Randomised comparison of percutaneous left ventricular assist device with open-chest cardiac massage and with surgical assist device during ischaemic cardiac arrest.

AIMS: A percutaneous left ventricular assist device can maintain blood flow to vital organs during ventricular fibrillation and may improve outcomes in ischaemic cardiac arrest. We compared haemodynamic and clinical effects of a percutaneous left ventricular assist device with a larger device deployed via endovascular prosthesis and with open-chest cardiac massage during ischaemic cardiac arrest. METHODS: Eighteen swine were randomised into three groups. After thoracotomy, coronary ischaemia and ventricular fibrillation was induced. Cardiac output was measured with transit-time flowmetry. Tissue perfusion was measured with microspheres. Defibrillation was performed after 20 min. RESULTS: Cardiac output with cardiac massage was 1129 mL min⁻¹ vs. 1169 mL min⁻¹ with the percutaneous- and 570 mL min⁻¹ with the surgical device (P < 0.05 surgical vs. others). End-tidal CO2 was 3.3 kPa with cardiac massage vs. 3.2 kPa with the percutaneous- and 2.3 kPa with the surgical device (P < 0.05 surgical vs. others). Subepicardial perfusion was 0.33 mL min⁻¹ g⁻¹ with cardiac massage vs. 0.62 mL min⁻¹ g⁻¹ with both devices (P < 0.05 devices vs. massage), cerebral perfusion was comparable between groups (all reported values after 3 min cardiac arrest, all P<0.05 vs. baseline, all P = NS for 3 min vs. 15 min). Return of spontaneous circulation was achieved in 5/6 subjects with cardiac massage vs. 6/6 with the percutaneous- and 4/6 with the surgical device (P = NS). CONCLUSION: The percutaneous device improved myocardial perfusion, maintained cerebral perfusion and systemic circulation with similar rates of successful defibrillation vs. cardiac massage. Increased delivery was not obtained with the surgical device during cardiac arrest.

Percutaneous left ventricular assist device can prevent acute cerebral ischaemia during ventricular fibrillation.

AIMS: A percutaneous left ventricular assist device has been shown to be able to perfuse cardiac and cerebral tissues during cardiac arrest and may be a useful supplement to current methods in resuscitation. We wished to assess device-assisted circulation during cardiac arrest with microspheres injections and continuous end-tidal CO(2) monitoring, and used cerebral microdialysis to detect ischaemia in the brain. METHODS: 12 anaesthetised pigs had microdialysis and pressure catheters implanted via craniotomy. The percutaneous assist device was deployed transfemorally. Ventricular fibrillation was induced by angioplasty-balloon occlusion of the left coronary artery. Cerebral microdialysis samples representing 0-20 and 20-40 min of cardiac arrest with assisted circulation were analysed for markers of cerebral injury (glucose, pyruvate, lactate, and glycerol). RESULTS: Microdialysis showed no ischaemic changes after 20 min of cardiac arrest (P=NS to Baseline for glucose, glycerol, lactate, pyruvate and lactate/pyruvate ratio) in subjects with maintained end-tidal CO(2) values above 1.3 kPa (10 mmHg). After 40 min only lactate showed a significant change compared to Baseline (P<0.05). Microspheres flow to the brain was 57% and myocardial flow was 72% compared to Baseline after 15 min (P<0.05). After 45 min flow declined to 22% and 40% of Baseline, respectively (P=NS vs. 15 min). CONCLUSIONS: A percutaneous left ventricular assist device may prevent ischaemic cerebral injury during cardiac arrest for a limited time. Cerebral injury and tissue perfusion were indicated by end-tidal CO(2).

An anaesthetic protocol in the young domestic pig allowing neuromuscular blockade for studies of cardiac function following cardioplegic arrest and cardiopulmonary bypass.

