Palliative treatment of malignant ascites by intraperitoneal bleomycin after dialytic ultrafiltration with haemofilter

Dialytic ultrafiltration with haemofilter was performed in 16 patients with malignant ascites refractory to treatment with sodium restriction, diuretic and systemic chemotherapy. A continuous flow of ascitic fluid at a rate of 300–400 ml/min through a haemofilter was maintained by a blood pump. The protein-rich ascitic fluid was re-infused into the peritoneal cavity with sodium and water removed. An average of 5.2 1 of filtrate was removed over a mean interval of 3.5 h. Bleomycin (60 mg) was administered intraperitoneally following the procedure. Complete response was observed in six patients (37.25%) and partial response occurred in four (25%). The remaining patients showed no response. Complications of the dialytic ultrafiltration procedure and toxicity of intraperitoneal administration of bleomycin were minimal. The technique of dialytic ultrafiltration is simple, safe and cost-effective and could be used as an adjuvant therapy for intraperitoneal chemotherapy.     

Intraperitoneal bupivacaine for analgesia after laparoscopic cholecystectomy

Background The effects of intraperitoneal administration of bupivacaine on pain after laparoscopic cholecystectomy were studied in a prospective, double-blind, randomised trial. Methods: Eighty ASA 1 and 2 patients were randomly assigned to one of two groups. Immediately after pneumoperi-toneum was obtained patients in group 1 were given 15 ml of 0.5% bupivacaine injected under direct vision into the hepato-diaphragmatic space, near and above the hepato-duodenal ligament and above the gallbladder. At the end of operation another 15 ml of bupivacaine was injected. Patients in group 2 were given 15 ml of 0.9% saline solution in a similar fashion. Postoperative pain was assessed using a visual analogue scale (VAS 100 mm) at 0.5,4, 8,12 and 24 h after surgery. Analgesic consumption was also recorded.     

In vitro biosynthesis of plasma proteins under ischemic conditions of closed-circuit perfusion of healthy and intoxicated rabbit liver

We are elaborating on the kinetics and mechanisms of septic rabbit liver to de novo biosynthesize acute-phase response (APR) proteins under in vitro conditions of deepening ischemia in reference to their in vivo prevalence in serum and cerebrospinal fluids (CSF) collected at predetermined times. The significance of the data is interpreted as relevant to grafting cadaveric liver into end-stage liver diseased patients and APR-induced ischemic heart diseases (IHD). Hepatic APR was induced by CCl(4)-intubation, and the administration of cholera toxin (CT) or scorpion venom (SV), or both, to rabbits. Hepatic functional efficiency, in terms of biosynthesis of APR proteins in closed circuit perfusion of the isolated intoxicated liver with oxygenated saline or L-15 media paralleled the two-dimensional immunoelectrophoresis (2D-IEP) spectrum of APR serum proteins at time of liver isolation. We are suggesting: (a) in vitro biosynthesis of plasma proteins by isolated perfused liver is the result of in vivo decoded and retained APR inflammatory signals; and (b) decoded inflammatory signals are expressed not withstanding the perfusate's organic composition. Furthermore, 90 min of ischemic perfusion in saline or L-15 medium precipitated mitochondrial aberrations which resulted in further deterioration of de novo biosynthesis of APR plasma proteins. Regardless of the nature of the inflammatory stimuli, mitochondrial aberrations rendered the perfused organ a biologically inert tissue mass that was incapable of resuming biological function upon perfusion with oxygenated L-15 medium. This is most likely due to ischemia-induced irreversible hepatic necrosis. Thus, in vitro aberrations of mitochondrial function(s) critically limit the capability of the isolated liver to resume its organic function to sustain biosynthesis of de novo plasma proteins. Extrapolation of these results to the surgical management of end-stage liver diseases points to the importance of the status and the handling protocol(s) of the cadaver donor liver prior to successful grafting. We conclude that although histology of a cadaver liver may reveal well-preserved hepatic cellular organelles with at least minimal intra- and intercellular communication required for viable hepatic function, we deem it essential to further define acceptable minimal capabilities to de novo biosynthesize plasma proteins by a cadaver liver as a measure of its functional viability and suitability for transplantation. Ultimately, this measure may improve the success of liver transplants with minimal surgical and drug interventions.     

Ability of rosetting or non-rosetting individual control and inflammatory macrophages to kill Escherichia coli X43 intracellularly

An autoradiographic method combined with a rosette technique was used to assess the bactericidal activity of individual control and inflammatory peritoneal macrophages (PM phi) in the presence or absence of expression of Fc receptor for IgG (FcR). There was a lack of FcR reactivity in a certain percentage of both categories of PM phi exposed to E. coli X43, a bacterium which is readily phagocytosed in the presence of specific antibody. Both rosetting and non-rosetting PM phi were capable of phagocytosing E. coli X43, but inflammatory PM phi showed a marked reduction in their capacity to ingest these bacteria compared with control PM phi. Once ingested the E. coli X43 were killed equally well by non-rosetting and rosetting control and inflammatory PM phi.     

