Virtual reality in surgical practice in vitro and in vivo evaluations.

This paper describes a method for the acquisition and integrative processing of laparoscopic and endoluminal ultrasound images. We used a stepping motor attached to a stabilizing rig, interfaced to the laparoscope, or the ultrasound probe. 360 degrees laparoscopic scenes were constructed during minimally invasive surgery, and three-dimensional reconstructions were made of related ultrasound data. Integration of 360 degrees panoramas with geometric ultrasound models could be displayed as interactive scenes. This resulted in a better demonstration of the surgical field and topographic anatomy. In conclusion, this type of visualizations may be used in virtual reality simulations for documentation, education and in operative planning.

Tissue metabolite levels in different types of skeletal muscle during sepsis.

The effect of sepsis on energy and metabolite levels in the white, fast-twitch extensor digitorum longus (EDL) and the red, slow-twitch soleus (SOL) muscles was studied in rats. Sepsis was induced by cecal ligation and puncture (CLP). Control rats were sham-operated. Sixteen hours later, metabolite levels in muscle tissue were determined. Adenosine triphosphate (ATP) levels and energy charge were reduced during sepsis in SOL, but were unchanged in EDL muscles. In contrast, phosphocreatine (PCr) concentration was reduced during sepsis in EDL, but not in SOL. Tissue glycogen levels were reduced and lactate concentrations were increased in both muscles during sepsis. Results suggest that sepsis affects energy metabolism differently in different types of skeletal muscle. Tissue lactate accumulation may be consistent with muscle hypoperfusion following CLP, although other mechanisms may also be involved.

Effect of the glucocorticoid receptor antagonist RU 38486 on muscle protein breakdown in sepsis.

The role of glucocorticoids in muscle catabolism during sepsis was tested with the glucocorticoid receptor antagonist RU 38486. Sepsis was induced in male Sprague-Dawley rats (40 to 60 gm) by cecal ligation and puncture (CLP). Other animals underwent sham operation. Two hours before CLP or sham operation, rats received RU 38486 (5 mg/kg) or a corresponding volume of vehicle by gavage. Sixteen hours after CLP or sham operation, protein synthesis rate was determined by measuring incorporation of 14C-phenylalanine into protein in incubated extensor digitorum longus muscles. Total and myofibrillar protein breakdown rates were determined by measuring net release of tyrosine and 3-methylhistidine, respectively. The protein synthesis rate was approximately 30% lower in rats with sepsis than in sham operated rats and was not affected by treatment with RU 38486. The total protein breakdown rate was increased by approximately 70% and myofibrillar protein degradation was increased more than fivefold in muscle from rats with sepsis. Treatment with RU 38486 resulted in a 28% reduction of total and a 44% reduction of myofibrillar protein breakdown in rats with sepsis but did not affect proteolysis in muscle from sham-operated animals. The results support a role of glucocorticoids in accelerated muscle proteolysis during sepsis. It is not clear whether glucocorticoids are the only required mediator or they interact with other substances to induce muscle protein breakdown during sepsis.

Influence of sepsis in rats on muscle protein turnover in vivo and in tissue incubated under different in vitro conditions.

