70例心脏骤停后复苏患者格拉斯哥昏迷评分及预后分析

正心脏骤停后综合征(post-cardiac arrest syndrome,PCAS)是指心脏骤停患者在急救复苏之后出现较长时间的严重全身缺血、再灌注损伤综合征等,也包含心脏骤停后脑损伤、心肌功能障碍等持续的致病     

Mu opioid receptor and orexin/hypocretin mRNA levels in the lateral hypothalamus and striatum are enhanced by morphine withdrawal

In this study, we investigated the effects of acute morphine administration, chronic intermittent escalating-dose morphine administration and spontaneous withdrawal from chronic morphine on mRNA levels of mu opioid receptor (MOP-r), and the opioid peptides pro-opiomelanocortin (POMC) and preprodynorphin (ppDyn) in several key brain regions of the rat, associated with drug reward and motivated behaviors: lateral hypothalamus (lat.hyp), nucleus accumbens (NAc) core, amygdala, and caudate-putamen (CPu). There was no effect on MOP-r mRNA levels in these brain regions 30 min after either a single injection of morphine (10 mg/kg, i.p.) or chronic intermittent escalating-dose morphine (from 7.5 mg/kg per day on day 1 up to 120 mg/kg per day on day 10). Activation of the stress-responsive hypothalamic-pituitary-adrenal axis by 12 h withdrawal from chronic morphine was confirmed; both POMC mRNA levels in the anterior pituitary and plasma adrenocorticotropic hormone levels were significantly elevated. Under this withdrawal-related stress condition, there was an increase in MOP-r mRNA levels in the lat.hyp, NAc core, and CPu. Recent studies have demonstrated a novel role for the lat.hyp orexin (or hypocretin) activation in both drug-related positive rewarding, and withdrawal effects. Around 50% of lat.hyp orexin neurons express MOP-r. Therefore, we also examined the levels of lat.hyp orexin mRNA, and found them increased in morphine withdrawal, whereas there was no change in levels of the lat.hyp ppDyn mRNA, a gene coexpressed with the lat.hyp orexin. Our results show that there is an increase in MOP-r gene expression in a region-specific manner during morphine withdrawal, and support the hypothesis that increased lat.hyp orexin activity plays a role in morphine-withdrawal-related behaviors.     

Changes in blood flow and permeability of vessels to protein preceding the development of cutaneous ulcers in the hind limb of the rabbit

The effect of sciatic nerve transection on the cutaneous and muscle nutritive blood flow in the hind limb of rabbits was studied. Vessel permeability to albumin was measured with ¹²⁵I-labeled human serum albumin periodically during the 2 weeks after transection. Cutaneous blood flow was measured with the ¹³³Xe washout technique. Two days after transection a decrease of blood flow was observed. The maximum drop in the blood flow occurred on the seventh day. A sharp increase in permeability to albumin was observed in the denervated leg starting on the fourth day after transection. Microscopic examination shows that peripheral nerve injury is responsible for structure disorders corresponding to the decrease of cutaneous blood flow and increase in the permeability to albumin.     

Differential leptin responses to acute and chronic biliary obstruction in rats

BACKGROUND/AIMS: Recently leptin, a protein released from adipocytes, has been identified as a potent circulating satiety factor. We therefore undertook this series of experiments to examine leptin's role in the anorexia associated with biliary obstruction. METHODS: Rats underwent either surgical bile duct resection (BDR) or sham resection (sham). Body weight, and food and water intake were measured during a baseline period and for 8 days after surgery. At 4, 8 and 16 h as well as on days 2, 4, 6, and 8 postsurgery, sham and BDR rats were sacrificed and sera collected for subsequent measurement of leptin hormone concentration by RIA. White adipose tissue was collected on days 2, 4, 6 and 8 for leptin mRNA determination by Northern blot. RESULTS: Obstructive cholestasis in BDR rats caused significant anorexia for up to 7 days post-surgery, whereas in sham rats, a significant decrease in food intake was only observed in the first 24-h period following surgery. In both sham and BDR rats, water intake was significantly decreased during the first 24-h period after surgery, but had recovered to baseline levels by day 2 in both groups. Fat pad mass corrected to body weight was not significantly different between the two experimental groups. Serum leptin levels were significantly increased 4 and 8 h after surgery, had normalized by 16 h post-surgery, and were then decreased in BDR rats on days 2, 4, 6 and 8 compared with controls. Leptin mRNA levels in epididymal fat pads were decreased by approximately 2-fold in BDR rats compared with sham rats on days 2, 4, 6 and 8. Furthermore, day 5 BDR and sham rats demonstrated similar anorectic responses to centrally administered leptin. CONCLUSIONS: Leptin production is significantly increased early after biliary obstruction but is reduced after prolonged biliary obstruction. Increased circulating leptin levels may contribute to the profound anorexia observed early after biliary obstruction but appear not to mediate the anorexia observed during more chronic biliary obstruction.     