Prophylactic interleukin-2 increases the survival rate of mice with acute intraperitoneal infection withStaphylococcus aureus

Laboratory of Cellular Immunity and Laboratory of Bacteriology, Department of Laboratory Animals. Oncologic Scientific Center, Russian Academy of Medical Sciences, Moscow. (Presented by Academician of the Russian Academy of Medical Sciences N. N. Trapeznikov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 10, pp. 383–385, October, 1992.     

Dynamics of some indices of blood clotting after intraperitoneal injection of thrombin into noninbred albino rats

The possibility of giving thrombin by intraperitoneal injection as a test of the function of the blood clotting system (the in vivo thrombin test) was demonstrated in experiments on noninbred albino rats.Department of Biochemistry, Tyumen' Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 12, pp. 675–677, December, 1978.     

Pharmacological evidence for stimulation of growth hormone secretion by a central noradrenergic system in dogs

The role of brain catecholamines in the regulation of growth hormone secretion was investigated in pentobarbital-anesthetized dogs by using drugs which modify the function of adrenergic neurons and receptors. Intravenous administration of L-dopa produced a prompt, statistically significant increase in plasma growth hormone concentration. This response was not significantly reduced by blockade of peripheral dopa decarboxylase activity with carbidopa. Clonidine, an alpha-agonist which penetrates the brain, increased plasma growth hormone secretion. Norepinephrine, epinephrine, dopamine and isoproterenol, catecholamines which do not penetrate the blood-brain barrier, failed to affect plasma growth hormone concentration when administered intravenously. Apomorphine did not produce a statistically significant increase in plasma growth hormone concentration when administered directly into the the third ventricle, and pimozide failed to abolish the increase in plasma growth hormone produced by L-dopa. The increase in plasma growth hormone concentration produced by intravenous L-dopa and clonidine was prevented by administration of phentolamine or phenoxybenzamine directly into the third ventricle. The response to L-dopa was also abolished by intraventricular procaine. In dogs in which central beta-adrenergic blockade was produced by intraventricular L-propranolol, the growth hormone response to L-dopa was greater than it was in control dogs treated with intraventricular D-propranolol. The data indicate that in pentobarbital anesthetized dogs, the increase in growth hormone secretion produced by L-dopa is mediated by norepinephrine, rather than dopamine, that the site of action of the norepinephrine is central, above the median eminence and inside the 'blood-brain barrier', and that the norepinephrine acts via alpha-adrenergic receptors.     

顺铂术中腹腔化疗对妇科恶性肿瘤患者术后的近期影响

目的 探讨顺铂术中腹腔化疗治疗妇科恶性肿瘤的可行性。方法 60例妇科恶性肿瘤患者术中腹腔置入100mg顺铂稀释液,观察其对患者术后胃肠功能、体温、切口愈合、腹水控制及术后并发症的影响。结果 术后24h内呕吐发生率增高,但使用止吐剂及水化效果好,尿量达标;胃肠道功能按期恢复;术后发热发生率低;服务部切口无一例丙级愈合;无并发症发生。14例伴发大量腹水患者11例得到控制。肝肾功能未发现损害。结论 术中腹腔化疗比较安全,切实可行。     

Imbalance between intraperitoneal coagulation and fibrinolysis during peritonitis of CAPD patients: the role of mesothelial cells

We compared peritoneal dialysis effluents from 18 CAPD patientswho had not suffered from peritonitis during the last 6 months(group 1) with the effluents from five patients with acute peritonitis(group 2), measuring activation markers of coagulation and fibrinolysis.These markers included prothrombin fragment F1+2 (F1+2), thrombin-antithrombinIII complex (TAT), fibrin monomer (FM), and fibrin degradationproducts (FbDP). In the dialysate of group 1 we found remarkablyhigh levels of F1+2, TAT and FM concomitant with a high concentrationof FbDP, indicating a high rate of intraperitoneal fibrin turnover.The balance between peritoneal generation and degradation offibrin was disturbed in untreated patients of group 2, who hadsignificantly higher levels of coagulation markers and a higherratio between FM and FbDP. Seven days after treatment with intraperitonealadministration of antibiotics and heparin, F1+2, TAT, FM andFbDP decreased significantly. To evaluate the role of mesothelial cells (MC) in the high peritonealfibrin turnover we investigated the expression of tissue-typeplasminogen activator (t-PA), urokinase-type plasminogen activator(u-PA), plasminogen activator inhibitor type-1 (PAI-1), andtissue factor in cultured human peritoneal MC under basal conditionsand after exposure to tumour necrosis factor (TNF) interleukin-1(IL-1), or bacterial lipopolysaccharide (LPS). The exposureof MC to TNF or to a lesser extent IL-1 or LPS reduced theirfibrinolytic activity by decreasing t-PA production and increasingPAI-1 synthesis. Furthermore the addition of TNF resulted inactivation of the coagulation cascade by the expression of tissuefactor. These in-vitro findings explain the imbalance betweenintraperitoneal coagulation and fibrinolysis during peritonitisof CAPD patients.