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S Lelcuk

Publications and source records attributed to S Lelcuk.

71 records · Page 4Linked to original sources
PubMed1986

Pulmonary and systemic consequences of localized acid aspiration.

Acid aspiration may recruit a generalized inflammatory reaction that can potentiate the local injury. After surgical isolation of bronchi in a group of 15 dogs, 1 milliliter per kilogram of 0.37 normal hydrochloric acid was instilled into either side. After five minutes, platelet and white blood cell counts fell to 10,000 and 1,000 per cubic millimeter (p less than 0.05). Platelet aggregates were noted in blood smears. 111Indium-platelet activity doubled over both the aspirated and nonaspirated lung (p less than 0.05). Physiologic dead space rose from 18 to 67 per cent and to 46 per cent in the aspirated and nonaspirated lung (p less than 0.05). Physiologic shunt increased from 12 to 47 per cent and to 43 per cent (p less than 0.05) on the two sides. Plasma thromboxane B2 levels at 30 minutes rose from 0.28 to 0.93 nanograms per milliliter (p less than 0.05). Edema fluid from the aspirated lung had thromboxane B2 values of 2.87 nanograms per milliliter, indicating pulmonary synthesis. Within five minutes of aspiration, systemic effects were prominent; mean arterial pressure fell from 114 to 46 milliliters of mercury (p less than 0.05), and the cardiac index fell 24 per cent from 106 to 81 milliliters per kilogram per minute (p less than 0.05) along with an 18 per cent decrease in contractility of a rat papillary muscle bathed in plasma from the aspirated dog. Mean pulmonary arterial pressure rose from 12 to 18 millimeters of mercury (p less than 0.05). Despite fluid infusion at 36 milliliters per kilogram per hour to keep wedge pressure constant at 5.5 millimeters of mercury, and sampling of one-third the blood volume, hemoglobin concentration rose 0.9 grams per cent (p less than 0.05) indicating increased microvascular permeability. At autopsy, the aspirated and nonaspirated lung were indistinguishable with congestion, interstitial hemorrhage, and white blood cell infiltrates. Systemic organs showed vascular congestion and edema. These data demonstrate that local aspiration leads to generalized inflammatory sequelae with cardiopulmonary failure.

Animals↗
PubMed1985

Thromboxane A2 moderates permeability after limb ischemia.

Reperfusion after limb ischemia results in muscle edema as well as excess secretion of thromboxane A2 (TxA2), an agent associated with permeability increase in other settings. This study tests whether TxA2 moderates the permeability following limb ischemia. A tourniquet inflated to 300 mmHg was applied for 2 hours around the hind limb of four groups of dogs. In untreated animals (N = 25), 2 hours following tourniquet release, plasma TxB2 values rose from 320 pg/ml to 2416 pg/ml (p less than 0.001), and popliteal lymph values rose from 378 pg/ml to 1046 pg/ml (p less than 0.001). Platelet TxB2 was unaltered and plasma 6-keto-PGF1 alpha levels did not vary. Following ischemia, lymph flow (QL) increased from 0.07 to 0.37 ml/h (p less than 0.05), while the lymph/plasma (L/P) protein ratio was unchanged at 0.41. These measurements indicate increased permeability since increase in hydrostatic pressure in a second group by tourniquet inflation to 50 mmHg (N = 7) led to a rise in QL from 0.07 to 0.22 ml/h, but a fall in the L/P ratio to 0.32, a value lower than the ischemic group (p less than 0.05). Pretreatment with the imidazole derivative ketoconazole (N = 11) reduced platelet Tx synthesis from 42 ng to 2 ng/10(9) platelets, but lymph TxB2 levels rose to 1703 pg/ml after ischemia, indicating an extravascular or vessel wall site of synthesis not inhibited by ketoconazole. Pretreatment with a lower molecular weight imidazole derivative OKY 046 (N = 9) inhibited all Tx synthesis after ischemia. Prior to tourniquet inflation, both OKY 046 and ketoconazole lowered plasma TxB2 levels as well as the L/P ratio (p less than 0.05). After ischemia, OKY 046, but not ketoconazole, maintained the L/P ratio at 0.33, a value below that of untreated animals (p less than 0.05). These results indicate that nonplatelet-derived TxA2 modulates both baseline and ischemia-induced increases in microvascular permeability in the dog hind limb.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Prostacyclin and thromboxane A2 moderate postischemic renal failure.