BACKGROUND: Neuromuscular blockade should, for ethical reasons, not be allowed in animal experiments unless the use is strongly motivated. Beforehand, the anaesthetic protocol must be documented without muscle relaxation in the species studied. Documentation is difficult to obtain from the scientific literature. When focusing on cardiac function over time, in particular, the ideal anaesthetic protocol should cause no or minor alterations in cardiac variables. METHODS: We intended to document an anaesthetic protocol involving ventilation with N(2)O combined with loading doses and continuous infusions of pentobarbital, fentanyl and midazolam in seven pigs by applying potentially painful stimuli every 15 min for 7 h. Subsequently, left ventricular global and regional function was studied with conductance catheter and strain rate imaging by echocardiography in eight pigs with pancuronium included. RESULTS: Pigs without pancuronium were completely immobilized and unresponsive to potentially painful stimuli and sternotomy, with no accumulation or degradation of anaesthetic agents. With pancuronium included, left ventricular preload gradually decreased together with reduction of cardiac index from 3.52 +/- 0.14 at 2 h to 2.84 +/- 0.11 L min(-1). m(-2) (+/-SEM) after 7 h of observation. Preload recruitable stroke work decreased after 7 h, whereas peak systolic strain in the anterior left ventricular wall and load-independent indices of diastolic function were not significantly altered. CONCLUSION: In specific experimental protocols, the anaesthetic protocol described could allow the use of muscular paralysis in young domestic pigs, for instance when involving hypothermic cardiopulmonary bypass, cardioplegic arrest and reperfusion.

Fluid resuscitation improves intestinal blood flow and reduces the mucosal damage associated with strangulation obstruction in pigs.

BACKGROUND: Strangulation obstruction of the small bowel is associated with local and systemic circulatory changes, local loss of fluid, and damage of the strangulated bowel segment. We wanted to examine to which extent these changes can be prevented by intravenous fluid administration. MATERIALS AND METHODS: In anesthetized pigs, strangulation obstruction was induced by increasing the pressure in a baby pressure gasket placed around a loop of ileum until venous pressure in the loop reached 50 mm Hg. During the strangulation period (180 min), a group of eight animals (Fluid(min) group) received 10 ml. kg(-1). hour(-1) Ringer acetate solution intravenously, whereas another eight animals (Fluid(max) group) received 55 ml. kg(-1). hour(-1) Ringer acetate solution intravenously. Blood flow to the strangulated bowel was measured by transit time flowmetry and colored microspheres. After completed experiments, whole wall samples of the strangulated loop were selected for microscopy. RESULTS: In the Fluid(min) group, the heart rate increased, the arterial pressure decreased markedly, and the urine output decreased toward zero. In the Fluid(max) group, the heart rate and arterial pressure remained fairly constant and the urine output increased. Blood flow to the strangulated bowel decreased in both groups, but significantly more in the Fluid(min) group. The intestinal blood flow was highly dependent on the arterial blood pressure. The strangulated mucosa showed markedly more damage in the Fluid(min) group than the Fluid(max) group. The degree of mucosal damage correlated linearly with the mucosal blood flow. CONCLUSION: The administration of large amounts of fluid to animals with strangulation obstruction normalized the arterial pressure and improved the intestinal blood flow thus minimizing damage to the intestinal mucosa.

Effects of the aldosterone receptor antagonist potassium canrenoate on renal blood flow and urinary output during prolonged increased intraabdominal pressure (IAP) in pigs.

BACKGROUND: Increased intraabdominal pressure can be found after major abdominal trauma and necrotizing pancreatitis and is used during laparoscopic surgery. The purpose of this study was to investigate the effect of the aldosterone receptor antagonist (potassium canrenoate) on renal hemodynamics and urinary output in pigs during increased intraabdominal pressure (IAP). METHODS: The IAP was kept at 30 mmHg for 3 h by instillation of Ringer's solution into the peritoneal cavity. Eight animals were treated with potassium canrenoate and eight animals served as controls. Renal blood flow, hormones in femoral artery blood, and the urinary output were measured. RESULTS: The administration of potassium canrenoate was followed by increased aldosterone concentrations in arterial blood, increased blood concentration of potassium, and increased concentration of sodium in the urine, indicating satisfactory inhibition of aldosterone. Potassium canrenoate did not cause changes in cardiac output and arterial pressure. It did not affect the renal vascular resistance that increased at an IAP of 30 mmHg, or the renal blood flow that remained constant during the experiments. The group treated with potassium canrenoate had higher mean urinary output than the controls, but the difference was not significant. CONCLUSION: Increased IAP in pigs is associated with markedly reduced urinary output and increased serum concentrations of aldosterone. Although the urinary output did not increase significantly, the increased sodium concentration in the urine of canrenoate-treated animals suggests that the high blood level of aldosterone contributes to the oliguria under increased IAP.

Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs.

BACKGROUND: The aim of the study was to investigate the effect of the angiotensin II receptor antagonist losartan on renal hemodynamics and diuresis in pigs with increased intraabdominal pressure (IAP). METHODS: The IAP was maintained at 30 mmHg for 3 h by intraperitoneal instillation of Ringer's solution. Ten animals were treated with losartan; another 10 animals served as controls. Renal blood flow, hormones in renal vein blood, and diuresis were measured. RESULTS: In control animals, the renal vascular resistance increased renal blood flow remained constant, the blood concentration of aldosterone increased and the diuresis decreased during increased IAP. Losartan prevented the increase in vascular resistance and improved renal blood flow under increased IAP. It also prevented the rise in aldosterone concentration and increased the urine output to baseline level. CONCLUSION: Our results suggest that the renal vasoconstriction associated with increased IAP is due to increased production of angiotensin II. The oliguria associated with increased IAP is probably due, at least partly, to increased reabsorbtion of sodium and water in the renal tubuli caused by increased tissue concentration of aldosterone.

Effects of prolonged increased intra-abdominal pressure on gastrointestinal blood flow in pigs.

BACKGROUND: The aim of the study was to investigate the effects of prolonged intra-abdominal pressure on systemic hemodynamics and gastrointestinal blood circulation. METHODS: The intra-abdominal pressure in anesthetized pigs was elevated to 20 mmHg (7 animals), 30 mmHg (7 animals), and 40 mmHg (4 animals), respectively. These pressures were maintained for 3 h by intra-abdominal infusion of Ringer's solution. A control group of seven animals had normal intra-abdominal pressure (IAP). Transit time flowmetry and colored microspheres were used to measure blood flow. RESULTS: An IAP of 20 mmHg did not cause significant changes in systemic hemodynamics or tissue blood flow. An IAP of 30 mmHg caused reduced blood flow in the portal vein, gastric mucosa, small bowel mucosa, pancreas, spleen, and liver. Serum lactate increased in animals with an IAP of 30 mmHg, but microscopy did not disclose mucosal damage in the stomach or small bowel. An IAP of 40 mmHg was followed by severe circulatory changes. CONCLUSIONS: Prolonged IAP at 20 mmHg did not cause changes in general hemodynamics or gastrointestinal blood flow. Prolonged IAP at 30 mmHg caused reduced portal venous blood flow and reduced tissue flow in various abdominal organs, but no mucosal injury. A prolonged IAP of 40 mmHg represented a dangerous trauma to the animals.

Rewarming from accidental hypothermia by extracorporeal circulation. A retrospective study.

