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Biomedical subjects

G Goldman

Publications and source records attributed to G Goldman.

At least 73 records · Page 4Linked to original sources
PubMed1990

Attenuation of acid aspiration edema with phalloidin.

Acid aspiration leads to pulmonary endothelial and epithelial cell (EC/EpC) injury characterized by increased permeability and polymorphonuclear (PMN) leukocyte diapedesis. Actin in the EC/EpC cytoskeleton has been shown to play a significant role in maintenance of the microvascular junction barrier. This study tests indirectly whether the development of permeability and diapedesis following acid aspiration is via disruption of the pulmonary cytoskeleton. Manipulation was achieved by the actin microfilament assembler phalloidin. Anesthetized rats (n = 88) underwent segmental lung installation of 0.1 ml saline or phalloidin (2 x 10(-6) M). Twenty minutes later 0.1 N HCl, saline, or phalloidin was introduced. After 3 h there was an increase in wet-to-dry weight (W/D) ratio of 6.6 and 5.1 in the HCl-injected and noninjected sides, protein concentration, 3,970 and 2,530 micrograms/ml, and accumulation of 93 PMN/ml (x 10(4] in bronchoalveolar lavage (BAL) of the HCl-injected lung. These values were higher than control animals. Local pretreatment with phalloidin attenuated acid-induced localized but not generalized permeability with reduction in W/D ratio, BAL protein concentration, and diapedesis (P less than 0.05). Acid injection into airways also led to elevated thromboxane B2 and leukotriene B4 levels in plasma and BAL (P less than 0.05) and generalized lung leukosequestration, events not affected by phalloidin. Taken together, these data suggest that acid aspiration lung injury is determined largely by loss of integrity of the pulmonary EC/EpC cytoskeleton with resultant loss of barrier function.

Administration, Inhalation↗
PubMed1990

Ischemia-induced neutrophil activation and diapedesis is lipoxygenase dependent.

Ischemia and reperfusion lead to eicosanoid- and neutrophil (PMN)-dependent injury. This study tests the role of ischemia-induced lipoxygenase activity in mediating PMN activation and diapedesis. Anesthetized rabbits (n = 8) underwent 3 hours of bilateral hindlimb ischemia. At 10 minutes of reperfusion, leukotriene B4 (LTB4) levels in femoral venous effluent were 0.49 +/- 0.05 ng/ml compared with 0.04 +/- 0.07 ng/ml in sham-treated animals (n = 10) (p less than 0.05). Intracellular H2O2 production of circulating PMNs assayed flow cytometrically by dichlorofluorescein (DCF) oxidation, increased from a preischemic value of 74 +/- 14 femtomoles DCF/cell to 135 +/- 8 fmol DCF/cell (p less than 0.05). PMNs were treated with phorbol myristate acetate (PMA), 10(-7) mol/L. In contrast to a 162% increase in H2O2 production before ischemia, PMNs at 10 minutes of reperfusion had an enhanced response to PMA of 336% (p less than 0.05). Addition of authentic LTB4 (0.5 ng/ml) to PMN from sham-treated animals led to their activation, manifest by an oxidative burst, 127 +/- 12 fmol DCF/cell, and an enhanced response of 337% to PMA stimulation. To study diapedesis, plasma collected at 10 minutes of reperfusion was introduced into plastic chambers taped atop skin abrasions in rabbits (n = 8). After 3 hours, 1610 +/- 246 PMN/mm3 accumulated and LTB4 levels in blister fluid were 0.83 +/- 0.03 ng/ml, higher than values of 44 +/- 23 PMN/mm3 (p less than 0.05) and 0.04 +/- 0.03 ng LTB4/ml (p less than 0.05) with saline solution and 68 +/- 16 PMN/mm3 (p less than 0.05) and 0.19 +/- 0.02 ng/ml (p less than 0.05) with nonischemic plasma. The introduction of LTB4, 3.3 ng/ml, into the chambers resulted in an accumulation of 536 +/- 352 PMN/mm3 (p less than 0.05). Pretreatment of animals before hindlimb ischemia (n = 5) with the lipoxygenase inhibitor diethylcarbamazine abolished PMN activation (51 +/- 12 fmol DCF/cell) and ischemic plasma-induced diapedesis into the plastic chamber (38 +/- 18 PMN/mm3). Pretreatment of nonischemic animals (n = 13) used for the dermabrasion bioassay with diethylcarbamazine abolished diapedesis into the plastic chambers induced by ischemic plasma (n = 5) (32 +/- 24 PMN/mm3) or LTB4 (n = 3) (36 +/- 28 PMN/mm3). These data indicate that PMN activation after reperfusion of ischemic tissue is mediated by a lipoxygenase product, perhaps LTB4, and that both reperfusion plasma and authentic LTB4 induce diapedesis by stimulating de novo lipoxygenase activity.