Since prostacyclin (PGI2) is known to regulate renal cortical blood flow and since ischemia stimulates thromboxane (Tx) A2 synthesis, the role of these prostanoids in moderating the response to renal ischemia was studied in the rat. At baseline, plasma TxB2 concentration in untreated animals (n = 13) was 357 pg/ml. The left renal pedicle was clamped for 45 minutes after a right nephrectomy (n = 16), which led after 5 minutes of reperfusion to a rise in TxB2 to 2825 pg/ml (p less than 0.001), but there was no change in 6-keto-PGF1 alpha. After 24 hours creatinine levels rose from 0.4 to 3.0 mg/dl (p less than 0.001), and left renal weight rose from 94% to 117% (p less than 0.001) relative to the weight of the right kidney. In nephrectomized but nonischemic sham control rats (n = 7), creatinine level was 0.9 mg/dl and kidney weight 91% after 24 hours. Pretreatment with OKY 046 (n = 13) (2 mg/kg administered intravenously) blocked ischemia-induced TxB2 synthesis, while 6-keto-PGF1 alpha levels rose from 96 to 302 pg/ml (p less than 0.001). There was no increase in creatinine levels or kidney weight relative to the sham group. Pretreatment with ibuprofen (n = 10) (12 mg/kg) or OKY 046 and ibuprofen (n = 9) inhibited TxB2 and 6-keto-PGF1 alpha synthesis, but creatinine levels and renal weight rose (p less than 0.001). Renal histology in OKY 046-pretreated animals was equal to that in nephrectomized controls, while all other ischemic groups showed tubular necrosis. Results indicate that a high PGI2/TxA2 ratio protects against renal ischemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Disadvantages of prostacyclin infusion during cardiopulmonary bypass: a double-blind study of 50 patients having coronary revascularization.

Prostacyclin (PGI2) has been suggested for use in cardiopulmonary bypass (CPB) because of its positive effects on platelet number and function. Fifty patients who underwent coronary artery bypass grafting using a bubble oxygenator received heparin, 3 mg per kilogram of body weight, and then were randomly assigned to receive PGI2, 25 ng/kg/min, beginning 5 minutes before and until the end of CPB (26 patients) or a placebo (24 patients). Both groups were similar in sex, age, heparin dose, protamine dose, and CPB time. During CPB, mean arterial pressure fell significantly with PGI2 (76 +/- 2 mm Hg to 53 +/- 2 mm Hg; p less than 0.05) and necessitated pressor substances. Platelet counts fell significantly in both groups with the start of CPB, but after 60 minutes were similar in both groups (118 +/- 9 X 10(3) versus 130 +/- 8 X 10(3); not significant [NS]) and were unchanged 3 hours after CPB. Total chest tube output was 647 +/- 51 ml (placebo group) versus 576 +/- 34 ml (PGI2 group) (NS); 18 of the patients given PGI2 required 26 transfusions compared with 16 transfusions in 8 of the patients given a placebo (p less than 0.05). In PGI2 patients, arterial oxygen tension on 100% oxygen fell from 281 +/- 18 mm Hg before CPB to 223 +/- 17 mm Hg immediately after CPB (p less than 0.05). The placebo patients did not show a change in this variable.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Determinants of cardiovascular stability during abdominal aortic aneurysmectomy (AAA).

