Penetrating trauma; experience from Southwest Finland between 1997 and 2011, a retrospective descriptive study.

BACKGROUND: (1) There is lack of epidemiological data on penetrating trauma in European countries. (2) In Finland most acts of violence are performed under the influence of alcohol. The aim of this study was to determine the incidence and types of injury, treatment and survival of patients with penetrating injuries to the thorax and abdomen. METHODS: This study includes two trauma centers with combined catchment area of approximately 720,000 patients. Patients were identified from patient records using ICD-10 codes. RESULTS: Patients were predominantly young males and they were stab victims. The average yearly incidence for penetrating trauma was 0.9/100,000 inhabitants. Thirteen percent of patients admitted gave a negative toxicology screen or breathalyzer test for alcohol. Twenty two percent of wounds were self-inflicted. Fifty five percent of patients received a chest tube and 30 patients (23%) underwent emergent thoracotomy after sustaining critical injury to the thorax. A considerable proportion (12%) of the study group also later died due to alcohol and/or violence, highlighting the psychosocial co-morbidity among penetrating trauma victims. DISCUSSION: Chest tube insertion is a skill to be mastered by any on-call physician. This simple procedure can be potentially life-saving. There is also a call for assessment of psychosocial well-being among penetrating trauma victims.

Treatment of esophageal perforation in octogenarians: a multicenter study.

Esophageal perforation is associated with significant mortality, and this may markedly increase with advanced age. This multicenter study investigates this issue in patients older than 80 years. Data on 33 patients >80 years old who underwent conservative (10 patients), endoclip (one patient), stent grafting (11 patients), or surgical treatment (11 patients) for esophageal perforation were collected from nine centers. Surgical repair consisted of repair on drain in one patient, primary repair in seven patients, and esophagectomy in two patients. Among patients who underwent stent grafting, one required repeat stenting and another stent graft repositioning. One patient was converted to surgical repair after stent grafting. Thirteen patients (39.4%) died during the 30-day and/or in-hospital stay. Their mortality was significantly higher than in a series of patients<80 years old (13.0%, 21/161 patients, P=0.001). Three patients (30.0%) died after conservative treatment, one (100%) after treatment with endoclips, five (45.5%) after stent grafting, and four (36.4%) after surgical repair (P=0.548). Early survival with salvaged esophagus was 42.4% (conservative treatment: 70.0% endoclips 0%, stent grafting: 54.5%, and surgical repair: 54.5%, respectively, P=0.558). Estimated glomerular filtration rate<60 mL/minute/1.73 m2 (70.0% vs. 25.0%, P=0.043) and sepsis (100% vs. 32.1%, P=0.049) at presentation were associated with increased risk of early mortality in univariate analysis. Esophageal perforation in octogenarians is associated with very high early and intermediate high mortality irrespective of the treatment method used.

The prognostic significance of declining health-related quality of life scores at 6 months after coronary artery bypass surgery.

PURPOSE: Health-related quality of life (HRQoL) measured on the EQ-5D (European quality of life-5 dimensions)-questionnaire has been shown to improve after coronary artery bypass grafting (CABG), this study investigated whether changes in HRQoL predict later morbidity. METHODS: Included were 404 consecutive patients undergoing isolated CABG between 2008 and 2010 who filled the EQ-5D-questionnaire at baseline and 6 months postoperatively. Records were reviewed for later major adverse cardiac and cerebrovascular events (MACCE) after 6 months. Follow-up was 38.6 months (10-58). RESULTS: Patients who suffered later MACCE more often had suffered an in-hospital postoperative stroke, had a longer in-hospital stay, had lower HRQoL scores at 6 months and deteriorated on several EQ-5D-subscales. Logistic regression showed 6 months visual analogue scale scores and declining function scores to be independent predictors of later MACCE. CONCLUSION: Deteriorating function and HRQoL-scores at 6 months as compared to baseline postoperatively predict later adverse cardiovascular events after CABG.

Splanchnic and pancreatic tissue perfusion in experimental acute pancreatitis.

