neurofibroma originating in the plexus of Meissner. This condition was clearly confirmed by macroscopic and microscopic evaluation.     

Role of Intrahepatic Portal-Systemic Shunts in the Reduction of Portal Blood Supply to Liver Cells in Cirrhosis

To assess the role of intrahepatic portal-systemic shunts in the reduction of portal blood supply to the liver cells in cirrhosis, we measured portal venous flow (blood flow in the portal trunk) by the pulsed Doppler flowmeter and intrahepatic portal-systemic shunt index from the counts over the lungs and liver in both the anterior and posterior projections after instillation of 99mTc-macroaggregated albumin in the portal vein, and calculated portal sinusoidal flow (blood flow into the sinusoids via the portal vein), using the equation, (sequence; see text) in 47 patients with posthepatitic cirrhosis, and measured portal venous flow in 63 healthy adults in whom portal sinusoidal flow should be comparable to portal venous flow. Portal sinusoidal flow was significantly reduced in cirrhotics with an intrahepatic portal-systemic shunt index averaging 24%, whereas portal venous flow was similar in the cirrhotics and control. There was a significant inverse correlation between intrahepatic portal-systemic shunt index and portal sinusoidal flow. When cirrhotics were divided into three stages, based on Child's grading, intrahepatic portal-systemic shunt index was significantly increased in the group order of Child's A (8 +/- 9%), Child's B (27 +/- 22%), and Child's C patients (46 +/- 19%), and portal sinusoidal flow was decreased in the same order. Portal sinusoidal flow was significantly reduced in Child's B and Child's C patients, but not in Child's A patients, compared with the control. In conclusion, intrahepatic portal-systemic shunts may play a role, at least in part, in the reduction of portal blood supply to the liver cells in patients with advanced stage of posthepatitic cirrhosis when large intrahepatic portal-systemic shunts develop.     

Flowcharts for the management of biliary tract and ampullary carcinomas

No strategies for the diagnosis and treatment of biliary tract carcinoma have been clearly described. We developed flowcharts for the diagnosis and treatment of biliary tract carcinoma on the basis of the best clinical evidence. Risk factors for bile duct carcinoma are a dilated type of pancreaticobiliary maljunction (PBM) and primary sclerosing cholangitis. A nondilated type of PBM is a risk factor for gallbladder carcinoma. Symptoms that may indicate biliary tract carcinoma are jaundice and pain in the upper right area of the abdomen. The first step of diagnosis is to carry out blood biochemistry tests and ultrasonography (US) of the abdomen. The second step of diagnosis is to find the local extension of the carcinoma by means of computed tomography (CT), magnetic resonance imaging (MRI), magnetic resonance cholangiopancreatography (MRCP), percutaneous transhepatic cholangiography (PTC), and endoscopic retrograde cholangiopancreatography (ERCP). Because resection is the only way to completely cure biliary tract carcinoma, the indications for resection are determined first. In patients with resectable disease, the indications for biliary drainage or portal vein embolization (PVE) are checked. In those with nonresectable disease, biliary stenting, chemotherapy, radiotherapy, and/or best supportive care is selected.     

Functional heterogeneity of colony-stimulating factor-induced human monocyte-derived macrophages

Objectives:   Macrophages (Mφs) have various functions and play a critical role in host defense and the maintenance of homeostasis. Mφs exist in every tissue in the body, but Mφs from different tissues exhibit a wide range of phenotypes with regard to their morphology, cell surface antigen expression and function, and are called by different names. However, the precise mechanism of the generation of macrophage heterogeneity is not known. In the present study, the authors examined the functional heterogeneity of Mφs generated from human monocytes under the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage-CSF (M-CSF).
Methodology:   CD14 positive human monocytes (Mos) were incubated with M-CSF and GM-CSF for 6–7 days to stimulate the generation of M-CSF-induced monocyte-derived Mφs (M-Mφs) and GM-CSF-induced monocyte-derived Mφs (GM-Mφs), respectively. The expression of cell surface antigens and several functions such as antigen presenting cell activity, susceptibility to oxidant stress, and the susceptibility to HIV-1 and mycobacterium tuberculosis infection were examined.
Results:   GM-Mφs and M-Mφs are distinct in their morphology, cell surface antigen expression, and functions examined. The phenotype of GM-Mφs closely resembles that of human Alveolar-Mφs (A-Mφs), indicating that CSF-induced human monocyte-derived Mφs are useful to clarify the molecular mechanism of heterogeneity of human Mφs, and GM-Mφs will become a model of human A-Mφs.     