Patients undergoing abdominal aortic aneurysmectomy (AAA) develop depressed cardiac function during aortic clamping. The importance of volume status and thromboxane (Tx) mediated declines in cardiac contractility in determining this event was studied. In a blinded fashion, patients received the cyclo-oxygenase inhibitor ibuprofen 12 mg/kg by mouth (n = 11) or a placebo (n = 15), 1.5 hours prior to surgery. In the placebo group levels of 6-keto-PGF1 alpha, the hydrolysis product of prostacyclin (PGI2) rose from 20 +/- 10 to 1170 +/- 80 pg/ml (p less than 0.05) soon after incision. Concentrations of TxB2, the stable hydrolysis product of TxA2, were unchanged until 30 minutes after the aorta was clamped when arterial TxB2 concentrations rose from 90 +/- 20 to 230 +/- 30 pg/ml (mean +/- SEM) (p less than 0.05). A pulmonary source for PGI2 and TxA2 was indicated by the observation that arterial 6-keto-PGF1 alpha and TxB2 levels exceeded those in pulmonary arterial blood by 180 +/- 50 and 110 +/- 30 pg/ml, respectively (p less than 0.05). Levels of TxB2 in circulating platelets remained unchanged from baseline in the placebo group. During aortic clamping, cardiac index (CI) fell 0.7 +/- 0.2 1/min X m2 (p less than 0.05) in placebo treated patients, and there was a 6% decline in plasma contractility as bioassayed with a rat papillary muscle (p less than 0.05). Placebo patients entered surgery with a PAWP greater than or equal to 10 mmHg (mean 13 mm). Ibuprofen suppressed production of TxB2, such that 30 minutes after aortic clamping TxB2 was 70 +/- 30 pg/ml, a value lower than control patients (p less than 0.05). Further, plasma no longer depressed contractility of the papillary muscle. Five patients given ibuprofen had an initial pulmonary arterial wedge pressure (PAWP) of 10 mmHg or greater (mean 12 mmHg). During aortic clamping there was an insignificant decrease in CI of 0.2 +/- 0.1 1/min X m2. This was in contrast to the CI decrease in six other ibuprofen treated patients of 0.9 +/- 0.2 1/min X m2 whose PAWP at the start of surgery was less than 10 mmHg (mean 6 mmHg) (p less than 0.05), and to placebo patients whose initial PAWP was greater than or equal to 10 (p less than 0.05). Platelet counts fell from 185,000 to 121,000/mm3 in placebo patients (p less than 0.05), but did not fall when ibuprofen was given. Creatinine concentrations were unaffected by ibuprofen. Blood replacement in placebo and ibuprofen patients was similar, 1.90 +/- 0.20 and 0.65 +/- 0.15 1, respectively. Results indicate that CI will not decrease during AAA if sufficient volume is given before surgery to increase PAWP above 10 mmHg, and secondly, if TxB2 synthesis is inhibited.

Aged↗
PubMed1984

Role of serotonin in patients with acute respiratory failure.