We studied the influence of sepsis on muscle protein synthesis and degradation in vivo and in muscles, incubated flaccid or at resting length. Sepsis was induced in rats by cecal ligation and puncture (CLP). Control rats were sham-operated. A flooding dose of 14C-phenylalanine was used to determine muscle protein synthesis rate in vivo, and protein breakdown was calculated from the difference between protein synthesis and growth rates. Protein synthesis rate in vitro was assessed by determining incorporation of 14C-phenylalanine into protein in incubated extensor digitorum longus (EDL) and soleus (SOL) muscles. Total and myofibrillar protein breakdown rates were determined from release into incubation medium of tyrosine and 3-methylhistidine (3-MH), respectively. Muscle protein synthesis rate in vivo was reduced by 35%, similar to the reduction observed in muscles incubated flaccid or at resting length. The calculated protein breakdown rate in vivo was increased by 31% in septic rats. In incubated muscles, the increase in total protein breakdown (ie, tyrosine release) during sepsis was almost identical in muscles incubated flaccid or at resting length, ie, 83% to 88% in EDL and 47% to 49% in SOL. Myofibrillar protein degradation in vitro (ie, 3-MH release) was increased approximately 10-fold in EDL muscles incubated flaccid or at resting length, but was not significantly affected by sepsis in SOL. Results suggest that sepsis-induced changes in protein synthesis observed in muscles incubated either flaccid or at resting length reflect changes in vivo. Changes in protein breakdown were qualitatively similar in vivo and in vitro, but results in incubated muscles may overestimate the increase in muscle proteolysis caused by sepsis.

Myofibrillar proteinase, cathepsin B, and protein breakdown rates in skeletal muscle from septic rats.

Muscle catabolism during sepsis is mainly caused by myofibrillar protein breakdown. The mechanism of this metabolic response is not known. We tested the hypothesis that increased protein breakdown in the extensor digitorum longus (EDL) muscle of septic rats is caused by increased activity of the so-called myofibrillar proteinase, which is a nonlysosomal proteolytic enzyme, and cathepsin B, which is a lysosomal proteinase. Sepsis, induced in male Sprague-Dawley rats (50 to 60 g) by cecal ligation and puncture (CLP), resulted in an approximately 50% increase in myofibrillar proteinase activity and an approximately 30% increase in cathepsin B activity. Concomitantly, both total and myofibrillar protein breakdown rates, measured as release of tyrosine and 3-methylhistidine (3-MH), respectively, by incubated EDL muscles, were substantially elevated. Treatment of septic rats with the mast cell degranulating compound 48/80 or the lysosomal protease inhibitor leupeptin significantly reduced myofibrillar proteinase and cathepsin B activities, but did not affect protein breakdown rates. The results suggest that increased protein breakdown in septic skeletal muscle is associated with, but not caused by, myofibrillar proteinase or cathepsin B activity. The data also support the concept of a mast cell origin of the myofibrillar proteinase activity, but do not suggest an obligatory involvement of mast cell proteinase in increased protein degradation during sepsis.

Reduced levels of mRNA for myofibrillar proteins in skeletal muscle from septic rats.

The influence of sepsis on transcription of myofibrillar proteins in skeletal muscle was studied in rats. Sepsis was induced by cecal ligation and puncture (CLP); control rats were sham-operated. Sixteen hours later, muscle levels of mRNA for myofibrillar proteins were determined by using cDNA probes specific for transcripts for alpha actin and myosin heavy chain. Sepsis resulted in a 2-6 fold decrease in alpha actin mRNA levels and an even more pronounced reduction in myosin heavy chain mRNA levels. Results suggest that sepsis-induced reduction of muscle protein synthesis is at least partly regulated at the transcriptional level.

Registration of post-operative wound infections: a method for reducing the rate of infections.

Continuous registration of postoperative wound infections reduces the rate of infection per se at the same time as enabling special risk groups to be identified. By improving or changing hygiene and antibiotic routines, the rate of infection in these especially exposed groups can be reduced. Major postoperative infectious complications prolong postoperative hospital stay by 17 days on average. Reduction of the rate of infections would save hundreds of treatment days.

Interaction between corticosterone and tumor necrosis factor stimulated protein breakdown in rat skeletal muscle, similar to sepsis.