Animals↗
PubMed1989

Role of thromboxane in interleukin 2-induced lung injury in sheep.

Interleukin (IL)-2 administration leads to respiratory dysfunction due to increased vascular permeability. This study examines the role of thromboxane (Tx)A2 in IL-2 induced lung injury in sheep with chronic lung lymph fistulae. This preparation enables evaluation of permeability prior to the development of gross edema. IL-2, 10(5) units/kg (n = 6), or its excipient control (n = 5) was given as an i.v. bolus over 2 min. After 2 h of IL-2 administration, plasma TxB2 increased from 168 to 388 pg/ml (P less than 0.05) and lung lymph TxB2 from 235 to 694 pg/ml (P less than 0.05). Mean pulmonary artery pressure (MPAP) rose from 13 to 29 mm of Hg (P less than 0.05) at 30 min and remained elevated for 4 h while the pulmonary artery wedge pressure was unchanged at 4 mm of Hg. Arterial oxygen tension (PaO2) fell from 88 to 77 mm of Hg (P less than 0.05). Lung lymph flow (QL) rose from 2.2 to 3.8 ml/30 min (P less than 0.05) at 1 h and to 6.4 ml/30 min at 3 h. This rise coincided with an increase in the lymph/plasma (L/P) protein ratio from 0.67 to 0.77 (P less than 0.05). In contrast, the non-IL-2-infused sheep (n = 3) recruitment of the lung vasculature by left atrial balloon inflation led to a rise in QL from 2.4 to 8.2 ml/30 min, whereas the L/P ratio declined from 0.62 to 0.25, suggesting that the protein-rich lymph flow after IL-2 administration reflected increased microvascular permeability. In further proof of an increase in permeability, IL-2 administration into sheep (n = 2) with an inflated left atrial balloon led, after a pressure-independent L/P protein ratio had been achieved, to an increase in L/P protein ratio and decrease in protein reflection coefficient. At 2 h after IL-2, the blood leukocyte count fell from 8156 to 4375/mm3 (P less than 0.05) primarily due to a 73% drop in lymphocytes. The platelet count declined from 292 to 184 x 10(3)/mm3 (P less than 0.05). Body temperature rose from 38.9-40.3 degrees C (P less than 0.05), and shaking chills were common. Pretreatment with the Tx synthetase inhibitor OKY 046 (n = 7) lowered baseline plasma and lymph TxB2 levels to 22 and 52 pg/ml (P less than 0.05) and prevented the IL-2-induced increase in plasma and lung lymph TxB2 (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Biliary micellar cholesterol nucleates via the vesicular pathway.

Biliary cholesterol nucleates primarily from phospholipid vesicles. In this study, we investigated the mode of nucleation of micellar cholesterol. Ten biles (four human and six model) were examined. The vesicular and micellar fractions of each bile were separated by gel chromatography. The whole biles and their isolated carriers were incubated at 37 degrees C until nucleation time. In whole human biles, the proportion of total cholesterol in vesicles rose throughout the incubation (from zero time to nucleation time) from 15.5 +/- 8.6% to 28.0 +/- 12.5%, and in model biles from 46.8 +/- 22.4% to 75.5 +/- 8.2%. The vesicular isolated fraction remained unchanged throughout incubation. In isolated micelles devoid of vesicles at zero time, new vesicles formed during incubation, carrying increasing proportions of cholesterol. At nucleation time, these vesicles contained 11.0% of originally micellar cholesterol in human biles, and 41.2% in model biles. The new vesicles formed in whole bile and in the micellar fraction were chromatographically and chemically similar to the vesicles originally present in bile. These data suggest that micellar cholesterol nucleates via the neoformation of phospholipid vesicles, which seem to be the final common pathway for cholesterol nucleation in bile.