An early event in the evolution of acute respiratory failure (ARF) is thought to be the activation of platelets, their pulmonary entrapment and subsequent release of the smooth muscle constrictor serotonin (5HT). This study tests the thesis that inhibition of 5HT will improve lung function. The etiology of ARF in the 18 study patients was sepsis (N = 10), aspiration (N = 3), pancreatitis (N = 1), embolism (N = 2), and abdominal aortic aneurysm surgery (N = 2). Patients were divided into two groups determined by whether their period of endotracheal intubation was less than or equal to 4 days (early ARF, N = 12) or greater than 4 days (late ARF, N = 6). Transpulmonary platelet counts in the early group showed entrapment of 26,300 +/- 5900 platelets/mm3 in contrast to the late group where there was no entrapment (p less than 0.05). The platelet 5HT levels in the early group were 55 +/- 5 ng/10(9) platelets, values lower than 95 +/- 15 ng/10(9) platelets in the late ARF group (p less than 0.05), and 290 +/- 70 ng/10(9) platelets in normals. The selective 5HT receptor antagonist, ketanserin was given as an intravenous bolus over 3 minutes in a dose of 0.1 mg/kg, followed by a 30-minute infusion of 0.08 mg/kg. During this period mean arterial pressure (MAP) fell from 87 +/- 5 to 74 +/- 6 mmHg (mean +/- SEM) (p less than 0.05). One and one-half hours following the start of therapy, MAP returned to baseline. At this time, patients with early ARF showed decreases in: physiologic shunt (Qs/QT) from 26 +/- 3 to 19 +/- 3 (p less than 0.05); peak inspiratory pressure from 35 +/- 2 to 32 +/- 2 cmH2O (p less than 0.05) and in mean pulmonary arterial pressure from 32 +/- 2 to 29 +/- 1 mmHg (p less than 0.05). At 4 hours all changes returned to baseline levels. In early ARF ketanserin did not alter pretreatment values of: pulmonary arterial wedge pressure, 17 +/- 3 mmHg; cardiac index, 2.8 +/- 0.3 L/min X m2; platelet count, 219,000 +/- 45,000/mm3; platelet 5HT, 55 +/- 5 ng/10(9) platelets; plasma 5HT, 142 +/- 21 ng/ml; plasma thromboxane B2, 190 +/- 30 pg/ml; or plasma 6-keto-PGF1 alpha, 40 +/- 10 pg/ml. Ketanserin infusion in patients with late ARF yielded no benefit. In both ARF groups the decreases in QS/QT were inversely related to the duration of intubation (r = 0.70; p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Inhibition of ischemia-induced thromboxane synthesis in man.

The ability of the imidazole derivative, ketoconazole, to inhibit thromboxane (Tx)A2 synthesis in response to ischemia was tested in ten volunteers. Two hours after taking placebo or ketoconazole 400 mg by mouth, plasma levels of the stable degradation product of TxA2, TxB2, were 300 +/- 129 pg/ml (mean +/- SEM) and 297 +/- 80 pg/ml, respectively. Arm ischemia for 10 min induced by inflation of a cuff to 220 mm Hg led to a rise in TxB2 levels to 657 +/- 157 pg/ml after placebo (p less than 0.05) and 337 +/- 81 pg/ml after ketoconazole. One hour after cuff deflation, TxB2 returned to pre-ischemia levels in both groups. Platelet TxB2 concentrations were 27 +/- 6 ng in the placebo and 35 +/- 6 ng/10(9) platelets in the ketoconazole group, and were unchanged by cuff inflation. The fact that plasma and platelet TxB2 values were not lower 2 hr after ketoconazole treatment was explored in another group of four nonstressed volunteers who received 400 mg of drug. After 2 hr, TxB2 values had fallen from 170 +/- 30 pg to 120 +/- 10 pg; at 4 hr, 6 hr, and 8 hr they were 30 +/- 20 pg, 5 +/- 5 pg, and 5 +/- 5 pg/ml, respectively. These results indicate that tourniquet ischemia provokes TxA2 synthesis, and that the source of this prostanoid is likely to be ischemic tissue and not platelets. Finally, ketoconazole can profoundly inhibit both background and stimulated TxA2 synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Arachidonic acid metabolites mediate early burn edema.

Standard burns were sequentially produced on the backs of Sprague-Dawley rats at 0, 1, 2, and 2 1/2 hr, followed by the IV injection of Evans blue dye. All animals were killed at 3 hr, and burns evaluated by wet/dry weight ratios, and Evans blue extravasation scored 1-4 by two observers. Five groups of rats were compared to controls. Rats made neutropenic by exposure to 137cesium showed no significant difference in wet/dry weight ratio or Evans blue extravasation compared to controls. At 1 1/2 hr four other groups were treated with various inhibitors of arachidonic acid metabolism including ibuprofen, a cyclo-oxygenase inhibitor; FPL 55712, a leukotriene (LT) receptor antagonist; ketoconazole, an inhibitor of thromboxane (Tx) synthetase; and lodoxamide, a calcium channel inhibitor. All treated groups showed significant reduction of Evans blue dye extravasation. Wet/dry weight ratios were significantly reduced in rats treated with FPL 55712 and ketoconazole before or after burning. These data support the postulate that oxygenation products of arachidonic acid, particularly Tx and LT, are important mediators in early burn edema.

