Gastric microcirculatory disturbance and behaviour of leucocytes after thermal injury: Intravital observation of arteriovenous shunting channels in the gastric submucosal layer

In order to investigate the pathogenesis of acute gastric mucosal lesion after thermal injury, microcirculatory disturbance was assessed and observation of the behaviour of leucocytes was performed. Gastric blood flow decreased at 15 min post-thermal injury, and partially improved at 2 h; however, it decreased again at 5 h post-thermal injury. Mucosal microcirculatory disturbance was observed by using vascular labelling with monastral blue B. Deposits of monastral blue B were observed centring mainly on collecting venules but were also observed in the capillaries. Submucosal microcirculatory disturbance was observed through an intravital microscope. The irregularity of the wall and segmental constriction in the venules and presence of an arteriovenous shunting channel was observed in the submucosal layer at 5 h post-thermal injury. The percentage of rolling or sticking leucocytes that passed the confluence of a prevenule and a venule were significantly increased at 5 h after thermal injury. The present study revealed depression of gastric blood flow, mucosal and submucosal microcirculatory disturbance, and a significant increase of rolling and sticking leucocytes in the peripheral part of venules after thermal injury. Leucocyte-endothelial interactions may occur under such conditions and this interaction may play an important role in inducing the microcirculatory disturbance that results in an acute gastric mucosal lesion after thermal injury. The present study also demonstrated the possibility of intravital study of gastric submucosal arteriovenous shunting channels.     

EFFECT OF I.V. LOW-DOSE ADRENALINE AND PHENYLEPHRINE INFUSIONS ON PLASMA CONCENTRATIONS OF BUPIVACAINE AFTER LUMBAR EXTRADURAL ANAESTHESIA IN ELDERLY PATIENTS

Thirty patients undergoing primary total hip replacement underlumbar extradural anaesthesia with 0.75% bupivacaine 25ml wereallocated randomly to receive either low-dose adrenaline orpheny/ephrine infusions i.v. throughout surgery. Haemodynamicmeasurements and arterial blood samples were obtained beforethe extradural injection and at 10, 20, 30, 40, 50, 60 and 90min thereafter. Peak arterial plasma concentrations of bupivacainewere observed 10 min after extradural anaesthesia and were significantlylower in patients receiving adrenaline infusions. Cardiac outputwas significantly greater in patients receiving adrenaline infusions(P < 0.01). It is postulated that the smaller circulatingconcentrations of bupivacaine observed in patients receivingadrenaline were caused by increased cardiac output and a greatervolume of distribution than in patients receiving phenyl-ephrine. Presented at The IX Annual Congress of the European Societyof Regional Anaesthesia, Bern, Switzerland, September 1990.     

LEARNING CURVE AND CONVERSION TO OPEN SURGERY IN CASES OF LAPAROSCOPIC ADRENALECTOMY AND NEPHRECTOMY

Purpose

We examine how the level of experience acquired by the laparoscopist affects the outcome of laparoscopic adrenalectomy and nephrectomy, and what is necessary to avoid complications in these surgeries.

Materials and Methods

We retrospectively evaluated the experience levels of 8 urological laparoscopists between 1991 and 1995. In addition, other cases that were converted to open surgery were collected from the institutes with which the 8 laparoscopists were affiliated.

Results

The rates of conversion to open surgery were 6.4% in 204 cases of adrenalectomy and 14.3% in 63 of nephrectomy. Conversion rates were related to blood loss volume but not operative time. The major causes of conversion were bleeding in 45% of cases and adhesion in 34%. There were no mortalities. Mean operative time decreased significantly, reaching that of open surgery as the number of procedures increased up to 20 adrenalectomies and 10 nephrectomies. The volume of blood lost remained low from the early experience. Blood transfusion rates were 4.4% for adrenalectomy and 11.1% for nephrectomy.

Conclusions

Operative time of these procedures decreased significantly with surgeon experience and reached that of open surgery. Cases in which adhesion is anticipated should be restricted to avoid conversion. These laparoscopic procedures are acceptable as a standard operative techniques for adrenal and renal diseases.     

美国国家骨髓库20年回顾:成人无关供者造血干细胞移植

自1987年起,美国国家骨髓库(NMDP)提供了>30 000份URD-HCT,其中70%以上的受者是患有恶性血液病或获得性血液疾病的成人.在此期间发生很大变化,包括无偿捐献队伍的扩大、PBSCs采集、脐血库(UCB)的加入、HLA分型技术的进步、新药物的使用、低强度预处理(RIC)以及移植后免疫调节等.本文就过去20年NMDP成人受者HCT的数据及分析作一介绍.     

Capsaicin-evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation

Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague-Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10-300 microm), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 microm). The specific, capsaicin receptor antagonist, capsazepine (300 microm), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.     

Afferent drive elicits ongoing pain in a model of advanced osteoarthritis

Osteoarthritis (OA) is a chronic condition characterized by pain during joint movement. Additionally, patients with advanced disease experience pain at rest (ie, ongoing pain) that is generally resistant to nonsteroidal antiinflammatory drugs. Injection of monosodium iodoacetate (MIA) into the intraarticular space of the rodent knee is a well-established model of OA that elicits weight-bearing asymmetry and referred tactile and thermal hypersensitivity. Whether ongoing pain is present in this model is unknown. Additionally, the possible relationship of ongoing pain to MIA dose is not known. MIA produced weight asymmetry, joint osteolysis, and cartilage erosion across a range of doses (1, 3, and 4.8 mg). However, only rats treated with the highest dose of MIA showed conditioned place preference to a context paired with intraarticular lidocaine, indicating relief from ongoing pain. Diclofenac blocked the MIA-induced weight asymmetry but failed to block MIA-induced ongoing pain. Systemic AMG9810, a transient receptor potential V1 channel (TRPV1) antagonist, effectively blocked thermal hypersensitivity, but failed to block high-dose MIA-induced weight asymmetry or ongoing pain. Additionally, systemic or intraarticular HC030031, a TRPA1 antagonist, failed to block high-dose MIA-induced weight asymmetry or ongoing pain. Our studies suggest that a high dose of intraarticular MIA induces ongoing pain originating from the site of injury that is dependent on afferent fiber activity but apparently independent of TRPV1 or TRPA1 activation. Identification of mechanisms driving ongoing pain may enable development of improved treatments for patients with severe OA pain and diminish the need for joint replacement surgery.