Bile↗
PubMed1989

Prostaglandin E2 in pyloric stenosis.

Prostaglandins are presumed to have many cytoprotective properties that play a role in the pathogenesis of duodenal ulcer and its complications where decreased levels of prostaglandin E2 (PGE2) impair gastric motility, oppose ionic membrane influx, and enhance obstructive changes. These are just some of the mechanisms that may cause pyloric obstruction and may result from decreased PGE2 levels. To evaluate this hypothesis, 17 patients with duodenal ulcer complicated by pyloric stenosis were examined. Biopsy specimens were obtained from the duodenal bulb, ulcer margins, gastric antrum, fundus, and gastric secretions. Prostaglandin E2 levels were measured and compared with those taken from the same areas during a second endoscopy in a later quiescent or exacerbated phase. During the active phase of pyloric stenosis, decreased levels of PGE2 were found in the gastroduodenal tissues and secretions were compared with levels found during convalescence. These level differences were statistically significant. A correlation between the severity of the clinical and endoscopic findings and the PGE2 levels was found. A further decrease in PGE2 levels in the second endoscopy were indicative of the presence of scar tissue, representing an irreversible obstructive peptic disease.

Aged↗
PubMed1989

Biliary colic treatment and acute cholecystitis prevention by prostaglandin inhibitor.

Sixty patients were treated in the emergency ward for biliary colic. Cholelithiasis was proven by ultrasonography. Twenty patients (group I) were treated by placebo. Twenty patients (group II) were treated by papaverine, and 20 patients were treated by diclofenac sodium (Voltaren) (group III). Twenty more patients (group IV) with low back pain (LBP) were treated with diclofenac sodium (Voltaren) as a control to assess the analgesic effect of Voltaren. Two interesting observations were made: Voltaren was proven more efficient for pain relief (P less than 0.002), and none of the patients treated with Voltaren were in need of hospitalization and immediate surgery. In comparison, nine patients of the other two groups progressed to acute cholecystitis and needed surgical intervention. The possible anticolic and anti-biliary inflammation properties and the indications for use of Voltaren are discussed.

Acute Disease↗
PubMed1989

The endothelial cell cytoskeleton modulates extravascular polymorphonuclear leukocyte accumulations in vivo.

Actin microfilaments, key elements in the endothelial cell (EC) cytoskeleton, have been noted in in vitro studies to play a modulating role in the diapedesis of polymorphonuclear leukocytes (PMN). The role of the cytoskeleton in PMN diapedesis in vivo was the subject of this study. Small skin abrasions were produced in rabbits. Cytoskeletal manipulation was accomplished by local application of phalloidin which promotes microfilament assembly or cytochalasin B which causes their disassembly, prior to addition of a chemotaxin. When the initial treatment to the abrasion site was saline, the secondary addition of more saline resulted in PMN accumulations, expressed as PMN/mm3 of 36 +/- 19, while 10(-4) M cytochalasin B led to 91 +/- 32 (P less than 0.05). Secondary addition of chemotaxins or histamine also led to significant PMN accumulations of 169 +/- 54 with 10(-8) M leukotriene (LT) B4, 318 +/- 85 with zymosan-activated plasma (ZAP), and 158 +/- 48 with 10(-4) M histamine. When the initial treatment was 10(-8) M phalloidin, PMN accumulations were reduced to 31 +/- 22 with cytochalasin B (P less than 0.05 relative to saline as initial treatment); 63 +/- 43 with LTB4 (P less than 0.05); 137 +/- 48 with ZAP (P less than 0.05); and 51 +/- 35 with histamine (P less than 0.05). In contrast, initial blister treatment with cytochalasin B rather than saline increased PMN accumulations in response to LTB4, 291 +/- 71 (P less than 0.05), and histamine, 270 +/- 56 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Postischemic renal injury is mediated by neutrophils and leukotrienes.