Subcutaneous administration of insulin-like growth factor (IGF)-II/IGF binding protein-2 complex stimulates bone formation and prevents loss of bone mineral density in a rat model of disuse osteoporosis.

Elevated serum levels of insulin-like growth factor binding protein-2 (IGFBP-2) and a precursor form of IGF-II are associated with marked increases in bone formation and skeletal mass in patients with hepatitis C-associated osteosclerosis. In vitro studies indicate that IGF-II in complex with IGFBP-2 has high affinity for bone matrix and is able to stimulate osteoblast proliferation. The purpose of this study was to determine the ability of the IGF-II/IGFBP-2 complex to increase bone mass in vivo. Osteopenia of the femur was induced by unilateral sciatic neurectomy in rats. At the time of surgery, 14-day osmotic minipumps containing vehicle or 2 microg IGF-II+9 microg IGFBP-2/100g body weight/day were implanted subcutaneously in the neck. Bone mineral density (BMD) measurements were taken the day of surgery and 14 days later using a PIXImus small animal densitometer. Neurectomy of the right hindlimb resulted in a 9% decrease in right femur BMD (P<0.05 vs. baseline). This loss in BMD was completely prevented by treatment with IGF-II/IGFBP-2. On the control limb, there was no loss of BMD over the 14 days and IGF-II/IGFBP-2 treatment resulted in a 9% increase in left femur BMD (P<0.05). Bone histomorphometry indicated increases in endocortical and cancellous bone formation rates and in trabecular thickness. These results demonstrate that short-term administration of the IGF-II/IGFBP-2 complex can prevent loss of BMD associated with disuse osteoporosis and stimulate bone formation in adult rats. Furthermore, they provide proof of concept for a novel anabolic approach to increasing bone mass in humans with osteoporosis.     

Persistent sciatic artery: an uncommon cause of intermittent claudication.

Persistent sciatic artery (PSA) is a rarely seen variation of the lower limb vessels. Anatomically the PSA is the continuation of internal iliac arteries. It follows the sciatic nerve from the sciatic foramen to the level of the knee. We report our experience with conservative therapy in a patient with complete occlusion of a PSA. A 54-year-old man with typical symptoms of intermittent claudication on the left limb was referred to our Department. After clinical examination Doppler and duplex sonography were performed. Angiography showed bilateral PSA. On the left side the PSA was occluded. The patient received 20 intravenous courses of prostaglandin E1 for 4 weeks, followed by oral anticoagulation with phenprocoumon for life (INR: 2.5-3.5). After 3 years therapy he does not show any typical symptoms of intermittent claudication or limb ischemia. This case shows that conservative therapy may be effective. However, it has to be emphasised that this approach requires frequent clinical and duplex sonography follow-up every 3 to 6 months with oral anticoagulation.     

