Biomedical subjects

G W Machiedo

Publications and source records attributed to G W Machiedo.

At least 19 recordsLinked to original sources

PubMed1992

The role of laparoscopy in abdominal trauma.

Thirty-nine hemodynamically stable trauma patients were evaluated prospectively by laparoscopy before planned celiotomy. Laparoscopy was performed using a forward-viewing laparoscope connected to two high-resolution video monitors. The mechanism of injury was blunt trauma in eight, stab wounds (SWs) in 16, and gunshot wounds (GSWs) in 15. Laparoscopy correctly identified the presence of an intraperitoneal injury in 26 patients. Six other patients had retroperitoneal injuries, five of which were seen on laparoscopy. The remaining seven patients had no demonstrable intraperitoneal or retroperitoneal injuries, did not undergo celiotomy, and were observed without morbidity. In comparison with findings at surgery, laparoscopy identified injuries to the liver in eight of ten, to the diaphragm in three of three, to the colon in two of three, to the stomach in three of three, to the kidney in one of one, to the spleen in none of three, and to the small bowel in none of four patients. Visualization of the spleen was achieved in only one patient. The extent of the hemoperitoneum was underestimated from the laparoscopic examination in all nine patients with greater than 750 mL of peritoneal blood, four of whom had undetected active bleeding. Laparoscopy was performed easily in all patients and there were no complications associated with its use. In conclusion, the absence of an intra-abdominal injury was correctly identified with laparoscopy in 11 patients and laparoscopy may decrease the need for celiotomy in selected patients. However, the inability to "run the small bowel," visualize the spleen, and evaluate hemorrhage limits the utility of laparoscopy in determining which patients with laparoscopically visualized injuries will require celiotomy.

Abdominal Injuries↗

PubMed1991

Reoperative versus conservative management for gastrointestinal fistulas.

Development of a fistula is a serious complication. It is necessary to identify its anatomic and pathologic features, as these can influence the outcome of treatment independent of the primary disease. Electrolyte abnormalities should be addressed as volume deficits are being restored. Sepsis, the most common cause of death in patients with fistulas, must be controlled, and the skin must be protected. Reoperation and conservative management are not opposing forms of therapy but rather are complementary.

Fistula↗

PubMed1991

Red cell deformability is an early indicator of infection.

Red blood cells (RBC) have been shown to become less deformable during infection. The RBC deformability index (DI) was measured within 24 hours of admission in 37 patients who had suffered trauma and every 48 to 72 hours thereafter while they were in the surgical intensive care unit to assess whether DI could be used as an early indicator of infection after injury. Infection was defined as a temperature of 101 degrees F or more and a white blood cell count of more than 12,000/cm3 associated with a positive culture. Eighteen patients developed an infection, and 19 patients did not. On day 1, both groups showed a significant decrease in DI, compared to controls (0.33 +/- 0.18 and 0.34 +/- 0.25 for patients with infection and patients with no infection vs 1.52 +/- 0.12 for control volunteers; p less than 0.05). In the group with no infection, the DI improved in 16 of 19 patients after injury; the DI in patients with infection continued to decrease in 17 of 18 patients. The decrease in DI occurred 4 +/- 2 days (range, 2 to 8 days) before the diagnosis of infection. No significant differences were apparent in the absolute white blood cell count between the group with infection and the group with no infection at any time after injury. Differences in maximal temperature were noted on day 3 and beyond; however, 30% of patients with no infection had a temperature of more than 101 degrees F for 7 days. These data show that trauma results in a significant decrease in RBC deformability and that serial changes in DI appeared to predict which patients would develop an infection and which patients would recover uneventfully. RBC deformability may be helpful in early detection of infection in patients who have suffered trauma.

Adolescent↗

PubMed1991

Effect of oxygen-free radical scavengers on survival in sepsis.