BACKGROUND: Gut hypoperfusion has a major role in the pathogenesis of multiple organ failure, which is the main cause of death in severe acute pancreatitis. The effects of experimental acute pancreatitis on splanchnic and pancreatic perfusion and oxygenation were studied to find out whether gut hypoperfusion occurs already at the same time as changes in pancreatic perfusion. METHODS: Twenty-four domestic pigs weighing 21-27 kg were randomized to severe or mild acute pancreatitis or control groups. Eight anaesthetized and mechanically ventilated pigs were intraductally infused with taurocholic acid to induce severe acute pancreatitis and eight received intraductal saline to induce mild acute pancreatitis. Eight pigs served as controls. RESULTS: Intraductally infused taurocholic acid rapidly induced severe necrotizing acute pancreatitis as assessed macroscopically and histologically. Histological changes of mild acute pancreatitis were seen in animals after intraductal saline infusion. After the induction, pancreatic tissue oxygen tension decreased promptly in severe acute pancreatitis and increased in mild acute pancreatitis. Laser-Doppler red cell flux decreased in severe acute pancreatitis. Gut pH gap and pCO2 gap decreased in 2 h after the induction of severe acute pancreatitis. Central haemodynamics were fairly stable throughout the study period in all groups. CONCLUSION: In experimental severe acute pancreatitis, splanchnic malperfusion seems to begin with pancreatic hypoperfusion before disturbances in gut microcirculation.

Pancreatic tissue perfusion in experimental acute pancreatitis.

OBJECTIVE: To investigate pancreatic tissue perfusion and oxygenation in severe and mild experimental acute pancreatitis in pigs. DESIGN: Randomised controlled experiment. SETTING: Animal laboratory, Finland. ANIMALS: 24 domestic pigs weighing 21-27 kg. INTERVENTIONS: 24 pigs were randomised into severe acute pancreatitis, mild acute pancreatitis and control groups (n = 8 in each). The pancreatic duct of eight anaesthetised and mechanically ventilated pigs was cannulated and taurocholic acid was infused into the pancreatic duct to induce severe acute pancreatitis. Eight animals received intraductally infused saline and developed mild acute pancreatitis. Eight pigs had their ducts cannulated alone, and served as controls. MAIN OUTCOME MEASURES: Pancreatic tissue oxygenation, laser Doppler red cell flux, central haemodynamics. RESULTS: Intraductally infused taurocholic acid rapidly induced macroscopically and histologically proven severe necrotising acute pancreatitis. Histological changes characterising mild acute pancreatitis were seen in animals after intraductal saline infusion. Pancreatic tissue oxygen tension decreased in the severe group and increased in the mild group during the six-hour study period. Laser Doppler red cell flux decreased in the severe group. Central haemodynamics, arterial blood gases, and acid base balances were stable throughout the study period in all groups. CONCLUSION: The present model of severe acute pancreatitis significantly impairs pancreatic oxygenation in the early phase. In mild acute pancreatitis, pancreatic oxygenation increases.

Tissue gas tensions in patients with necrotising fasciitis and healthy controls during treatment with hyperbaric oxygen: a clinical study.

OBJECTIVE: To investigate the effect of hyperbaric oxygen (HBO) treatment on tissue oxygen and carbon dioxide tensions in patients with necrotising fasciitis and healthy volunteers. DESIGN: Clinical study in patients and healthy controls. SETTING: University hospital, Finland. SUBJECTS: 6 patients with necrotising fasciitis and 3 healthy volunteers. INTERVENTIONS: Subcutaneous tissue PO2 and PCO2 tensions were measured directly in patients with necrotising fasciitis and in healthy volunteers during normobaric and hyperbaric conditions. Arterial blood PO2 and PCO2 tensions were measured only in the patients. Tissue gas tensions were measured with a Silastic tube tonometer implanted in the brachial subcutaneous tissue of both patients and controls as well as in the subcutaneous tissue of the patients in the immediate vicinity of the necrotising process. The diagnosis of necrotising fasciitis was made on the basis of the presence of typical clinical signs and symptoms, intraoperative findings, and microbiological observations. MAIN OUTCOME MEASURES: Arterial and subcutaneous tissue PO2 and PCO2 tensions. RESULTS: In patients with necrotising fasciitis the arterial PO2 rose about 7-fold whereas the arterial PCO2 increased only slightly during exposure to 2.5 absolute atmospheres (ATA) of oxygen. During HBO the subcutaneous tissue PO2 increased four to five fold from the baseline and CO2 tensions also increased, but to a lesser degree, in both healthy and infected tissues. In patients with necrotising fasciitis, the PO2 was higher, but not significantly so, in the vicinity of the infected area than in the healthy tissue. CONCLUSION: Under hyperbaric conditions the subcutaneous PO2 in patients with necrotising fasciitis rose higher in the vicinity of the infected area than in the healthy tissue, which may be the result of vasodilatation and increased microcirculation induced by the inflammatory process associated with infection or it may be the result of decreased local tissue oxygen utilisation, or both. The tissue PCO2 values tended to rise during HBO probably from hypoventilation or reduced CO2 washout from tissue because venous blood haemoglobin was fully saturated with oxygen.