Transcutaneous electric nerve stimulation for the treatment of postthoracotomy pain: a randomized prospective study

BACKGROUND: Insufficient relief of postthoracotomy pain is a major cause of increased rates of postoperative complications including inadequate coughing, mucous plugging, hypoxia, compromised ventilation or even bacterial lung infection. We aimed to assess the efficacy of transcutaneous electric nerve stimulation (TENS) in patients with postthoracotomy pain. METHODS: Forty patients scheduled to undergo posterolateral thoracotomy were randomly allocated to receive either TENS or patient-controlled intravenous morphine. Postoperative pain was evaluated using a visual analogue scale (VAS) and the Prince Henry pain scale. Pulmonary function was evaluated and an intergroup comparison was done. RESULTS: On the first three days following surgery, the VAS intensity of the TENS group did not differ significantly from that of the morphine group ( P > 0.05), and on the first two days following thoracotomy, the Prince Henry scale of the TENS group was not statistically significantly different. However, the VAS intensity was significantly lower than that of the control group on the fourth ( P = 0.044), fifth ( P = 0.016), sixth ( P = 0.009), seventh ( P = 0.008), eighth ( P = 0.004), ninth ( P = 0.002), tenth ( P = 0.001), fifteenth ( P = 0.002), thirtieth ( P < 0.001), forty-fifth ( P < 0.001) and sixtieth ( P < 0.001) days. The Prince Henry scale of the TENS group was found to be significantly diminished from the 3rd to the 60th day. TENS significantly reduced the analgesic requirements from day 5 to 60 ( P < 0.01). No noticeable side effect was observed in the TENS group during the study period. CONCLUSION: This study demonstrated that TENS provided a better pain relief and comfort compared to PCA from the fourth postoperative day onwards, and this pain-reducing effect continued for at least two months postoperatively.     

Changes induced by morphine administration in the hypothalmic neurosecretory system of the spotted owlet, Athene brama Temminick.

The effect of chronic administration of morphine, in gradually increasing doses, on the histology of the HNS of the spotted owlet was investigated. Administration of morphine in low doses (0.25-0.75 mg/day), for 9 days, induced marked depletion of NSM from all regions of the HNS, except the zona externa of the AME. Maximum depletion of NSM was noticed in the HNS of birds treated with morphine for 9 days. Beyond the 9th day, the HNS did not exhibit further depletion of its NSM. Administration of morphine in high doses (1.5-4 mg/day), for 18 days, did not cause depletion of NSM from the HNS. On the other hand there was noticeable increase of the NSM in the HNS over that of the controls. The histological changes in the HNS induced by low doses of morphine are comparable to the changes induced by hypertonic saline administration and are presumably indicative of augmented secretion of the ADH. The accumulation of NSM in the HNS of birds receiving high doses of morphine suggests a decrease in neurohypophysial activity. The results therefore indicate that the effect of morphine on the HNS of the spotted owlet is dose-dependent. The mechanism of action of morphine on the neurohypophysis is briefly discussed.     

磁刺激疗法对坐骨神经损伤大鼠神经传导速度及损伤运动神经元内GAP-43表达的影响

目的探讨磁刺激疗法治疗坐骨神经损伤的临床效果及机制。方法将60只SD大鼠随机分为观察组、对照组各24只和假手术组12只,前两组制备坐骨神经损伤模型。制模后观察组给予表面场强为0．09T磁刺激,30min／d,1次／d;其余两组不予干预。各组分别于第2、4、8、12周采用免疫组化法检测L4-L5脊髓运动神经元内生长相关蛋白（GAP-43）表达,于12周末行电生理检查测定神经传导速度（MCV）。结果与对照组比较,观察组各时点GAP-43表达明显升高（P均〈0．05）,术后第12周再生神经传导速度加快、波幅升高、潜伏时缩短（P〈0．05）。结论磁刺激疗法能促进大鼠周围神经损伤后MCV的恢复,其机制可能为增加损伤脊髓运动神经元中GAP-43的表达。     

Treatment of acute hepatic porphyria with hematin

The efficacy of hematin has been evaluated in eight patients with acute intermittent porphyria: six with acute attacks and two with chronic subacute symptoms. Hematin suppressed the chemical signs of porphyria in all patients and the symptoms in those with acute attacks. The clinical response to hematin occurred uniformly on the third or fourth day of treatment, suggesting that a stereotypic response to this form of therapy can be defined. Hematin had no effect on chronic subacute symptoms. The indications for hematin therapy, its rationale and the details of its administration are reviewed.     