UNLABELLED: Sepsis remains a leading cause of death in the surgical intensive care unit (SICU) patient following major surgery or trauma. Recent work has demonstrated that oxygen-free radicals (OFR) generated during sepsis contribute to the pathogenesis of this syndrome. The purpose of this study was to evaluate the effect of various new free radical scavengers on survival in sepsis. A total of 85 male Sprague-Dawley rats were placed into one of the following treatment groups. CONTROL: cecal ligation and puncture (CLP); PRE-AT: pretreatment with alpha-tocopherol (AT) 10 mg/100 gm SC x 3 days, and 5 mg/100 gm IV prior to CLP; AT: 20 mg/100 gm at time of CLP and 4 hours following CLP; U74006F: (21-aminosteroid which inhibits lipid peroxidation) 3 mg/kg IV at the time of and 4 hours following CLP; U78517F: (alpha-tocopherol analogue) 3 mg/kg at the time of and 4 hours following CLP. Survival was determined at various time points up to 72 hours. Pretreatment with AT resulted in improved survival, whereas the novel OFR scavengers U78517F and U74006F significantly improved survival and were efficacious without pretreatment. It was concluded that OFR scavengers can improve survival in sepsis.

Animals↗

PubMed1991

Oxygen free radicals: effect on red cell deformability in sepsis.

OBJECTIVE: To examine the effect of alpha-tocopherol, a free radical scavenger, on RBC deformability, mixed venous hemoglobin saturation (SvO2), arterial-venous oxygen content difference (C[a-v]O2), pHv, and survival during sepsis. DESIGN: Randomized controlled study. INTERVENTIONS: Sprague-Dawley rats were randomized to three groups: sham, cecal ligation and puncture, or alpha-tocopherol/cecal ligation and puncture (pretreatment with alpha-tocopherol before cecal ligation and puncture). MEASUREMENTS AND MAIN RESULTS: The cecal ligation and puncture group had a significantly (p less than .05) higher SvO2 and lower C (a-v)O2, pHv, and survival rate when compared with alpha-tocopherol/cecal ligation and puncture and sham groups. No difference in pHa existed between groups. CONCLUSIONS: The alpha-tocopherol treatment improves survival in sepsis. RBC deformability during sepsis is prevented by alpha-tocopherol, suggesting that free radicals may cause the decrease in RBC deformability. This study provides indirect evidence that decreased RBC deformability may play a role in the physiologic peripheral shunting and decreased microcirculatory flow that occurs during sepsis.

Animals↗

PubMed1990

Kupffer cell-hepatocyte interactions and the changes in 1-14C-arachidonate incorporation in response to endotoxin in vitro.

The present experiments were undertaken to elucidate the effect of either the hepatocyte (HC) or hepatocyte supernatant on prelabeled endotoxin (LPS)-stimulated Kupffer cell (KC) arachidonic acid utilization. HC, KC, or their coculture were incubated for 18 hours with labeled 1-14C- arachidonic acid followed by a 24 hour incubation with 10 micrograms/ml LPS. LPS had no effect on the percent distribution of labeled arachidonate into the HC phospholipid or neutral lipid. KC showed a decreased percent neutral lipid labeled arachidonic acid distribution with generally no effect on the phospholipid. However, KC:HC cocultures or the addition of HC supernatant to KC exposed to LPS dramatically reversed the labeled arachidonate distribution into the KC with an increased incorporation into neutral lipid. Labeled PGE2 and PGD2 were increased in the KC following incubation with HC supernatant while only labeled PGE2 levels were elevated in the cocultures. The changes in the distribution of cell's labeled arachidonate required the addition of LPS. These results suggest that the HC can promote changes in the lipid fraction during sepsis by elaborating a substance that can modulate labeled arachidonate distribution in the KC lipids as well as stimulate prostaglandin production.

Animals↗

PubMed1990

Organ distribution of gut-derived bacteria caused by bowel manipulation or ischemia.

Translocation of carbon-14-labeled Escherichia coli from the gut was studied at the specified times in the following groups of rats: Group 1, 5 hours after ligation of the superior mesenteric artery; Group 2, 5 hours after laparotomy and exposure of the superior mesenteric artery with gentle removal and replacement of the intestines; and Group 3, 5 hours after handling but no surgical manipulation. Both living and dead bacteria were administered by means of gavage, and the effect of viability, intestinal ischemia without reperfusion, and bowel manipulation on the translocation of enteric bacteria was assessed. We demonstrated that (1) even gentle bowel manipulation causes bacteremia as great as that associated with ligation of the superior mesenteric artery; (2) dead E. coli are absorbed into the blood in the presence of bowel manipulation or ischemia but less effectively than are live E. coli; (3) live bacteria are found in highest concentration in the lung and in descending order in the liver, kidney, heart, and spleen; (4) dead bacteria absorbed from the gut are found in highest concentration in the kidney and the liver. Lesser amounts are found in the lung, spleen, and heart.