Social support and physical and psychological recovery one year after myocardial infarction or coronary artery bypass surgery.

The aim of this study was to evaluate the role of different support factors supposed to explain physical and psychological recovery after myocardial infarction (MI) or coronary artery bypass surgery (CABS). The subjects comprised 147 MI patients and 159 CABS patients. Support factors included formal services, semi-formal assistance, and informal social support. The outcome measures used for analysis were functional activities level (Duke Activity Status Index, DASI), physical working capacity, anxiety, and depression one year after MI or CABS. In general, support factors had a limited role in this study. The patient's functional and psychological status at three months was the main determinant to recovery at one year. The outcome factors measured at three months explained 36-56% of their variance at one year, and the support factors increased the explanatory power by 0-10%. The support model employed in this study revealed that some single factors may have a positive or negative role in the recovery after MI or CABS.

Effect of carbogen inhalation on peripheral tissue perfusion and oxygenation in patients suffering from sudden hearing loss.

The effects of repeated carbogen inhalation on peripheral tissue perfusion and oxygenation were assessed in 5 patients suffering from sudden hearing loss by means of continuously measured subcutaneous tissue oxygen and carbon dioxide tension, transcutaneous oxygen tension, laser Doppler red cell flux, and fingertip temperature. The subcutaneous oxygen tension increased clearly during the carbogen inhalation periods, and also, a smaller increase in subcutaneous carbon dioxide tension was simultaneously noticed. The changes in transcutaneous oxygen tension were even greater and the latency was shorter as compared with the subcutaneous gas tensions. The laser Doppler measurements showed no signs of vasoconstriction during the study. In conclusion, carbogen inhalation increases peripheral tissue oxygenation without microvascular vasoconstriction and with only a minor retention of carbon dioxide.

Subcutaneous tissue oxygen and carbon dioxide tensions during hyperbaric oxygenation: an experimental study in rats.

OBJECTIVE: To investigate the response of subcutaneous tissue oxygen (O2) and carbon dioxide (CO2) tensions to hyperbaric oxygenation. DESIGN: Experimental study. SETTING: University hospital, Finland. SUBJECTS: 10 Wistar rats. INTERVENTION: Subcutaneous tissue PO2 and PCO2 were directly measured with an implanted Silastic tube tonometer and capillary sampling technique while breathing air and exposed to hyperbaric oxygen (HBO) at 2.5 or 2.8 ATA pressure. Hyperbaric exposures were carried out in a large multiplace chamber pressurised with air. MAIN OUTCOME MEASURES: Subcutaneous tissue PO2 and PCO2. RESULTS: The mean subcutaneous PO2 rose from the baseline of 8 kPa (60 mmHg) to 16 kPa (112 mmHg) when rats breathed room air during pressurisation to 2.8 atm. When the rats breathed oxygen at 2.5 ATA the maximal mean tissue PO2 was four times higher than the mean starting value. During the HBO treatment at 2.8 ATA the tissue PO2 rose to a value about five times above baseline. The tissue PCO2 values almost doubled during the exposure to HBO at 2.5 ATA, probably because elimination of carbon dioxide was impaired. CONCLUSION: Measurements of tissue PO2 and PCO2 with an implanted Silastic tonometer and a capillary sampling technique can successfully be adapted to hyperbaric conditions. The method yielded reproducible results and is applicable to clinical use in hyperbaric medicine.