Properties of ICI 128,436, a novel aldose reductase inhibitor, and its effects on diabetic complications in the rat

ICI 128,436 (3-(4-bromo-2-fluorobenzyl)-4-oxo-3H-phthalazin-1-ylacetic acid) is a chemically novel, potent inhibitor of aldose reductase. It inhibits partially purified aldose reductase isolated from a number of sources including human tissue (human lens - IC50 2.0 X 10(-8) mol/L). Dulcitol accumulation in erythrocytes and sciatic nerves of galactose loaded rats was inhibited by five days of treatment with ICI 128,436 (oral ED50's 2.21 mg/kg and 8.56 mg/kg, respectively). On oral administration for five days to streptozotocin diabetic rats, ICI 128,436, reduced sorbitol levels in sciatic nerve, lens, retina, and renal cortex. The ED50 for inhibition of nerve sorbitol accumulation was 5 mg/kg. The effect of a single dose of ICI 128,436 in diabetic rats was prolonged, with little increase in nerve sorbitol for 48 hours. No tolerance to the ability of ICI 128,436 to reduce nerve sorbitol was found on treatment for 74 days. ICI 128,436 was effective in rodent models of the neural and lenticular complications of diabetes. At doses as low as 25 mg/kg/d it completely prevented the development of cataracts in diabetic rats. The deterioration in motor nerve conduction velocity velocity found in diabetic rats was ameliorated by treatment with ICI 128,436 (3.125 mg/kg/d). Thus, ICI 128,436 constitutes a chemically novel aldose reductase inhibitor that is now being assessed for therapeutic value in the diabetic patient.     

Effects of growth hormone in rats with postinfarction left ventricular dysfunction

Summary Growth hormone may affect cardiac function. In rats, chronic hypersecretion of growth hormone leads to increased maximum isometric contractile force of the left ventricular papillary muscle in vitro. In humans, administration of growth hormone can increase myocardial contractility. However, cardiac effects of growth hormone in heart failure or cardiac dysfunction have not been studied to date. The current study was to evaluate the cardiac effects of growth hormone in conscious rats with postinfarction left ventricular dysfunction and sham controls. Ligation of the left coronary artery or sham operation was performed, then 4 weeks after surgery, recombinant human growth hormone (2 mg/kg/day, SC) or vehicle was administered for 15 days. Catheters were implanted 13 days after treatment with growth hormone or vehicle. Hemodynamic parameters were measured in conscious rats 2 days after catheterization. In vehicle-treated rats, left ventricular systolic pressure, maximum dP/dt, and arterial pressure were significantly decreased and left ventricular end-diastolic pressure was significantly increased in the ligation group compared with sham controls. Growth hormone treatment increased left ventricular systolic pressure (p<0.05) and dP/dt (p<0.05) and reduced left ventricular end-diastolic pressure (p<0.05), significantly in the ligated rats. In sham rats, growth hormone tended to decrease arterial pressure but did not alter ventricular contractility. Neither ligation nor growth hormone significantly altered heart rate and right atrial pressure. These results suggest that growth hormone treatment may improve cardiac function by increasing myocardial contractility in cardiac dysfunction or heart failure.     

Renin activity and blood pressure in response to chronic episodic hypoxia.

Previous studies in several strains of rats have demonstrated that 35 days of recurrent episodic hypoxia (EH) (7 hours per day), with a fractional concentration of inspired oxygen that produces desaturation equivalent to the recurrent hypoxemia of sleep apnea, results in an 8 to 13 mm Hg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. Both renal artery denervation and adrenal demedullation block the BP response to chronic EH. The present study was undertaken to define further the role of the kidneys and the renin-angiotensin system in this BP increase. Separate groups of male Sprague-Dawley rats had either (1) bilateral renal artery denervation with EH, (2) sham surgery with EH, (3) sham surgery with sham EH (compressed air), (4) EH with losartan, (5) unhandled with losartan, or (6) unhandled. The experimental period lasted 35 days. Both renal-artery denervated and losartan-treated animals showed no BP change or a lowering of BP in response to EH, whereas the sham-operated EH animals showed a progressive, sustained increase in resting room air BP. BP remained at basal levels or fell in unhandled and unhandled losartan-treated animals. Plasma renin activity was elevated 4-fold versus basal levels in EH animals with renal nerves intact but remained at baseline levels in denervated animals. At the end of the experiment, renal tissue catecholamines confirmed renal denervation in those animals. In conclusion, EH causes a progressive increase in BP, mediated in part through renal sympathetic nerve activity that acts to increase renin-angiotensin system activity through angiotensin II type 1 receptors.     