Animals↗
PubMed1983

Breast carcinoma originating in cystosarcoma phyllodes.

Only three cases of carcinoma infiltrating the stroma of cystosarcoma phyllodes have been reported. An additional case is presented. Unlike the treatment of cystosarcoma phyllodes which is limited to complete removal of the tumor, carcinosarcomas should be treated in the same manner as carcinoma by mastectomy and axillary dissection.

Adenocarcinoma↗
PubMed1983

Thromboxane mediation of cardiovascular dysfunction following aspiration.

Acid aspiration leads to an inflammatory response characterized by the activation and pulmonary entrapment of platelets and while blood cells (WBCs. We speculate that thromboxane (Tx) produced by these activated cells alters lung permeability and diminishes cardiac performance. The lungs of dogs were aspirated with 0.1N HCl (3 ml/Kg). Within 30 minutes in six untreated controls, cardiac index (CI) decreased from 121 to 104 ml/min . kg (P less than ).05), mean arterial pressure decreased from 142 to 120 mm Hg (P less than 0.05), Pao2 decreased from 91 to 73 mm Hg (P less than 0.05), and TxB2 levels increased from 70 to 130 pg/ml (P less than 0.05). Pulmonary WBC sequestration occurred after 2 hours, while at 21/2 hours edema fluid was noted in the endotracheal tube. Six dogs were treated with infusion of the imidazole derivative ketoconazole 1 hour after aspiration (2.5 mg/kg bolus followed by 10 mg/kg . hr for 2 hours). After 30 to 60 minutes of treatment, CI rose from 106 to 143 ml/min . kg (P less than 0.05), TxB2 decreased from 130 to 70 pg/ml (P less than 0.05). At 21/2 hours, plasma from treated animals used to incubate a papillary muscle led to developed tension 8% higher than that in controls (P less than 0.05). Sequestration of WBC was not observed. After 4 hours, 24 ml endotracheal edema fluid was collected in contrast to 127 ml in controls (P less than 0.05). A hamster cheek pouch used for bioassay of microvascular permeability yielded 78 leakage sites/cm2 with control edema fluid and 26/cm2 with fluid from treated animals (P less than 0.05). The importance of WBC Tx synthesis in the induction of permeability was tested by stimulation of isolated WBCs with ionophore in the presence or absence of ketoconazole (0.4 Microgram/ml). Ketoconazole reduced the number of leakage sites in the hamster cheek pouch from 196/cm2 noted in controls to 28/cm2 (P less than 0.05). These data support our hypothesis that Tx directly or indirectly lead to cardiac depression and WBC-mediated permeability.

Animals↗
PubMed1983

Cholelithiasis in Dubin-Johnson syndrome.

Only one instance of Dubin-Johnson syndrome associated with cholelithiasis has been reported. We present one additional patient, a 30 year old man with Dubin-Johnson syndrome in whom pancreatitis and cholecystitis, secondary to cholesterol gallstones, developed. A possible cause for the lithogenicity of the bile in the Dubin-Johnson syndrome is considered.

Adult↗
PubMed1983

Ischemia of the limb stimulates thromboxane production and myocardial depression.