Central haemodynamics in experimental acute pancreatitis.

OBJECTIVE: To investigate central haemodynamics in severe and mild acute pancreatitis in pigs. DESIGN: Randomised controlled experiment. SETTING: Animal laboratory, Finland. SUBJECTS: 24 domestic pigs weighing 21-27 kg. INTERVENTIONS: In 8 anaesthetised and mechanically ventilated pigs the pancreatic duct was cannulated and taurocholic acid was infused to induce severe acute pancreatitis. Eight animals received intraductal saline infusion and developed mild acute pancreatitis. Eight pigs were cannulated alone and served as controls. MAIN OUTCOME MEASURES: Cardiac index, heart rate, mean arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, haemoglobin, arterial blood gases and acid base balance. RESULTS: Intraductally infused taurocholic acid rapidly induced severe necrotising acute pancreatitis as assessed both macroscopically and histologically. Histological changes of mild acute pancreatitis were seen in animals after intraductal saline infusion. Central haemodynamics, arterial blood gases, and acid base balances were stable throughout the study period in all groups. The main finding was haemoconcentration as indicated by the increase in arterial haemoglobin concentration in pigs with mild and severe acute pancreatitis. CONCLUSION: Haemoconcentration precedes central haemodynamic alterations in experimental acute pancreatitis.

Central hemodynamic changes in experimental muscle crush injury in pigs.

To investigate central and pulmonary hemodynamics in a standardized normovolemic experimental muscle injury model, 8 anesthetized and mechanically ventilated test pigs were intracavally infused with 100 ml of autologous muscle extract over a period of 100 min; 8 control pigs received Ringer's solution. The cardiac index decreased 20% and the heart rate decreased 10% within 30 min of starting the infusion in the muscle extract group and remained depressed. Mean arterial pressure increased significantly in both groups. The pulmonary capillary wedge pressure and central venous pressure remained relatively unchanged during the 5-hour study. A 2-fold increase in mean pulmonary arterial pressure and a nearly 4-fold increase in the pulmonary vascular resistance index was seen in the muscle extract infusion group, which however returned to normal. Arterial hemoglobin concentration and systemic vascular resistance index remained fairly stationary in both groups. Immediate significant decreases in both arterial oxygen saturation and arterial oxygen tension were observed in the muscle extract group, however both variables recovered towards the end of the experiment. A slight increase in arterial blood pH value was noted during the experiment. In conclusion, autologous muscle extract infusion causes decreases in heart rate and cardiac index, as well as a significant increase in pulmonary vascular tone and systemic hypoxemia, emphasizing the detrimental effects of skeletal muscle injury following severe trauma.

Experimental fat embolism induces urine 2,3-dinor-6-ketoprostaglandin F1alpha and 11-dehydrothromboxane B2 excretion in pigs.