Serotonin blockade in conscious, unrestrained cirrhotic dogs with portal hypertension

It has recently been reported that the administration of ketanserin, a serotonin antagonist, was associated with a significant reduction in portal pressure both in portal hypertensive rats and cirrhotic patients. However, this beneficial effect on splanchnic hemodynamics was accompanied by a significant reduction in arterial pressure. Using conscious dogs, we investigated the effect of the chronic oral administration of a new specific antiserotonergic drug, ritanserin (10 mg per day for 5 days), on portal pressure and systemic hemodynamics. Eleven dogs with secondary biliary cirrhosis and portal hypertension due to chronic bile duct ligation were evaluated. One week prior to study, heparinized catheters were placed in the portal vein and brought subcutaneously to the dorsal cervical area. Measurements were made under baseline conditions, following ritanserin administration and 72 hr after the last dose. Ritanserin administration caused a significant reduction in portal pressure (from 17.3 +/- 3.1 mmHg to 13.6 +/- 4.5 mmHg; mean decrease: 23.1%; p less than 0.001). Maximal effects on portal pressure were reached on the fourth day. During the recovery period, hemodynamic parameters returned to baseline values. In six of the 11 cirrhotic dogs with successful chronic catheterization of the inferior vena cava and aorta, ritanserin administration did not cause significant changes in the mean arterial pressure, heart rate, cardiac output and peripheral vascular resistance. These data indicate that chronic implantation of venous and arterial catheters in dogs with secondary biliary cirrhosis is a useful experimental model for pharmacological studies of portal hypertension in conscious animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic endothelin blockade in dogs with pacing-induced heart failure: possible modulation of sympathoexcitation

BACKGROUND: Endothelin-1 (ET-1) is a potent vasoconstrictor peptide elaborated by many cell types. Plasma ET-1 levels are significantly augmented in patients and experimental animals with heart failure. Enhanced levels of ET-1 may contribute to myocardial depression and alterations in sympathetic nerve activity in the setting of chronic heart failure. The effects of chronic blockade of endothelin A (ET(A)) receptors on the development and severity of experimental heart failure and sympathoexcitation were evaluated in these experiments using the specific ET(A) antagonist, PD156707. METHODS AND RESULTS: Four groups of conscious, chronically instrumented mongrel dogs were administered either PD156707 (750 mg orally thrice daily) or a placebo starting 1 day before ventricular pacing or a sham (nonpaced) period. Before pacing or the sham period, baseline hemodynamic and plasma norepinephrine (NE) measurements were made. Hemodynamic and NE measurements were made every 3 to 4 days for the next 28 days. All parameters were relatively stable in nonpaced dogs administered placebo. Paced placebo dogs showed classic hemodynamic and sympathoexcitatory changes indicative of heart failure. Nonpaced dogs administered PD156707 showed a significant decrease in mean arterial pressure and total peripheral resistance beginning 3 days after drug administration. Myocardial function was not affected by PD156707 in nonpaced dogs. In paced dogs, PD156707 also reduced arterial pressure and peripheral resistance. Changes in myocardial function were small and insignificant. Paced dogs administered PD156707 showed an approximately 50% lower increase in plasma NE level from days 10 to 24 compared with paced dogs administered placebo (941.8 +/- 122.8 vs 501.1 +/- 92.6 pg/mL at 17 days; P < .01). CONCLUSIONS: These data suggest that ET-1 contributes to the maintenance of arterial pressure in both sham dogs and dogs paced into heart failure. ET-1 does not appear to have a potent effect on inotropic state, but the data strongly suggest that ET-1 may contribute to the progressive deterioration of circulatory function in heart failure by mediating sympathoexcitation and enhancing plasma NE concentration.     