OBJECTIVE: Twenty-six patients with accidental hypothermia combined with circulatory arrest or severe circulatory failure were rewarmed to normothermia by use of extracorporeal circulation (ECC). The aim of the present study was to evaluate our results. PATIENTS AND METHODS: The treatment of six female and 20 male patients (median age: 26.7 years; range 1.9--76.3 years) rewarmed in the period 1987--2000 was evaluated retrospectively. Hypothermia was related to immersion/submersion in cold water (n=17), avalanche (n=1) or prolonged exposure to cold surroundings (n=8). Prior to admission, the trachea was intubated and cardiopulmonary resuscitation (CPR) initiated in all patients with cardiorespiratory arrest (n=22), whereas in those with respiration/circulation (n=4) only oxygen therapy via a face mask was given. RESULTS: Nineteen of the 26 patients were weaned off ECC whereas seven died because of refractory respiratory and/or cardiac failure. Eight of the 19 successfully weaned patients were discharged from hospital after a median of 10 days. One patient died 3 days after circulatory arrest (complete atrioventricular block) resulting in severe cerebral injury. The remaining ten patients died following 1--2 days due to severe hypoxic brain injury (n=5), cerebral bleeding (n=1) or irreversible cardiopulmonary insufficiency (n=4). Based on the reports from the site of accident, two groups of patients were identified: the asphyxia group (n=15) (submersions (n=14); avalanche accident (n=1)) and the non-asphyxia group (n=11) (patients immersed or exposed to cold environment). Seven intact survivors discharged from hospital belonged to the non-asphyxia group whereas one with a severe neurological deficit was identified within the asphyxia group. CONCLUSION: Patients with non-asphyxiated deep accidental hypothermia have a reasonable prognosis and should be rewarmed before further therapeutic decisions are made. In contrast, drowned patients with secondary hypothermia have a very poor prognosis. The treatment protocol under such conditions should be the subject for further discussion.

Role of endothelin in the circulatory changes associated with small bowel strangulation obstruction in pigs: effects of the endothelin receptor antagonist bosentan.

BACKGROUND: We have previously shown that experimental strangulation obstruction leads to increased release and concentration of endothelin-1 (ET-1) in venous blood from the strangulated bowel loop. The present study focuses on the microcirculatory effects of the released ET-1 in strangulation obstruction. METHODS: In anesthetized pigs strangulation obstruction was induced by increasing pressure in a baby pressure gasket placed around a loop of ileum until venous pressure reached 45 mm Hg. The pigs were randomly allocated into two groups. The nonselective ET(A)/ET(B) antagonist bosentan was administered intravenously (5 mg kg(-1)) to eight pigs (bosentan group) 30 min before strangulation, which was maintained for 90 min. Another eight pigs were treated in same manner except for the bosentan injection (control group). RESULTS: The concentration of ET in arterial and intestinal venous blood increased markedly after intravenous administration of bosentan. Intravenous infusion of bosentan was followed by a reduction in systemic arterial blood pressure. Bosentan reduced vascular resistance and increased blood flow in the normal intestinal mucosa. It also reduced muscularis blood flow in the beginning of the experiment. In strangulated small bowel bosentan inhibited the increase in vascular resistance usually caused by strangulation obstruction. Muscularis blood flow in strangulated small bowel was not affected by bosentan. CONCLUSION: Endothelin is involved in the normal regulation of arterial blood pressure. The increase in vascular resistance associated with strangulation obstruction is caused mainly by locally released endothelin.

[Rewarming of patients with accidental hypothermia with the help of heart-lung machine]. / Oppvarming av pasienter med aksidentell hypotermi ved hjelp av hjerte-lunge-maskin.

BACKGROUND: Different techniques have been used for treatment of victims with accidental hypothermia. We have used cardiopulmonary bypass (CPB) for rewarming hypothermic patients with circulatory failure or cardiac arrest. This report summarises our experiences with this patient group. MATERIAL AND METHODS: 23 patients, submersions (n = 15), avalanche (n = 1) and primary hypothermia (immersion/air cooling) (n = 7), were rewarmed using extracorporeal circulation with standard equipment for open-heart surgery. RESULTS: On a clinical basis, two patient populations could be identified; one group for whom asphyxia was probably present prior to and during cooling, and another group for whom asphyxia was unlikely. In the first group, one of 13 patients survived compared to the latter group where six out of ten survived. A search for laboratory and other variables that with certainty could contribute to the prediction of prognosis was unsuccessful. INTERPRETATION: Due to lack of safe prognostic predictors, all accidental hypothermic victims with circulatory failure should be rewarmed by cardiopulmonary bypass before further therapeutic decisions are made.