OBJECTIVE: To evaluate the in vivo production of prostacyclin and thromboxane A2 during the initial phase of experimental fat embolism as assessed, respectively, by determinations of urine 2,3-dinor-6-ketoprostaglandin F1alpha and 11-dehydrothromboxane B2 excretion. DESIGN: Randomized, controlled trial. SETTING: Animal laboratory. SUBJECTS: Twenty seven domestic pigs, weighing 24 to 31 kg. INTERVENTIONS: All pigs were anesthetized and mechanically ventilated during the experiment. Eighteen pigs were subjected to an intracaval infusion of 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins. Nine pigs received only bone marrow suspension (fat embolism group). Nine pigs were given an intravenous bolus of aspirin (300 mg) 1 hr before the bone marrow suspension infusion. After the induction of fat embolism, intravenous aspirin was administered at a dose of 150 mg/hr for 2 hrs (aspirin-treated group). Nine pigs were infused with saline (control group). MEASUREMENTS AND MAIN RESULTS: In the fat embolism group, cardiac index decreased within 30 mins, while mean arterial pressure remained unchanged. Central venous pressure and pulmonary artery occlusion pressure remained relatively stable over time in the animals with fat embolism. Mean pulmonary arterial pressure and pulmonary vascular resistance increased immediately after the bone marrow suspension infusion from 23 +/- 0.8 (SEM) to 34 +/- 1.3 mm Hg and from 305 +/- 28 to 585 +/- 45 dyne x sec/cm5, respectively; these variables remained increased throughout the study period. Simultaneously, pulmonary shunt in the fat embolism group increased persistently from the baseline of 12.3 +/- 2.8%, and reached its maximum of 26.1 +/- 4.8% at the end of the experiment. Instant and gradual decreases in PaO2 (from 95 +/- 4 to 67 +/- 5 torr [12.6 +/- 0.5 to 8.9 +/- 0.7 kPa]), hemoglobin oxygen saturation (from 97.2 +/- 0.4 to 91.8 +/- 1.8%), and oxygen delivery (from 16.3 +/- 1.0 to 12.6 +/- 0.4 mL/min/kg) were observed in the fat embolism group. In the bone marrow suspension-infused animals, urine 2,3-dinor-6-ketoprostaglandin F1alpha excretion increased transiently from 451 +/- 63 up to 1466 +/- 499 pg/micromol creatinine, while urine 11-dehydrothromboxane B2 excretion increased transiently from 385 +/- 36 up to 2307 +/- 685 pg/micromol creatinine. In the aspirin-treated animals, urinary excretion of these prostanoid metabolites was reduced by 81% and 88%, respectively. The changes in mean pulmonary arterial pressure and PaO2 were ameliorated, and the alterations in pulmonary shunt and SaO2 were abolished in the animals with aspirin treatment. CONCLUSIONS: Pulmonary hypertension, increased pulmonary vascular tone, and increased pulmonary shunt are hallmarks of the present fat embolism model. These hemodynamic responses may, at least partly, be related to the changed balance between prostacyclin and thromboxane A2 production.

Catalytic activity of phospholipase A2 in serum in experimental fat embolism in pigs.

OBJECTIVE: To investigate the catalytic activity of phospholipase A2 in serum during the early phase of experimental fat embolism. DESIGN: Randomised controlled experimental study. SETTING: Animal laboratory, Finland. SUBJECTS: 18 domestic pigs weighing 25-31 kg. INTERVENTIONS: Allogeneic bone marrow suspension at a dose of 100 mg/kg was infused intracavally in 9 anaesthetised, mechanically ventilated, and haemodynamically monitored pigs; 9 control pigs received saline. MAIN OUTCOME MEASURES: Central haemodynamics, blood gases, catalytic activity of phospholipase A2. RESULTS: In the fat embolism group, there were significant increases in mean pulmonary arterial pressure (p < 0.001), pulmonary vascular resistance (p < 0.001) and pulmonary shunting (p < 0.05) and simultaneously, systemic oxygenation was significantly impaired. The animals with fat embolism developed gradual fever and leucocytosis, whereas the catalytic activity of phospholipase A2 remained relatively unchanged. CONCLUSION: In this experimental model the measurement of serum phospholipase A2 activity does not provide a useful tool for the early detection of experimental fat embolism.

Resource support and heart patient recovery.

This prospective study examines the effects of resources utilized by myocardial infarction (MI) and coronary artery bypass (BY) patients in the recovery process. The resource support model incorporates formal (institutionalized) and semi-formal (mutual aid) services along with informal assistance (social networks). Patient interview data were collected on 147 MI and 159 BY patients at hospitalization and at 3 months. Sociodemographic, illness and resource data were obtained, and hospital records were abstracted. Two outcomes were evaluated: activity limitations and work capacity. Bivariate and multivariate analyses were used to assess individual and resource effects. Multivariate analyses revealed that, for MI patients, a higher level of activity prior to hospitalization and a shorter hospital stay were significantly related to recovery. A smaller social network with greater frequency of contact enhanced recovery. For BY patients, recovery was significantly associated with higher social class higher level of activity prior to hospitalization and fewer health care visits. Outcome based on work capacity revealed that MI patients who were younger in age, male sex and who had fewer prescribed medications were more likely to recover. By patients had a similar pattern as that observed for MI patients in terms of age and sex. Co-morbidity had a negative effect on recovery. Those with less affective informal support were more likely to have recovered. The resource support model employed in this prospective study proved to have mixed results. However, the model may be a useful multifactorial framework for examining the effects on patient recovery over a longer duration.

