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Biomedical subjects

E Zoucas

Publications and source records attributed to E Zoucas.

At least 37 records · Page 2Linked to original sources

Control of traumatic liver hemorrhage in the cirrhotic rat by intraportal infusion of norepinephrine.

The effect of intraportal infusion of norepinephrine (NE) on primary hemostasis in the cirrhotic rat was investigated at standardized liver trauma. Cirrhosis was induced by simultaneous administration of increasing amounts of carbontetrachloride (CCl4) and phenobarbitone. Infusion of norepinephrine took place after cannulation of the gastroduodenal vein. Intraportal infusion of NE resulted in a significant increase in arterial blood pressure and portal pressure in all animals. No difference was observed between cirrhotic and control rats. Cirrhotic animals bled longer and more profusely as compared with the controls. Infusion of NE resulted in significant decrease in bleeding time and blood loss. NE did not affect hematocrit, hemoglobin, platelet, or white cell count. Platelet aggregation was not influenced by the compound. In conclusion, intraportal infusion of NE proved effective in decreasing hemorrhage at liver trauma in cirrhotic rats.

Animals↗

Increased uptake of 5-FU in experimental liver tumours by simultaneous infusion of norepinephrine.

The effect of the simultaneous administration of norepinephrine and 5-fluorouracil (5-FU) on the uptake of radiolabelled 5-FU by liver tumours was studied in rats. Three different concentrations of 5-FU were used (15, 1.5 and 0.15 microgram/g body weight). The drugs were infused over a 30 min period via the hepatic artery, following cannulation of the gastroduodenal artery. The radioactivity in liver tumour, normal liver, lungs and intestines was estimated by liquid scintillation counting. At all concentrations tested, an increased uptake of radioactive 5-FU was found in the tumour when norepinephrine was infused. Tumour/liver ratios also increased significantly in all these cases. No significant differences were noted between norepinephrine infused and control animals in the radioactivity in normal liver, lungs and intestines. The effects noted were possibly due to changes in blood flow within the liver, but the possibility of a direct effect of norepinephrine on DNA metabolism is discussed.

Animals↗

The effect of intraportal six-hydroxy-dopamine on hemorrhage after standardized liver trauma in rats.

Sympathetic denervation of the liver was accomplished by intraportal injection of 6-hydroxy-dopamine in rats. The animals were subjected to standardized liver trauma 1 week later. Blood loss and duration of bleeding from the cut raw surface were more than doubled in the denervated animals. Mean arterial blood pressure was significantly lower in the denervated animals, but stable during hemorrhage in both denervated and innervated animals. Platelet aggregation and the intrinsic coagulation system were not affected by the chemical denervation. Hepatic norepinephrine was almost eliminated by the denervation procedure. These findings suggest that the liver nerves at the porta hepatis should be preserved during hepatic resections.

Animals↗

Inhibition of platelet aggregation by myeloid leukaemic cells demonstrated in vitro.

The effect of myeloid leukaemic cells, cells of the promyelocytic cell line HL-60 and normal polymorphonuclear granulocytes (PMN), enclosed in dialysis tubes, on the aggregation of allogeneic normal platelets after induction with arachidonic acid (AA) and with adenosine diphosphate (ADP) was investigated in vitro. Inhibition of aggregation was seen after preincubation of the platelets with leukaemic blood or bone marrow cells from 7/14 patients belonging to various FAB groups and with HL-60 cells, but not with normal PMN (14/14 cases). A dose-dependent inhibition was seen after lysis of some leukaemic cells with anti-human rabbit antiserum and active complement. Lysis of normal PMN inhibited platelet aggregation slightly and inconstantly and only at higher cell concentrations. Platelet inhibitory activity was not related to a higher rate of metabolism of the leukaemic cells which inhibited platelet aggregation since they did not differ from the cells not inhibiting aggregation with respect to heat production. Neither was a non-specifically increased cell membrane permeability the cause of the release of platelet inhibitory factor(s) since the release of 51Cr-labelled leukaemic cells was not related to the inhibition of platelet aggregation.