Protein synthesis and breakdown rates were determined in incubated extensor digitorum longus muscles of rats treated with tumor necrosis factor (TNF; 20 micrograms/100 gm body weight), corticosterone (20 mg/100 gm body weight), or a combination of the two substances. Protein synthesis was measured as incorporation of carbon 14-labeled phenylalanine into protein. Total and myofibrillar protein breakdown rates were assessed as release of tyrosine and 3-methylhistidine, respectively. Administration of TNF alone did not affect muscle protein turnover rates. Corticosterone inhibited muscle protein synthesis and stimulated total and myofibrillar protein breakdown. When TNF was administered together with corticosterone, total and myofibrillar protein breakdown rates were increased further compared with rats treated with corticosterone alone. Because plasma corticosterone levels in rats treated with both TNF and the glucocorticoid were higher than in animals treated with corticosterone alone, it is possible that muscle proteolysis noted after TNF, injected together with costicosterone, was caused by the high glucocorticoid levels. To test that hypothesis, corticosterone alone or in combination with TNF was injected in rats that had undergone adrenalectomy. In these experiments, TNF did not increase plasma corticosterone levels or muscle protein breakdown rates. The results suggest that muscle catabolism induced by administration of TNF is mediated by glucocorticoids.

Regulation of total and myofibrillar protein breakdown in rat extensor digitorum longus and soleus muscle incubated flaccid or at resting length.

The present study characterized total and myofibrillar protein breakdown rates in a muscle preparation frequently used in vitro, i.e. incubated extensor digitorum longus (EDL) and soleus (SOL) muscles of young rats. Total and myofibrillar protein breakdown rates were assessed by determining net production by the incubated muscles of tyrosine and 3-methylhistidine (3-MH) respectively. Both amino acids were determined by h.p.l.c. Both total and myofibrillar protein breakdown rates were higher in SOL than in EDL muscles and were decreased by incubating the muscles maintained at resting length, rather than flaccid. After fasting for 72 h, total protein breakdown (i.e. tyrosine release) was increased by 73% and 138% in EDL muscles incubated flaccid and at resting length respectively. Net production of tyrosine by SOL muscle was not significantly altered by fasting. In contrast, myofibrillar protein degradation (i.e. 3-MH release) was markedly increased by fasting in both muscles. When tissue was incubated in the presence of 1 munit of insulin/ml, total protein breakdown rate was inhibited by 17-20%, and the response to the hormone was similar in muscles incubated flaccid or at resting length. In contrast, myofibrillar protein breakdown rate was not altered by insulin in any of the muscle preparations. The results support the concepts of individual regulation of myofibrillar and non-myofibrillar proteins and of different effects of various conditions on protein breakdown in different types of skeletal muscle. Thus determination of both tyrosine and 3-MH production in red and white muscle is important for a more complete understanding of protein regulation in skeletal muscle.

Corticosterone alone does not explain increased muscle proteolysis in septic rats.

The mediators and mechanisms of muscle proteolysis in sepsis are not fully known. We investigated the role of corticosterone in increased muscle proteolysis during sepsis in rats. In one series of experiments, plasma corticosterone and total and myofibrillar protein breakdown rates, determined in incubated extensor digitorum longus muscles as release of tyrosine and 3-methylhistidine, respectively, were measured 16 hr after sham operation (control) or cecal ligation and puncture (sepsis). In other experiments, corticosterone (10 mg/100 g body wt) was injected subcutaneously twice over 16 hr; thereafter, plasma hormone levels and muscle protein breakdown rates were determined. Plasma corticosterone was increased from 14 +/- 1 micrograms/dl in control rats to 38 +/- 8 micrograms/dl in septic rats and total and myofibrillar protein breakdown rates were increased by 99 and 326%, respectively, in muscles from septic rats. When administration of corticosterone resulted in plasma levels similar to those observed in septic rats, total or myofibrillar protein breakdown rates were not altered. The results suggest that corticosterone alone is not responsible for increased muscle proteolysis in septic rats. The data, however, do not rule out the possibility that glucocorticoids may be a cofactor to some other substance or substances in the induction of muscle proteolysis during sepsis.

Effects of elevated temperature on protein breakdown in muscles from septic rats.