Angiotensin-converting enzyme inhibitors slow recovery from anemia following cardiac surgery

OBJECTIVES: Angiotensin-converting enzyme (ACE) inhibitors, which are frequently administered in patients with heart disease, have a known inhibitory effect on erythropoiesis. The aim of this study was to detect whether early ACE inhibitor administration slows recovery from anemia following recent cardiac surgery. METHODS AND RESULTS: Forty male patients with anemia (hemoglobin < 12 g/dL) an average of 9 days after cardiac surgery were randomized to receive enalapril (ACE inhibitor group) or not. All of the patients received ferrous sulfate, 525 mg, in addition to standard therapy. Patients with anemia due to other causes were excluded. Blood samples were obtained at baseline, and after 8 days, 16 days, and 60 days. A 6-min walking test and echocardioscan were performed at baseline, and after 16 days and 60 days of treatment, and a chest radiograph was obtained at baseline and after 60 days. The ACE inhibitor group showed a statistically significant lower increase in hemoglobin and RBC values. The peak between-group differences of 1 g/dL of hemoglobin (p = 0.012) and 444 RBCs per milliliter (p = 0.017) were observed on day 16. CONCLUSIONS: Early enalapril maleate administration in anemic patients after heart surgery significantly inhibits erythropoiesis. This unfavorable effect on anemia should be considered when prescribing ACE inhibitors for such patients.     

1型糖尿病对主动脉缩窄大鼠结构和功能的影响

目的探讨糖尿病是否能加重左心室超负荷引起的心力衰竭。方法 3周龄雄性Wistar大鼠54只,随机分为4组:假手术组14只,胸主动脉缩窄(TAC)组12只,假手术+链脲佐菌素(STZ)组15只(STZ组),TAC+STZ组(联合组)13只。记录大鼠的体质量演变,并分别于TAC术后15、50d对所有大鼠行超声心动图检查。在TAC术后66d处死大鼠,分离左心房、右心房、心室等,进行称重,天狼星红染色分析心肌纤维化。结果与假手术组比较,STZ组50d舒张末室间隔厚度(IVST)、左心室后壁舒张末厚度(PWT)、左心室质量、心率明显降低(P<0.01);TAC组15dIVST、PWT、LVM明显升高(P<0.01)。与15d比较,TAC组和联合组50d左心室肥厚百分比明显增高(P<0.01)。与假手术组比较,STZ组大鼠体质量、左心室质量、左心房质量、肺脏质量、左心室质量/胫骨长度明显降低,左心室质量/体质量明显升高;而TAC组大鼠左心室质量、左心房质量、肺脏质量、左心室质量/胫骨长度、左心室质量/体质量明显升高(P<0.05,P<0.01)。结论糖尿病明显增加了TAC诱导的左心室肥厚,但并没有加重TAC大鼠模型的心力衰竭指征,可能是因为糖基化终产物的聚集所致。     

Transcutaneous electrical nerve stimulation as a novel method of remote preconditioning: in vitro validation in an animal model and first human observations

Remote ischemic preconditioning (rIPC) induced by transient limb ischemia (li-rIPC) leads to neurally dependent release of blood-borne factors that provide potent cardioprotection. We hypothesized that transcutaneous electrical nerve stimulation (TENS) is a clinically relevant stimulus of rIPC. Study 1: seven rabbits were subjected to lower limb TENS; six to li-rIPC, and six to sham intervention. Blood was drawn and used to prepare a dialysate for subsequent analysis of cardioprotection in rabbit Langendorff preparation. Study 2: 14 healthy adults underwent upper limb TENS stimulation on one study day, 10 of whom also underwent li-rIPC on another study day. Blood was drawn before and after each stimulus, dialysate prepared, and cardioprotective activity assessed in mouse Langendorff preparation. The infarct size and myocardial recovery were measured after 30 min of global ischemia and 60 or 120 min of reperfusion. Animal validation: compared to control, TENS induced marked cardioprotection with significantly reduced infarct size (TENS vs. sham p < 0.01, rIPC vs. sham p < 0.01, TENS vs. rIPC p = ns) and improved functional recovery during reperfusion. Human study: compared to baseline, dialysate after rIPC (pre-rIPC vs. post-rIPC, p < 0.001) and TENS provided potent cardioprotection (pre-TENS vs. post-TENS p < 0.001) and improved myocardial recovery during reperfusion. The cardioprotective effects of TENS dialysates were blocked by pretreatment of the receptor heart with the opioid antagonist naloxone. TENS is a novel method for inducing cardioprotection and may provide an alternative to the limb ischemia stimulus for induction of rIPC clinically.     