[Back pain--when both patients and physicians are in deep waters]. / Ryggsmerter--når så vel pasient som lege går i vannet.

BACKGROUND: Intraosseous pneumatocysts are rare and represent a benign condition. Such cysts can be an incidental finding described as a lytic process on plain X-rays. Computed tomography (CT) will confirm the diagnosis. Bone cysts filled with air are most frequently described in the iliac bone and in the sacrum, very rarely in the vertebrae or other bones. MATERIAL AND METHODS: This paper describes a patient that over a four to five-years period experienced relapses of rather strong lower back and hip pain of short duration during shallow water diving and ascent, and also during air travel. RESULTS: Plain X-rays of the lower spine and left hip (prescribed because of an earlier hip trauma) demonstrated a lytic process in the left iliac bone. CT of the pelvis confirmed the diagnosis of an intraosseous pneumatocyst in the left iliac bone. A mini-invasive procedure with CT-guided puncture under local anaesthesia and destruction of the cyst relieved the patient's symptoms. INTERPRETATION: The physician should consider rear causes of lower back pain in otherwise healthy patients. As demonstrated here, the causal treatment can sometimes be quite simple.

Glutathione modulation changes the penetration of N-[3H]methyl-N-nitro-N-nitrosoguanidine into gastric mucosa of rats.

Glutathione plays a role in gastric mucosal protection and the glutathione level is elevated in some forms of gastritis. We studied the relevance of glutathione for the penetration of N-methyl-N-nitro-N-nitrosoguanidine in the glandular mucosa of the stomach. Male Wistar rats were treated with glutathione (0.5 mmol/kg intravenously), N-acetylcysteine (0.5 mmol/kg intravenously), or L-buthionine-[S,R,]-sulfoximine (BSO, 2 mmol/kg intraperitoneally), before the gastric mucosa was exposed to N-[3H]methyl-N-nitro-N-nitrosoguanidine for 10 min. Penetration of the carcinogen was evaluated by light microscopic identification of cells labeled with bromodeoxyuridine and N-[3H]methyl-N-nitro-N-nitrosoguanidine (double-labeled cells). Thiol substances were quantified by reversed-phase ion-pair liquid chromatography and fluorescence detection. The percentage double-labeled cells was higher in antrum mucosa (11.7 +/- 3.1%) than in corpus mucosa (1.1 +/- 0.2%) (P < 0.05). Total glutathione level was 1853 +/- 101 nmol/g in antrum and 1560 +/- 76 nmol/g in corpus mucosa. BSO administration reduced the amount of glutathione in antrum to 495 +/- 14 nmol/g (P < 0.05) and reduced the percentage double-labeled cells in antrum mucosa to 6.1 +/- 1.3% (P < 0.05). A positive correlation was found between the percentage of double-labeled cells in the antrum mucosa and the total amount of glutathione (r = 0.451, P = 0.002), and the amount of reduced glutathione (r = 0.449, P = 0.002). Glutathione modulation effects the penetration of N-[3H]methyl-N-nitro-N-nitrosoguanidine in the antrum but not in the corpus mucosa. Thiols do not explain the different penetration of carcinogen in antrum and corpus mucosa.

Velocity distribution in the ascending aorta in pigs during chronotropic and inotropic stimulation.

The influence of heart rate, stroke volume and myocardial contractility on temporal and spatial velocity distribution in the ascending aorta was investigated in 10 pigs. A pulsed Doppler ultrasound technique with intraluminal probe and a single crystal connected to a position-sensitive device was used to measure blood velocity. After baseline registration, the heart rate was increased in two discrete steps of 20 beats/min by right atrial pacing. Isoproterenol infusion was given to increase contractility. Finally, without isoproterenol, the heart rate was again raised to the values found during inotropic stimulation. The first three measuring situations did not differ haemodynamically, apart from increased heart rate and reduced stroke volume. Increased heart rates were not associated with significant change in the parameters for skewness of velocity distribution (peak systolic slope and ratio, maximum skewness slope and ratio). During inotropic stimulation the peak left ventricular dP/dt, aortic systolic pressure, cardiac output and stroke volume were greater than at comparable paced heart rate, and the peak systolic slope of velocity distribution was significantly increased. Velocity distribution in the ascending aorta thus was not altered by increased heart rate alone, whereas skewness of distribution was enhanced by increased inotropic drive of the myocardium and the concomitant central and peripheral vascular changes.