Elevated temperature has been proposed to contribute to accelerated muscle protein degradation during fever and sepsis. The present study examined the effect of increased temperature in vitro on protein turnover in skeletal muscles from septic and control rats. Sepsis was induced by cecal ligation and puncture (CLP); control rats were sham operated. After 16 h, the extensor digitorum longus (EDL) and soleus (SOL) muscles were incubated at 37 or 40 degrees C. Protein synthesis was determined by measuring incorporation of [14C]phenylalanine into protein. Total and myofibrillar protein breakdown was assessed from release of tyrosine and 3-methylhistidine (3-MH), respectively. Total protein breakdown was increased at 40 degrees C by 15% in EDL and by 29% in SOL from control rats, whereas 3-MH release was not affected. In muscles from septic rats, total and myofibrillar protein breakdown was increased by 22 and 30%, respectively, at 40 degrees C in EDL but was not altered in SOL. Protein synthesis was unaffected by high temperature both in septic and nonseptic muscles. The present results suggest that high temperature is not the primary mechanism of increased muscle protein breakdown in sepsis because the typical response to sepsis, i.e., a predominant increase in myofibrillar protein breakdown, was not induced by elevated temperature in normal muscle. It is possible, however, that increased temperature may potentiate protein breakdown that is already stimulated by sepsis because elevated temperature increased both total and myofibrillar protein breakdown in EDL from septic rats.

Protein synthesis in liver following infusion of the catabolic hormones corticosterone, epinephrine, and glucagon in rats.

The mediator(s) and mechanism(s) of acute-phase protein synthesis in the liver following injury and sepsis are not fully known. Elevated plasma levels of the catabolic hormones cortisol, glucagon, and epinephrine have been reported in trauma and sepsis. In previous reports, when these hormones were infused simultaneously (triple hormone infusion), several, but not all, of the metabolic alterations characteristic of sepsis occurred. In the current investigation, the effect of triple hormone infusion on hepatic protein synthesis was studied. Rats were infused intravenously during 16 hours with a solution containing corticosterone (4.2 mg/kg/h), glucagon (2.5 micrograms/kg/h), and epinephrine (6 micrograms/kg/h). Control animals were infused with a corresponding volume of vehicle. Total hepatic protein synthesis in vivo was measured with a flooding dose technique using [14C]-leucine. The synthesis of total secretory proteins and of the individual proteins albumin, complement component C3, and alpha 1-acid glycoprotein was measured in isolated, perfused liver using [3H]-leucine and a recirculating technique. Urinary excretion of nitrogen and plasma concentration of glucose were higher and plasma total amino acid concentration was lower in hormone-infused than in control rats. Total hepatic protein synthesis in vivo, expressed as the proportion of the protein pool that was replaced each day, was increased from 39% +/- 2% per day to 48% +/- 3% per day (P less than .05) by hormone infusion, but synthesis of secretory proteins in perfused liver was not significantly altered. The results suggest that although total hepatic protein synthesis may be increased by catabolic hormones, other mediator(s) are probably responsible for the stimulation of acute-phase protein synthesis in sepsis.

Total and myofibrillar protein breakdown in different types of rat skeletal muscle: effects of sepsis and regulation by insulin.