Neutrophils have been implicated as central mediators in myocardial and skeletal muscle ischemia-reperfusion injury. This study tests whether these cellular elements and the chemoattractant leukotriene (LTB4) play a role in postischemic renal failure. Anesthetized rats underwent 45 min of left renal pedicle clamping. Five minutes after reperfusion, LTB4 levels were elevated to 1.42 ng/ml (P less than 0.05); thromboxane (Tx)B2 was 2,840 pg/ml, higher than 503 pg/ml in sham controls (P less than 0.05); renal artery blood flow was 67% of preclamping values at 1 min of reperfusion compared with 111% in sham (P less than 0.05). At 24 h, creatinine levels were 4.6 mg/dl (P less than 0.05). At 24 h, creatinine levels were 4.6 mg/dl (P less than 0.05); histology showed acute tubular necrosis (ATN). Neutrophil depletion by rabbit antiserum (n = 8) led during reperfusion to reduced LTB4 and TxB2 levels, 1.04 ng/ml and 1.043 pg/ml (P less than 0.05); increased renal blood flow of 174% (P less than 0.05); reduced creatinine levels of 1.8 mg/dl (P less than 0.05); and limited ATN. Pretreatment with diethycarbamazine prevented the increases in LTB4 and TxB2 (P less than 0.05), increased renal blood flow (P less than 0.05), minimized creatinine increase to 1.7 mg/dl (P less than 0.05), and reduced ATN. These data indicate that neutrophils and LTB4 play a role in ischemia-induced Tx synthesis and mediate postischemic renal injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Thromboxane A2 mediates increased pulmonary microvascular permeability following limb ischemia.

Lower torso ischemia and reperfusion lead to respiratory dysfunction characterized by pulmonary hypertension and increased lung microvascular permeability. This is associated with lung leukosequestration and thromboxane (TX) generation. This study tests the role of elevated TX levels following muscle ischemia in mediating remote lung injury. Anesthetized sheep prepared with chronic lung lymph fistulae underwent 2 hours of bilateral hind limb tourniquet ischemia. In untreated controls (n = 7), 1 minute after reperfusion there was a transient increase in plasma immunoreactive (i)-TXB2 levels from 211 to 735 pg/ml (p less than 0.05), and at 30 minutes, lung lymph i-TXB2 levels rose from 400 to 1,005 pg/ml (p less than 0.05). At 1 minute, the mean pulmonary arterial pressure (MPAP) increased from 13 to 38 mm Hg (p less than 0.05) and pulmonary microvascular pressure (Pmv) from 7 to 18 mm Hg (p less than 0.05). Lung lymph flow (QL) rose from 4.3 to 8.3 ml/30 min (p less than 0.05), the lymph/plasma (L/P) protein ratio was unchanged from 0.6, and the lymph protein clearance increased from 2.6 to 4.6 ml/30 min (p less than 0.05). Two hours after reperfusion, neutrophils were observed sequestered in lung capillaries and proteinaceous exudates were found in alveoli in contrast to sham-operated animals (n = 3). To maximize lung vascular surface area and achieve a pressure independent L/P protein ratio a left atrial balloon was inflated during one group of ischemia-reperfusion experiments (n = 5). This resulted in a baseline rise in MPAP to 20 mm Hg (p less than 0.05); a 4.3-fold increase in QL (p less than 0.05), a decrease in the L/P ratio from 0.70 to 0.28 (p less than 0.05) and a protein reflection coefficient (sigma d) of 0.72. During reperfusion the L/P ratio rose to 0.49 (p less than 0.05) and the sigma d decreased to 0.51 (p less than 0.05), documenting an increase in lung microvascular permeability. In contrast to untreated ischemic controls, inhibition of TX synthetase with OKY 046 (n = 6) reduced plasma i-TXB2 levels to 85 pg/ml (p less than 0.05) but also increased i-6-keto-PGF1 alpha levels to 78 pg/ml relative to 15 pg/ml in untreated controls (p less than 0.05). OKY 046 prevented the increase in MPAP, Pmv, QL, and lymph protein clearance (p less than 0.05). Lung histology was normal in distinction to the leukosequestration in untreated ischemic controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Pulmonary edema after aneurysm surgery is modified by mannitol.

Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p less than 0.01), and MPAP rose from 19 to 27 mmHg (p less than 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p less than 0.01) and MPAP to 34 mmHg (p less than 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p less than 0.01). Four to eight hours after surgery, physiologic shunting (Q[sc]S[xsc]/Q[sc]T[xsc]) rose from 9% to 20% (p less than 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p less than 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 12 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and PaO2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p less than 0.01); MPAP to 21 and 26 mmHg (p less than 0.01); minimized the decline in WBC to 5850/mm3 (p less than 0.01), and the postoperative rise in Q[sc]S[xsc]/Q[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p less than 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10(-4)M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.

Aged↗
PubMed1989

Thromboxane mediates the ischemia-induced neutrophil oxidative burst.

Indirect evidence exists that the reperfusion of ischemic tissue activates white blood cells. Thus local and systemic reperfusion injuries are prevented by making animals leukopenic or by inhibiting white blood cell lung entrapment by blocking thromboxane A2 generation. This study tests directly whether ischemia and reperfusion activates neutrophils, as measured by their oxidative burst, and whether thromboxane mediates this event. Anesthetized rats underwent 4 hours of bilateral hind limb tourniquet ischemia followed by 60 minutes of reperfusion. Plasma thromboxane B2 levels increased to 2750 pg/ml at 5 minutes of reperfusion, higher than the sham control (n = 36) value of 370 pg/ml (p less than 0.01). In untreated ischemic animals (n = 30) the intracellular H2O2 production of circulating neutrophils, as assayed flow cytometrically by dichlorofluorescein oxidation, increased from a preischemic value of 133 to a peak of 251 femtomoles dichlorofluorescein/neutrophil at 5 minutes of reperfusion (p less than 0.01). Treatment of neutrophils with phorbol myristate acetate (PMA) 10(-7) mol/L led to a 91% increase in neutrophil H2O2 production before ischemia, and 5 minutes after reperfusion there was an enhanced response to PMA of 222% (p less than 0.01). Pretreatment of animals with the thromboxane-synthetase inhibitor OKY 046 (n = 36) prevented ischemia-induced thromboxane generation, neutrophil H2O2 production (p less than 0.05), as well as the enhanced response to PMA stimulation (p less than 0.05). Treatment with the thromboxane-receptor antagonist SQ 29,548 (n = 36) did not affect the increase in plasma thromboxane levels after ischemia but was as effective as OKY 046 in preventing the ischemia-induced increase in neutrophil H2O2 production and the enhanced response to PMA stimulation. These data indicate that lower-torso ischemia leads to neutrophil activation, manifest by H2O2 production, an event mediated by thromboxane.

Animals↗
PubMed1988

Alpha-adrenergic blocker for posthernioplasty urinary retention. Prevention and treatment.

In a prospective, randomized study, 102 patients over the age of 60 years underwent inguinal hernioplasty. We compared a group of 58 patients who received phenoxybenzamine hydrochloride with a control group of 44 patients. The phenolsulfonphthalein test was performed in all patients. Twenty-six (25.5%) of the 102 patients developed acute urinary retention after the hernioplasty; all of them were in the control group. All of these 26 patients had pathological phenolsulfonphthalein test. In 21 of these 26 patients, urinary retention disappeared within 48 hours following phenoxybenzamine administration.

Aged↗
PubMed1988

Effective technique of sternum closure in high-risk patients.