Administration, Oral↗

PubMed1990

Organ distribution of radiolabeled enteric Escherichia coli during and after hemorrhagic shock.

Translocation of intestinal bacteria to the blood during hemorrhagic shock (HS) has been confirmed in rats and humans. The current study was designed to trace the path of translocated intestinal bacteria in a murine HS model. Thirty-one rats were gavaged with 1,000,000 counts of viable 14C oleic acid-labeled Escherichia coli. Forty-eight hours later the animals were bled to 30 mmHg until either 80% of their maximal shed blood was returned or 5 hours of shock had elapsed and they were resuscitated with Ringer's lactate as previously described. Control animals were cannulated but not shocked. Eight rats immediately after shock and resuscitation, 6 rats 24 hours after shock, 3 rats 48 hours after shock, and 4 animals that died in shock had their heart, lung, liver, spleen, kidney, and serum harvested, cultured, and radioactive content measured. Translocated enteric bacteria are found primarily in the lung immediately after shock with redistribution to the liver and kidney 24 hours later. Animals surviving to 48 hours were capable of eliminating the majority of the bacteria from their major organ systems. Positive cultures for E. coli were also found in the blood, lung, liver, and kidney. We speculate that the inflammatory response stimulated by the bacteria in these organs may contribute to the multiple-organ failure syndrome seen after HS.

Animals↗

PubMed1990

Hepatocyte modulation of Kupffer cell prostaglandin E2 production in vitro.

It is likely that dynamic interactions between hepatocytes and Kupffer cells contribute to the responses of these cell types both under normal conditions and during sepsis. In this study, we examined the influences of hepatocytes on the concentration of the inflammatory mediator PGE2 in Kupffer cell cultures. Evidence to suggest that cultured rat hepatocytes both metabolize PGE2 and produce a substance that promotes LPS-stimulated Kupffer cell PGE2 biosynthesis include the following: 1) PGE2 levels in Kupffer cell: hepatocyte coculture were lower than the levels in Kupffer cell cultures early after LPS stimulation; 2) 36 h after LPS, coculture PGE2 levels exceeded the levels in Kupffer cell cultures despite the demonstrated capacity for hepatocytes to metabolize PGE2; 3) a transferable, non-dialyzable, and heat-unstable factor in hepatocyte supernatant promoted PGE2 production when added to Kupffer cells with LPS or after LPS; 4) there was no increased PGE2 synthesis when the hepatocyte supernatant was added without LPS or if hepatocyte supernatant was preincubated with the Kupffer cells for 6 or 18 h before LPS administration; 5) there was an inability of the hepatocyte factor to promote PGE2 production in response to other macrophage-activating agents, including calcium ionophore A23187 or phorphol myristate acetate; and 6) there was no increased cell replication or protein synthesis in the Kupffer cell cultures following hepatocyte supernatant incubation. The increased Kupffer cell PGE2 production by the hepatocyte supernatant was not due to contamination of the hepatocyte supernatant by endotoxin or PGE2. These in vitro results raise the possibility that hepatocytes have the capacity to modulate local PGE2 levels by two distinct mechanisms. Hepatocytes can metabolize PGE2 as well as release factor(s) which promote LPS-induced PGE2 production by Kupffer cells.

Animals↗

PubMed1990

A "treated" model for severe hemorrhagic shock: a comparison of conventional and germ-free animals.

In an unanesthetized "treated" model of severe hemorrhagic shock, a bacteremia originating from the animal's enteric flora was demonstrated by finding radiolabeled Escherichia coli in the blood as early as 2 hr after the onset of shock. In 50 patients admitted to our trauma unit, the observation was similar, with 56% positive blood cultures, when their mean arterial blood pressure was 80 mmHg or less. The relationship of bacterial translocation and the high post-shock mortality in our conventional (CV) animal model is being evaluated in germfree (GF) Sprague-Dawley rats. Preliminary observations in 15 GF animals showed 80% survival at 24 hr post-shock, 54% at 48 hr, and 42% at 72 hr compared with those of CV animals in previous experiments with survival at similar times of 73%, 20% and 7%, respectively.