Plasma levels of atrial natriuretic peptide and endothelin-1 in experimental fat embolism.

In order to understand the role of vasoactive peptides in fat embolism, arterial plasma atrial natriuretic peptide (ANP) and endothelin-1 concentrations were investigated in an experimental study. Nine anesthetized and mechanically ventilated pigs received an intracaval infusion of allogeneic bone marrow suspension at a dose of 100 mg/kg (fat embolism group); 9 control pigs received saline. The observation period was 5 h. In the fat embolism group, cardiac index and heart rate decreased within 30 min, whereas mean arterial pressure remained stationary. Pulmonary capillary wedge pressure rose transiently and central venous pressure rose slightly in time, while mean pulmonary arterial pressure, pulmonary vascular resistance and pulmonary shunt increased immediately and persistently after the bone marrow suspension infusion. Simultaneously, arterial oxygen tension and arterial hemoglobin oxygen saturation decreased markedly. Arterial plasma ANP and endothelin-1 concentrations remained stable in the fat embolism animals, whereas in the controls ANP and endothelin-1 levels decreased at 3 and 5 h. Arterial epinephrine concentrations were stable in animals receiving bone marrow suspension, while in the controls arterial epinephrine concentrations decreased towards the end of the experiment. Arterial norepinephrine concentrations remained unchanged in both groups. To conclude, impaired pulmonary function and consequent systemic hypoxemia distinguish the present fat embolism model. Unchanged arterial ANP and endothelin-1 concentrations in the fat embolism group suggest that these circulating vasoactive hormones have a minor impact on the pathogenesis of the current experimental fat embolism.

Splanchnic and peripheral tissue perfusion in experimental fat embolism.

OBJECTIVE: To investigate the acute effects of experimental fat embolism on splanchnic and peripheral perfusion and oxygenation in pigs. DESIGN: Randomized, controlled trial. SETTING: Animal laboratory. SUBJECTS: Eighteen domestic pigs, weighing 25 to 31 kg. INTERVENTIONS: The 18 pigs were randomized to either the fat embolism or control groups. Nine anesthetized and mechanically ventilated pigs were intracavally infused with a 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins (the fat embolism group); nine control pigs received normal saline in the same volume and speed (control group). MEASUREMENTS AND MAIN RESULTS: Mean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary shunt increased, and PaO2 decreased immediately after the bone marrow suspension infusion. In the fat embolism animals, oxygen delivery decreased, oxygen content difference widened, and total oxygen consumption remained high, indicating enhanced oxygen extraction. Further, superior mesenteric artery blood flow and mesenteric oxygen delivery decreased, while intramucosal pH in the small bowel was stable. Subcutaneous PO2 decreased in both groups, whereas transcutaneous PO2 decreased only in the animals receiving bone marrow suspension. Skin red cell flux showed no significant changes. CONCLUSIONS: The present model of fat embolism results in significant impairment in systemic oxygenation. Despite this fact, the intestinal oxygenation remains unaffected probably due to sufficient compensatory mechanisms. Transcutaneous PO2 measurements may provide a useful index for early detection of fat embolism.

Phospholipases A2 in the serum of patients after coronary artery bypass surgery.

OBJECTIVE: To study the catalytic activity of phospholipase A2 and the concentrations of group I and group II phospholipase A2 in the sera of patients during and after coronary artery bypass surgery. DESIGN: Prospective study. SETTING: University hospital and research laboratory. PATIENTS: Fourteen consecutive patients operated on for ischemic heart disease. INTERVENTIONS: The catalytic activity of phospholipase A2 and the serum concentrations of group I and group II phospholipases A2 were measured before, during, and after the operation until the seventh postoperative day. A total of 196 blood samples were taken from 14 patients. MEASUREMENTS AND MAIN RESULTS: The catalytic activity of phospholipase A2 and the concentration of group II phospholipase A2 increased in the sera of patients after coronary artery bypass surgery. The concentration of Group I phospholipase A2 did not change. The catalytic activity of phospholipase A2 correlated significantly with group II but not with group I phospholipase A2 values. CONCLUSIONS: The increase in the catalytic activity of phospholipase A2 in serum after coronary artery bypass surgery is due to group II phospholipase A2. The present results suggest that group II phospholipase A2 is responsible for the physiologic and pathophysiologic effects of catalytically active phospholipase A2 after coronary artery bypass surgery.