Thromboxane A2 is thought to be an important mediator of cardiopulmonary dysfunction, hence stimuli that effect synthesis of this prostanoid are of major interest. In this study, the thesis that ischemia of the limb is a significant stimulus to thromboxane A2 synthesis and the generation of a circulating negative inotrope is tested. Twelve healthy volunteers, taking no medications and ranging in age from 21 to 29 years, underwent inflation of an arm cuff to either 70 or 220 millimeters of mercury for ten minutes. Immediately after deflation of the cuff from 220 millimeters of mercury, the stable degradation product of thromboxane A2, thromboxane B2, rose from a base line plasma level of 34 +/- 6 picograms per milliliter (mean +/- SEM) to 70 +/- 18 picograms per milliliter. In contrast, deflation from a cuff pressure of 70 millimeters of mercury resulted in a lower thromboxane B2 level of 26 +/- 9 picograms per milliliter (p less than 0.05). Plasma obtained before and after inflation of the cuff to 220 millimeters of mercury was used to bathe a rat papillary muscle. Developed tension fell from a base line of 2.80 +/- 0.19 to 2.44 +/- 0.17 grams (p less than 0.01). There was no significant change in developed tension induced by plasma harvested after the cuff was inflated to 70 millimeters of mercury. The base line plasma level of 6-keto-prostaglandin F1 alpha, the hydrolysis product of prostacyclin, was 46 picograms per milliliter; the plasma serotonin, 51 nanograms per milliliter; the platelet serotonin, 1.02 micrograms per 10(9) platelets; platelet count, 220,000 per cubic millimeter, and white blood count, 6,094 per cubic millimeter. These values did not change significantly with cuff inflation to either 220 or 70 millimeters of mercury. The results show that ischemia of the limb leads to thromboxane A2 production. Possible adverse cardiac effects related to this event are suggested by the bioassay demonstrating that circulating plasma with high levels of thromboxane B2 is associated with the depression of tension of an isolated rat papillary muscle.

Adult↗
PubMed1982

Acute complications of metastatic melanoma to the gastrointestinal tract.

The gastrointestinal tract is a favoured site for metastatic melanoma. Complications such as obstruction, bleeding or perforation should be alleviated by surgery in order to improve the patient's condition for further systemic therapy. Six patients with melanoma involving the gastrointestinal tract are presented: 3 were operated upon for metastatic lesions in the small bowel causing intussusception, 2 patients were treated for perforation of the small bowel and 1 patient with massive bleeding from metastatic melanoma in the stomach underwent gastrectomy. Two of the patients are alive 6 months and 4 years respectively after these operations. The other 4 survived between 6 months and 2 years.

Adult↗
PubMed1981

[Rectus sheath hematoma].

Rectus sheath hematoma is rarely diagnosed preoperatively. It can mimic acute intra-abdominal disease and other familiar disorders. It is more frequent during pregnancy and debilitating diseases. Blunt trauma to the abdomen, straining, coughing and anticoagulant therapy are also common contributing factors. The presenting symptom is onset of acute, localized, abdominal pain soon after the precipitating event. A tender abdominal mass is palpated in one of the rectus muscles. There are no specific diagnostic laboratory tests. Ultrasonography is the procedure of choice for correct diagnosis. Most of these patients can be successfully managed conservatively. During a period of two years, five cases were treated. Three of the patients suffered from acute cough associated with upper respiratory infections. Two had had multiple childbirths, one had had an abdominal operation and another had Cushing's disease and morbid obesity. Three were misdiagnosed and operated on. The hematoma was evacuated but the peritoneum was not opened. In two patients the correct diagnosis was made by ultrasonography and they were successfully treated conservatively.

Abdomen, Acute↗
PubMedDate not supplied

Colitis cystica profunda: self-inflicted by rectal trauma? Report of a case.

Colitis cystica profunda (CCP) is a rare benign condition with a controversial etiology. We report a case of CCP in a patient with a history of anal masturbation, supporting an acquired traumatic etiology. Diagnosis was assisted by transrectal ultrasound. The patient was successfully treated by local excision.

Adult↗