Significance of coronary artery tone assessed by coronary responses to ergonovine and nitrate

The coronary artery response to ergonovine (EM) and nitrate of the proximal, middle and distal segments of the three major coronary artery branches and the main trunk was quantified in 67 patients without coronary spasm and in 69 patients with coronary spasm without significant organic stenosis. The changes in control diameter and diameter after EM administration compared to diameter after nitrate were used as the index of coronary artery tone. EM increased coronary artery tone regardless of the occurrence of coronary spasm (p less than 0.01). In all segments, basal coronary artery tone was greater in patients with spasm than in patients without spasm (p less than 0.01) in a way similar to the coronary responses to EM (p less than 0.01). In patients with spasm, both coronary artery tone after EM and basal coronary tone were greater in the spastic segments than in the nonspastic segments (p less than 0.01), which were greater than those in patients without spasm (p less than 0.01). Our data suggest that patients with spasm may have increased basal tone, and that coronary artery spasm may be based on increased coronary tone. Clinically, evaluation of the basal tone and response to EM in the entire coronary artery tree may be useful for predicting the presence of coronary artery spasm.     

Effect of the calcium antagonist,diltiazem, on beta-agonist-induced reduction of beta-adrenergic responsiveness in the guinea pig lung

This study was designed to clarify the mechanism of tolerance that occurs during prolonged administration of a beta-agonist in relation to membrane phospholipid degradation and to elucidate the effect of diltiazem, a calcium antagonist. Guinea pigs were divided into 3 groups: (1) control—physiological saline (0.5 ml) was injected once a day for 7 successive days; (2) metaproterenol (Mp)—Mp was injected intraperitoneally (10 mg/kg/day) for 7 successive days; (3) Mp + diltiazem—diltiazem was injected intraperitoneally (20 mg/kg/day) 30 min before Mp injection for 7 successive days. The number of beta-adrenoceptors and the 10⁻⁵ M (−)-isoproterenol-stimulated adenylate cyclase activity were significantly decreased in the metaproterenol group. Diltiazem reduced these decreases. Phospholipase activity was increased and phosphatidylcholine and phosphatidylethanolamine levels were decreased in the metaproterenol group. Diltiazem also reduced these changes. These results suggest that the degradation of membrane phospholipids by phospholipase may be involved in a decrease in beta-adrenergic response caused by successive administration of metaproterenol. Diltiazem protects membrane phospholipids from phospholipase attack, which in turn maintains beta-adrenergic responsiveness. Part of this study was presented at the Annual Meeting of the American Thoracic Society, May 12, 1987, New Orleans, Louisiana     

Aggressive surgical resection for hepatocellular carcinoma with tumor thrombus extending to inferior vena cava and synchronous pulmonary metastasis

We describe a 66-year-old man having hepatocellular carcinoma with tumor thrombus extending into the inferior vena cava and synchronous pulmonary metastasis. He was referred to Chiba University Hospital on May, 2000, complaining of emaciation. Radiological findings showed a huge hepatocellular carcinoma in the entire right lobe and tumor thrombus extended into the intrapericardial inferior vena cava. He also had a solitary pulmonary metastasis in the left pulmonary lobe (stage IVB). Right hemihepatomy was performed under total hepatic vascular exclusion without cardiopulmonary bypass, and tumor thrombus was completely removed. Thoracoscopic wedge resection of pulmonary metastasis was also performed. The patient had an uneventful postoperative course. Histopathological examination revealed that the tumor was moderately differentiated hepatocellular carcinoma The patient is still alive after 26 months with pulmonary recurrence, but without hepatic recurrence. To our knowledge, there has been no reported case of resection for both hepatocellular carcinoma invading the inferior vena cava and synchronous pulmonary metastasis. In conclusion, aggressive surgical resection for advanced hepatocellular carcinoma concomitant with pulmonary resection may bring about better prognosis in highly selected patients.     

Clinical and Portal Hemodynamic Features in Cirrhotic Patients Having a Large Spontaneous Splenorenal and/or Gastrorenal Shunt

Clinical and portal hemodynamic features in 28 cirrhotic subjects with a large spontaneous spleno- and/or gastrorenal shunt were studied in comparison with 30 control cirrhotic cases without such collaterals. Forty-six percent of the former had chronic hepatic encephalopathy, but none of the latter was encephalopathic. These patients with large renal shunts were divided into those with and those without encephalopathy. Large esophageal varices were significantly less common in patients with a large shunt and encephalopathy compared with those who had a large shunt but no encephalopathy, and the control. But there was no significant difference of past variceal bleeding among these three groups. In all those with encephalopathy, part of superior mesenteric venous blood was shunting through these collaterals into the left renal vein or inferior vena cava, but the same was not demonstrable in patients with a large shunt and no encephalopathy and control cirrhotics. In the chronic encephalopathic, portal venous flow was estimated to be less than one-half of that in control cirrhotics, and the portion of superior mesenteric venous blood that was flowing hepatofugally through a large shunt into the left renal vein seemed about the same or greater than the portal venous flow. Thus, a large spontaneous spleno- and/or gastrorenal shunt might prevent development of large esophageal varices but not variceal hemorrhage and it increased a risk of chronic hepatic encephalopathy.