Effects of experimental fat embolism on central hemodynamics and oxygenation in pigs.

Nine anesthetized and mechanically ventilated test pigs were intracavally infused with a 10% allogeneic bone marrows suspension at a dose of 100 mg/kg over 5 min; 9 control pigs received saline. The cardiac index decreased slightly in the fat embolism animals. Left ventricular stroke work remained unchanged in both groups, whereas right ventricular stroke work rose in the fat embolism animals. Mean arterial pressure remained stationary in the test group but rose in the controls. Pulmonary capillary wedge pressure and central venous pressure rose slightly in the test group. After infusion of the bone marrow suspension, mean pulmonary arterial pressure, pulmonary vascular resistance, pulmonary shunt and alveoloarterial oxygen tension difference increased immediately and remained elevated throughout the study period. Simultaneously, arterial and mixed venous oxygen tension and hemoglobin oxygen saturation decreased. Arterial carbon dioxide tension and hematocrit remained stationary. The fat embolism animals developed gradual fever. In conclusion, increased mean pulmonary arterial pressure, pulmonary vascular resistance, pulmonary shunt and alveoloarterial oxygen tension difference proved to be useful early indicators of experimental fat embolism.

Effects of dexmedetomidine on coronary hemodynamics and myocardial oxygen balance.

OBJECTIVE: alpha 2-adrenergic agonists decrease central sympathetic outflow and maintain normal transmural myocardial blood flow distribution, but intravenous bolus doses of these agents can also induce excessive coronary vasoconstriction and myocardial ischemia. The hypothesis of the present study was that a rapid intravenous bolus of dexmedetomidine, a specific alpha 2-adrenergic agonist, will cause coronary vasoconstriction and accompanying myocardial ischemia in young pigs. DESIGN: Prospective, controlled study on experimental animals. SETTING: Animal laboratory of a university cardiorespiratory research center. PARTICIPANTS: Twelve domestic 8-week-old open-chest pigs, anesthetized with high-dose fentanyl. Another six pigs served as controls. INTERVENTIONS: Sequential intravenous dexmedetomidine boluses of 3, 10, and 30 mg/kg were administered, and responses were measured during peak changes (2 minutes after injection) and during recovery after each dose. MEASUREMENTS AND MAIN RESULTS: Left anterior descending coronary artery blood flow, calculated regional coronary vascular resistance, myocardial extraction of oxygen and lactate, plasma catecholamine levels, and conventional central hemodynamic parameters were measured. The two higher doses of dexmedetomidine induced 21% and 29% immediate increases in left anterior descending coronary artery blood flow. At the same time mean systemic blood pressure and pulmonary capillary wedge pressure increased, and calculated regional coronary vascular resistance increased. Myocardial extraction of oxygen and lactate remained unchanged. CONCLUSIONS: Large intravenous doses of dexmedetomidine caused moderate regional coronary vasoconstriction without metabolic signs of myocardial ischemia in young domestic pigs at the same time as a marked vasoconstrictive response in the systemic circulation.

Serum phospholipases A2 after aortobifemoral reconstruction.

Phospholipase A2 has been implicated in the pathogenesis of local and distant tissue injury after ischaemia and reperfusion. A common operation inducing ischaemia and reperfusion is aortobifemoral reconstruction, during which the aorta is clamped and the blood supply via the inferior mesenteric artery and iliac arteries is interrupted. The purpose of the present work was to study the catalytic activity concentration of phospholipase A2 and the mass concentrations of group I and group II phospholipases A2 in the sera of patients undergoing aortobifemoral reconstruction. Both the catalytic activity concentration of phospholipase A2 and the mass concentrations of group I and group II phospholipases A2 increased in serum samples after the operation. The catalytic activity concentration of phospholipase A2 correlated well with group II phospholipase A2 mass values (r = 0.81, p < 0.001), whereas no correlation was found between the catalytic activity concentration of phospholipase A2 and group I phospholipase A2 mass values (r = 0.12, p = 0.54). The results emphasize the role of group II phospholipase A2 in tissue injury after ischaemia and reperfusion.