Negative extrathoracic pressure ventilation for phrenic nerve palsy after paediatric cardiac surgery.

OBJECTIVE--To investigate the feasibility of negative extrathoracic pressure ventilation as a respiratory support following phrenic nerve palsy after cardiac surgery. DESIGN--An uncontrolled pilot study. PATIENTS--14 patients aged one week to 30 months (median 5.3 months) with phrenic nerve palsy diagnosed by phrenic nerve conduction tests and diaphragmatic electromyograms. Four had bilateral and 10 unilateral palsy. Before treatment all required oxygen and 10 were receiving positive pressure ventilation. One of the patients with bilateral and four of the patients with unilateral palsies had undergone a plication before negative pressure ventilation was started. INTERVENTION--Treatment was started 6-65 days (median 23) after operation with a newly designed system which included a Perspex chamber, which gave easy access to the child, and an elastic latex neck seal. Continuous negative pressure was used in conjunction with intermittent positive pressure ventilation while continuous or intermittent negative pressure ventilation was used in extubated infants. RESULTS--All four patients with bilateral palsy survived with long-term intermittent negative pressure ventilation and did not require further surgery. Of the 10 with unilateral lesions, seven required no further surgery, two underwent plication, and one had a re-plication. Three patients with unilateral palsy died of non-respiratory causes. The duration of positive pressure ventilation after starting negative pressure ranged from 0 to 23 days (median 6). Treatment with negative pressure lasted for 3-241 days (median 32) and was predominantly administered off the intensive care unit, including at home. CONCLUSIONS--Negative pressure ventilation may be an alternative to positive airway pressure ventilation in the management of phrenic nerve palsy. A multicentre randomised controlled trial is now required to assess further the role of negative pressure ventilation in phrenic nerve palsy.     

Negative extrathoracic pressure ventilation for phrenic nerve palsy after paediatric cardiac surgery.

OBJECTIVE--To investigate the feasibility of negative extrathoracic pressure ventilation as a respiratory support following phrenic nerve palsy after cardiac surgery. DESIGN--An uncontrolled pilot study. PATIENTS--14 patients aged one week to 30 months (median 5.3 months) with phrenic nerve palsy diagnosed by phrenic nerve conduction tests and diaphragmatic electromyograms. Four had bilateral and 10 unilateral palsy. Before treatment all required oxygen and 10 were receiving positive pressure ventilation. One of the patients with bilateral and four of the patients with unilateral palsies had undergone a plication before negative pressure ventilation was started. INTERVENTION--Treatment was started 6-65 days (median 23) after operation with a newly designed system which included a Perspex chamber, which gave easy access to the child, and an elastic latex neck seal. Continuous negative pressure was used in conjunction with intermittent positive pressure ventilation while continuous or intermittent negative pressure ventilation was used in extubated infants. RESULTS--All four patients with bilateral palsy survived with long-term intermittent negative pressure ventilation and did not require further surgery. Of the 10 with unilateral lesions, seven required no further surgery, two underwent plication, and one had a re-plication. Three patients with unilateral palsy died of non-respiratory causes. The duration of positive pressure ventilation after starting negative pressure ranged from 0 to 23 days (median 6). Treatment with negative pressure lasted for 3-241 days (median 32) and was predominantly administered off the intensive care unit, including at home. CONCLUSIONS--Negative pressure ventilation may be an alternative to positive airway pressure ventilation in the management of phrenic nerve palsy. A multicentre randomised controlled trial is now required to assess further the role of negative pressure ventilation in phrenic nerve palsy.