Effect of gastric secretion on penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine into gastric mucosa of rats.

Clinical conditions with low gastric acid secretion have been associated with increased risk of gastric cancer. There has also been concern about gastric acid inhibition and N-nitroso compound formation in the stomach. This study investigates the effect of gastric acid secretion on the penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine, an N-nitroso compound and gastric carcinogen, into the gastric mucosa of rats. Gastric acid secretion was stimulated by pentagastrin (40 microg/kg/hr) and inhibited by omeprazole (40 micromol/kg) before mucosal exposure to N-3H-methyl-N-nitro-N-nitrosoguanidine. Penetration of the carcinogen was evaluated by light microscopic identification of cells in the S-phase labeled with N-3H-methyl-N-nitro-N-nitrosoguanidine. This population of double-labeled cells is considered at risk from N-methyl-N-nitro-N-nitrosoguanidine-induced carcinogenesis. The percentage of double-labeled cells was significantly higher in antrum than in corpus mucosa (P < 0.0001). Stimulation or inhibition of gastric acid secretion did not affect the penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine in antrum or corpus mucosa. We conclude that modulation of gastric acid secretion does not affect the penetration of the carcinogen into the gastric mucosa nor does it explain the different penetration of the carcinogen into corpus and antrum mucosa.

Acute erosions of the gastric mucosa in burned rats: effect of sucralfate.

The effect of intragastric sucralfate on development of gastric erosions in burns was studied in 20 rats anaesthetised with midazolam/fentanyl/fluanisone. Gastric blood flow was measured by radioactive microspheres immediately before, and 20, 40, and 120 minutes after the rats had been burned. Significantly fewer erosions were found in the 10 rats treated with sucralfate (less than 2% of the gastric mucosal surface was affected) compared with the controls (16% of the mucosa affected). There was no difference in the rate of gastric blood flow in any part of the stomach between the rats treated with sucralfate and the controls. We conclude that sucralfate is effective in preventing gastric erosions in burned rats, but that other mechanisms of action than increase gastric blood flow are responsible for its protective effect.

Glutathione and N-acetylcysteine reduce gastric mucosal blood flow in rats.

Glutathione has been studied as a possible mediator in gastric mucosal protection and healing, but its extracellular function is not fully understood. This study evaluates blood flow changes in normal gastric mucosa secondary to glutathione modulation under stable central hemodynamic conditions. Thiol substances were quantified by reverse-phase ion-pair liquid chromatography and fluorescence detection. Central hemodynamics remained stable when glutathione and N-acetylcysteine were administered in a dose of 0.5 mmol/kg. Higher doses than 0.5 mmol/kg of glutathione and N-acetylcysteine caused unstable hemodynamics. Glutathione (0.5 mmol/kg intravenously) and N-acetylcysteine (0.5 mmol/kg intravenously) reduced corpus mucosal blood flow by 28% and 26% (P < 0.0005), respectively, and glutathione reduced antral mucosa blood flow by 22% (P < 0.01). L-Buthionine-[S,R]-sulfoximine (2 mmol/kg intravenously) did not effect gastric mucosal blood flow. Cysteine content in mucosa and plasma increased while mucosal glutathione levels were largely unchanged after administration of reduced glutathione and N-acetylcysteine. Plasma glutathione only increased after injection of glutathione. L-Buthionine-[S,R]-sulfoximine reduced the glutathione level in both plasma and mucosa. We conclude that glutathione and N-acetylcysteine reduce gastric mucosal blood flow and that the effect may be related to increased cysteine levels in plasma or mucosa.