Animals↗

PubMed1990

A comparison of intravenous access sites for bolus injections during shock and resuscitation after emergency room thoracotomy with and without aortic crossclamping.

Thoracotomy with aortic crossclamping is used to resuscitate trauma victims. Pharmacologic boluses are often given via intravenous lines of central, brachial, or femoral origin. This study was undertaken to determine the efficacy of intravenous access site on delivery of a bolus injection to the heart with thoracotomy and aortic crossclamping during shock and resuscitation. Six dogs were anesthetized, intubated, and underwent brachial and femoral venotomy and Swan-Ganz insertion (central). Baseline measurements of central, brachial, and femoral transit times for 10 cc cold saline were obtained via Swan-Ganz thermistor. Each animal then underwent thoracotomy, aortic crossclamping alone, hemorrhage to blood pressure (BP) 50 mm Hg for 30 minutes with aorta unclamped and then aorta crossclamped and resuscitation with lactated Ringer's Solution with aorta unclamped and then crossclamped. Femoral-Brachial Index (FBI) was determined by dividing femoral transit time by brachial transit time at each observation. The data suggest that femoral access significantly prolongs bolus transit time when compared with central or brachial access during aortic crossclamping in the euvolemic, shock, or aggressively resuscitated model. Brachial access is therefore the preferred route for bolus injection delivery in the emergency room thoracotomy with or without aortic crossclamping because it provides expedient bolus delivery equal to central access and superior to femoral access.

Analysis of Variance↗

PubMed1989

The incidence of decreased red blood cell deformability in sepsis and the association with oxygen free radical damage and multiple-system organ failure.

We studied the incidence of decreased red blood cell deformability (RBCD) in sepsis and the association between decreased RBCD and oxygen free radical generation (as measured by malonyldialdehyde) and the occurrence of multiple-system organ failure (MSOF). Patients were divided into three groups: septic (n = 28), nonseptic (n = 15), and control (n = 5). Serial measurements of deformability index, malonyldialdehyde, and MSOF were made. The deformability index for the septic group (0.23 +/- 0.17) was significantly less than that for the nonseptic (1.12 +/- 0.48) and control (1.11 +/- 0.25) groups. The malonyldialdehyde levels for the septic group (4.5 +/- 1.0 nmol/mL) were significantly greater than those for the nonseptic (2.7 +/- 0.9 nmol/mL) and control (2.6 +/- 0.8 nmol/mL) groups. The MSOF index for the septic group (10.1 +/- 2.5) was significantly greater than that for the nonseptic (7.6 +/- 1.7) and control (6.0 +/- 0.0) groups. An inverse correlation existed between malonyldialdehyde and deformability index ( = .501, less than .001, n = 40) and between deformability index and MSOF index (= .350, less than .05, n = 61). We conclude that RBCD is decreased during human sepsis; free radicals generated during sepsis may play a role in the decrease in RBCD. Decreased RBCD may contribute to the MSOF that occurs during sepsis.

Adult↗

PubMed1989

Does the bacteremia observed in hemorrhagic shock have clinical significance? A study in germ-free animals.

We have recently reported the rapid appearance of bacteria and endotoxin in the blood of rats and of trauma patients in the course of 30 minutes to 2 hours of hemorrhagic shock. The current study was designed to determine the effect of this bacteremia and endotoxemia on survival. Thirty-three conventional (C:group 1) and 36 germ-free (GF:group 2) Sprague Dawley rats were subjected to our previously described model of treated hemorrhagic shock. Survival in the GF group was significantly better than the C group at 24, 48, and 72 hours after shock. Endotoxin levels were elevated in 88% of C group during shock and in 28% of GF group. The gut of the GF animal contains endotoxin (26 ng/gm of stool) as does the sterile food supply (393 ng/gm of rat chow).

Animals↗

PubMed1988

Red blood cell deformability in human and experimental sepsis.

Red blood cell (RBC) "deformability" is necessary for maintenance of normal microcirculation. To determine whether RBC deformability was affected in human or murine sepsis, a deformability index was determined in a human study and a murine model. Deformability was decreased postoperatively in patients with sepsis (0.49 +/- 0.12) compared with patients without sepsis (1.62 +/- 0.13) and normal control volunteers (1.51 +/- 0.17). Deformability was decreased in rats that had undergone cecal ligation and puncture (0.37 +/- 0.06) compared with that of sham-operated rats (0.76 +/- 0.12), as well as in endotoxemic rats (0.38 +/- 0.4) compared with control rats (0.82 +/- 0.11). These data suggest that RBC deformability decreases in both human and murine sepsis. This effect could be an important factor in the disordered oxygen utilization noted in human sepsis, and its correction could lead to better tissue oxygenation and preserved organ function.