A successful technique of closing the sternum in a selected group of poor-risk patients involves the combination of a mattress suture and a fixative single-wire suture, both of 0 stainless-steel monofilament. Our technique was used on 100 high-risk patients and compared with double control groups, one consisting of 200 normal-risk patients and the second of 100 high-risk patients. We found that the incidence of wound infections was reduced to 1% with our new technique compared with 3% and 1% in the control groups (the high- and normal-risk groups, respectively). There was neither dehiscence nor mediastinitis in the study group, compared with 1% and 0.5% incidences of these complications in the controls. Also, there was no mortality in the combined-closure group compared with mortality of 0.5% and 1% in the control groups. We believe that this closure effectively strengthens the complex of bone and wire, improving the stability of the chest by giving a correct axis to the sternum. It is also cost-effective and easy to perform and does not prolong operation time.

Aged↗
PubMed1988

Epitheloid hemangiomatosis mistaken for carcinomatosis.

We present a unique case of intra and extra-peritoneal epitheloid hemangioma which was mistaken for diffused carcinomatosis, representing a clinical-pathological problem, and emphasizing the unpredictable behaviour of this tumour. We are dealing with epitheloid vascular tumours, and briefly touch on the differential diagnosis, the principle of biological, pathological and clinical behaviour. Knowledge of this entity would provide an accurate diagnosis and would hence improve dealing with the problem. The conclusion is that this group of Histiocytoid-epitheloid vascular lesions have varying biological potential and this unusual functional state represents a large spectrum of cells, from normal to neoplastic endothelium.

Abdominal Neoplasms↗
PubMed1988

Low-energy CO2 laser intestinal anastomosis: an experimental study.

Intestinal anastomosis was performed in 17 Wistar rats via tissue welding by the low-energy CO2 laser. The postoperative course in the animals studied was uneventful. The integrity of the anastomosis was investigated manometrically, immediately upon completion of the anastomosis as well as 20 days later. Ten additional Wistar rats served as controls in which conventional interrupted one-layer anastomosis was performed. The results show a significant superiority of the intestinal anastomoses that were constructed by means of laser tissue welding. The time to complete the anastomosis was also significantly shorter when laser rather than manual suturing was used. Serial histological examinations for up to 90 days following surgery revealed complete healing and epithelization of the anastomotic site.

Anastomosis, Surgical↗
PubMed1988

Leukergy in inflammatory bowel disease.

In the phenomenon of leukergy, white blood cells agglomerate in peripheral blood slides. This agglomeration has been described in inflammatory infections of various causes. This study assesses this phenomenon in inflammatory bowel disease. A correlation was found between the severity of inflammatory bowel disease activity and the percentage of leukergy. Leukergy was found to parallel the clinical and endoscopic findings of inflammatory bowel disease. Furthermore, leukergy was found to be more accurate than white blood count and erythrocyte sedimentation rate. It is also found to accurately assess the course of the disease when clinical and other laboratory tests were masked by steroid and antibiotic administrations. Leukergy is a quick, inexpensive test that can easily be performed at the patient's bedside.

Adolescent↗
PubMed1988

Intrarectal bypass graft in low anterior resection and sigmoid obstruction--an experimental study.

The most common causes for morbidity and mortality in colorectal resections are anastomotic leaks. In low anterior resection, the incidence of anastomotic leakage ranges from 17 to 50%. With the use of the stapler technique, leakage incidence rate remains high and ranges from 10 to 25%. Colostomy formation and closures are associated with considerable morbidity and mortality. Due to the high incidence of anastomotic leakage rate in low anterior resection, and the additional complications of diverting colostomy formation and closure, the use of a rectal stent-intrarectal bypass graft has been instituted. This is carried out by means of a silastic graft, which prevents the fecal stream and gas pressure from coming into contact with the anastomotic site at the low rectum. The efficacy of intrarectal bypass graft was examined in two high-risk surgical situations, the first in very low anterior resection and the other, after early sigmoid obstruction. In both situations the intrarectal bypass graft provided for a safe anastomosis. Even when dehiscence and early obstructions occur, the tube may prevent leakage. This procedure presents effective practical implications which obviate the need for a proximal colostomy formation, thereby eliminating the physical and psychological stress that accompanies colostomies.

Anastomosis, Surgical↗