Carvedilol retards sudden loss of contraction during early regional myocardial ischemia in feline hearts.

The purpose of our study was to investigate whether loss of myocardial contraction immediately after coronary occlusion was nonuniform, and if pretreatment with carvedilol, a vasodilating nonselective beta-adrenoceptor antagonist, could retard loss of contraction after coronary artery occlusion. Feline hearts were subjected to acute regional ischemia by total occlusion of the left anterior descending coronary artery. The animals were either treated with vehicle (control group) or with carvedilol 1 mg/kg i.v. before left anterior descending coronary artery occlusion (n = 9 in each group). Regional contraction in the left anterior descending coronary artery perfused region of the heart was studied by cross-oriented sonomicrometry. In control animals, circumferential (subepicardial) contraction ceased after 10 sec, whereas longitudinal (subendocardial) contraction ceased immediately after left anterior descending coronary artery occlusion. Loss of contraction in animals treated with carvedilol was significantly slower compared to controls. Circumferential contraction ceased between 30 sec and 1 min, whereas longitudinal contraction ceased after 20 sec. In conclusion, loss of contraction during the first seconds after coronary occlusion was nonuniform, with most rapid dysfunction in the subendocardium. Pretreatment with carvedilol retarded loss of contraction in both axes.

Small intestinal perforation and peritonitis after abdominal suction lipoplasty.

Suction lipoplasty for abdominal contouring in nonoperated patients is considered a safe procedure with a low incidence of local and systemic complications. Suction lipoplasty combined with a full abdominoplasty is, however, still controversial with a higher rate of local complications. A 56-year-old woman with a history of four laparotomies and two abdominoplasties was hospitalized with abdominal pain and signs of peritonitis after an ambulatory suction lipoplasty. During laparotomy for peritonitis the abdominal wall was found to be stiff and fibrotic, with massive adhesions to the intestine. Two small intestinal perforations caused soiling into the peritoneum. The perforated intestinal segment was resected and the postoperative history was uneventful. Both recent and former laparotomies in the lower abdomen represent a possible risk when suction lipoplasty is performed. An ultrasonographic or computed tomographic scan of the abdominal wall would identify or rule out any underlying fascial defect or hernia.

Carvedilol improves function and reduces infarct size in the feline myocardium by protecting against lethal reperfusion injury.

This study examined the effect of carvedilol, a vasodilating beta-adrenoceptor antagonist and antioxidant, on lethal reperfusion injury in feline hearts subjected to 40 min of regional ischemia and 180 min of reperfusion. 30 open chest anaesthetized cats were randomized into three groups. A control (n = 10) was compared with a group given carvedilol before coronary artery occlusions (n = 10) and a group given carvedilol immediately before and during early reperfusion (n = 10). Regional myocardial function was measured by sonomicrometry. Infarct size was determined by staining the left ventricle with triphenyl tetrazolium chloride. Myocardial blood flow was measured by radiolabeled microspheres. Tissue levels of glutathione were measured after reperfusion. Infarct size was significantly reduced compared to control both when carvedilol was given before ischemia (0.2 +/- 0.1 vs. 17.6 +/- 3.6%, P < 0.05). and when given immediately before reperfusion (3.7 +/- 1.3 vs. 17.6 +/- 3.6%, P < 0.05). Regional shortening improved significantly and the incidence of ventricular fibrillation during early reperfusion was reduced in both groups treated with carvedilol compared to control. Oxidized glutathione did not differ between groups in the post-ischaemic myocardium. This study supports that lethal reperfusion injury is a significant phenomenon. Furthermore, carvedilol reduces infarct size and reperfusion arrhythmias, and improves post-ischaemic regional myocardial function by protecting against both ischaemic and lethal reperfusion injury. The present study does not answer whether it is the non-selective beta- or alpha 1-receptor antagonism, the antiarrhythmic or the antioxidant actions of carvedilol that is responsible for the protective effect.