Animals↗

PubMed1988

Temporal relationship of hepatocellular dysfunction and ischemia in sepsis.

To determine whether hepatic dysfunction in sepsis results from hypoperfusion or direct cellular injury, Sprague-Dawley rats underwent either cecal ligation and puncture or sham operation. After either two or six hours, effective hepatic blood flow was measured using the galactose clearance method. Hepatocytes were isolated and intracellular sodium and potassium and glucose production were measured. Hepatic blood flow in septic rats decreased as early as two hours after sepsis when compared with sham-operated rats (3.8 +/- 1.4 vs 8.7 +/- 3.1 mL/min/100 g body weight). Intracellular sodium and potassium levels and glucose production in septic rats were not significantly different when compared with controls at two hours. After six hours, hepatic blood flow remained depressed and intracellular sodium level was increased compared with sham-operated rats (41.7 +/- 10.4 vs 31.4 +/- 5.9 mmol/L [41.7 +/- 10.4 vs 31.4 +/- 5.9 mEq/L]) and potassium decreased compared with controls (90.7 +/- 7.9 vs 111.5 +/- 6.7 mmol/L [90.7 +/- 7.9 vs 111.5 +/- 6.7 mEq/L]). Glucose production was decreased in septic rats after six hours when compared with controls (4.7 +/- 1.5 vs 15.4 +/- 6.4 mumol/g hepatocytes). These data suggest that hepatic blood flow is decreased before alterations in intracellular sodium and potassium as well as glucose production.

Animals↗

PubMed1988

The gut as source of sepsis after hemorrhagic shock.

In a model of severe hemorrhagic shock in rats, blood culture findings became positive within 2 to 4 hours of shock. The organisms cultured were primarily gram-negative. To test the hypothesis that the gut was the source of the bacteria, E. coli labeled with carbon-14 oleic acid were fed to rats undergoing hemorrhagic shock. Their plasma was then assayed for carbon-14 activity. Seven of the 14 shocked animals demonstrated increased plasma carbon-14 activity during or after shock. The mortality rate was 100 percent 80 hours postshock, and all animals had E. coli on subsequent blood culture. The seven rats without increased plasma carbon-14 activity had a survival rate of 83 percent postshock. Sham-shocked animals did not exhibit plasma carbon-14 levels greater than the background levels. These data suggest that bacterial translocation occurs during hemorrhagic shock and that the gut is the source of the bacteremia seen during hemorrhagic shock.

Animals↗

PubMed1988

Detection of sepsis in the postoperative patient.

It becomes evident, therefore, that there is no one indicator, either clinical or laboratory, sufficient to diagnose infection in the postoperative patient. Only a skillful clinician using the multiple modalities available and combining them with a careful history and physical examination and a high index of suspicion will be able to diagnose and treat infection in a timely manner and so avoid the physical, emotional, and fiscal costs of a late or missed diagnosis.

Abdomen↗

PubMed1988

Endotoxemia and bacteremia during hemorrhagic shock. The link between trauma and sepsis?

Previous investigations of a treated model of hemorrhagic shock in the rat indicated the frequent occurrence of bacteremia that appeared to derive from the gut. This paper determines the incidence of bacteremia and endotoxemia during the acute shock period and compares this with similar observations in humans in varying degrees of shock. Studies in 26 rats indicated that bacteremia and endotoxemia was present in 50% and 87%, respectively, by the end of 2 hours at a mean arterial pressure of 30 mmHg. Observations in 50 patients admitted to the trauma unit showed that positive bacterial blood cultures were present in 56% when the admission systolic blood pressure was 80 mmHg or less (p less than 0.01 compared with either of the other groups). Endotoxemia was noticed in two such patients. Direct access of bacteria and endotoxin to the blood stream may occur during hemorrhagic or traumatic shock and is the probable cause of subsequent sepsis in traumatized patients when no other source is apparent.

Acute Disease↗