Proteolysis is increased in sepsis, but it is not known whether myofibrillar and non-myofibrillar proteins are broken down in the same fashion, or respond to the same regulatory forces as in non-septic muscle. In this study, therefore, the effect of sepsis on total and myofibrillar protein breakdown in incubated rat extensor digitorum longus (EDL) and soleus (SOL) muscles was determined, and the response in vitro to different concentrations of insulin (10 to 10(5) microU/mL) of protein degradation was studied in incubated EDL muscles from control and septic rats. Sepsis was induced in rats weighing 40 to 60 g by cecal ligation and puncture (CLP). Control animals were sham operated. Sixteen hours after CLP or sham operation, intact EDL and SOL muscles were incubated for two hours in oxygenated Krebs-Henseleit bicarbonate buffer containing glucose (10 mmol/L) and cycloheximide (0.5 mmol/L), and total and myofibrillar protein breakdown was assessed from release into incubation medium of tyrosine and 3-methylhistidine (3-MH), respectively. Tyrosine and 3-MH were determined fluorometrically by high performance liquid chromatography (HPLC). Tissue levels of tyrosine and 3-MH remained stable both in control and septic muscles during incubation for two hours. The rate of tyrosine release was increased during sepsis by 58% (P less than .001) and 15% (NS) in EDL and SOL muscle, respectively. The corresponding figures for 3-MH were 103% (P less than .001) and 21% (NS). Tyrosine release was reduced by insulin at a concentration of 10(3) microU/mL in control muscle and at a concentration of 10(4) microU/mL in septic muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Rupture of the stomach complicating bleeding peptic ulcer. Case report.

Three cases of overdistension and rupture of the stomach complicating bleeding ulcer are reported. Despite early surgery two of the patients died of multiorgan failure and rebleeding. The pathogenesis, clinical picture and treatment of this rare condition are discussed. The literature is reviewed.

Effect of methylprednisolone, indomethacin, and diethylcarbamazine on survival rate following trauma and sepsis in rats.

The role of steroids in the treatment of sepsis and septic shock remains controversial, and it is not known if a possible beneficial effect is due to inhibition of the cyclooxygenase or lipoxygenase pathway of arachidonic acid metabolism. In this investigation we studied the effect of methylprednisolone (MP), the cyclooxygenase inhibitor indomethacin (IM), and the lipoxygenase inhibitor diethylcarbamazine (DE) on survival rate in an experimental trauma-sepsis model in rats consisting of laparotomy and intravenous infusion of live E. coli. Groups of rats received saline (control) or MP (30 mg/kg) intravenously 30 min before or after induction of trauma-sepsis. In other groups of animals IM (4 mg/kg) or DE (0.2 mmol/kg) was administered intravenously 30 min before trauma-sepsis. Survival rate was significantly improved by MP or DE given 30 min before trauma-sepsis while the other treatments did not affect the outcome. The results indicate that the beneficial effect of MP on survival rate in the present trauma-sepsis model did not reflect inhibited prostaglandin synthesis but might have been due to inhibited production of leukotrienes.

Penetrating wounds of the neck. Experience from a Swedish hospital.

Stab wounds of the neck were retrospectively studied in 28 patients. Neck stabbings constituted 9% of all stab wounds recorded during the same period. Vascular injuries were most frequent, and the mortality rate was 14%. The management of neck stab wounds is discussed and three cases are presented to illustrate the difficulties and pitfalls. It is proposed that all wounds penetrating the platysma should be explored in general anaesthesia.

Pharmacologic influence on esophageal varices: a preliminary report.

Selective catheterization of the left gastric vein was performed after percutaneous transhepatic portography (PTP) in patients with portal hypertension and esophageal varices. Following the hypothesis that drugs increasing the lower esophageal sphincter (LES) pressure may obstruct the variceal blood flow through the lower esophagus, the effect of different drugs (i.e., intravenous injection of vasopressin, pentagastrin, domperidone and somatostatin and subcutaneous injection of metacholine) on the variceal blood flow was examined. Vasopressin did not change the variceal blood flow; pentagastrin, with its known effect of increasing the LES pressure produced a total interruption of the flow in four of eight patients; domperidone, also known to increase the LES pressure obstructed the variceal blood flow in the only patient examined with this drug; somatostatin has no reported action on the LES but blocked the flow in one of two patients; and metacholine, reported to increase the LES pressure did not produce any change in the flow in the three patients examined. LES pressure was recorded before and during vasopressin infusion in seven patients with portal hypertension and esophageal varices. No reaction on the pressure was found. The patient number in the study is small and the results are nonuniform but still they suggest that drugs increasing the LES tonus might be useful to control variceal blood flow.