Adenosine Diphosphate↗

Effect of intraarterial, intraportal or combined norepinephrine infusion on hemorrhage at experimental liver trauma in the rat.

The effect of intraarterial, intraportal or simultaneous intraarterial and intraportal norepinephrine (NE) infusion on hemorrhage after standardized liver trauma was evaluated in the rat. Infusion of NE through a catheter in the gastroduodenal artery or/and vein, was started 5 min prior to the liver trauma and continued throughout the experiment. Blood pressure was continuously registered after cannulation of the femoral artery. Standardized liver trauma involved resection of the left anterior liver lobe. Bleeding time, blood loss from the traumatized liver surface, hemoglobin (Hb), hematocrit (Hct), platelet count (PC) and white blood cell count (WBC) were measured. Infusion of NE resulted in significant increase of blood pressure compared with controls. Infusion of NE (i.a., i.p., i.a. + i.p.) caused significant decrease in bleeding time and blood loss. Hb, Hct, PC and WBC were not affected. NE infusion proved effective in decreasing hemorrhage at liver trauma; the route of administration did not influence the results.

Animals↗

Hypersplenism--effect on haemostasis. An experimental study in the rat.

Hypersplenism induced by methylcellulose given to rats i.p. was characterized by splenomegaly, anaemia, leucocytopenia and thrombocytopenia. Hb, Hct and WBC count were normalized, and platelet count rose to supernormal values by splenectomy. At a standardized liver resection, the hypersplenic rats had an increased blood loss and prolonged bleeding time in comparison with control rats. Removal of the large spleen normalized these abnormalities. Hypersplenism also shortened APT time and impaired ADP and collagen-induced platelet aggregation, findings not normalized by splenectomy.

Animals↗

Hemostasis following inoculation and during spreading of colon carcinoma in the rat.

Platelet function following inoculation of chemically induced carcinoma was evaluated in the rat. The original line of tumor (NGW1) was obtained using N-methyl-N-nitrosoguanidine. After trypsin homogenation a cell suspension of 0.3 X 10(6) viable tumor cells was injected subserosally in the cecum of each animal. Controls received injections of equal volumes of 0.9% NaCl solution or trypsin. The animals were subjected to laparotomy 2, 4, and 6 weeks after inoculation. Platelet function was assessed in vivo by measuring bleeding time and blood loss during mesenteric vessel transection or liver resection upon laparotomy. Hemoglobin, hematocrit, platelet count, activated partial thromboplastin time, platelet aggregation, thromboxane B2, platelet factor 4, and fibrinogen levels were evaluated after sacrifice by exsanguination. Significant decrease in bleeding time and blood loss was observed in animals with local primary tumors as well as in rats with lymph node metastases. Hemoglobin and hematocrit were decreased in the presence of metastases. Platelet count was not changed. Activated partial thromboplastin time was not affected by the presence of tumor. Platelet aggregation in vitro was accelerated in the presence of primary tumor or lymph node metastases, as well as following addition of tumor cells to platelet suspensions. No changes in thromboxane B2 or platelet factor 4 could be registered. Fibrinogen levels were decreased in the presence of liver metastases. Enhancement of primary hemostasis and platelet function in the presence of colon carcinoma in the rat was demonstrated both in vivo and in vitro. Direct or indirect interaction of the tumor cell with thrombocytes may play a role in determining the metastatic potential of the neoplasm.

Adenosine Diphosphate↗

Increased bleeding during liver resection after sympathetic block in normal rats.

The effect of sympathetic block on hemostasis after standardized liver resection was studied in the rat. Sympathetic block was undertaken by paravertebral block or surgical sympathectomy. Blood loss was significantly increased, but the bleeding time was not prolonged after paravertebral block. Surgical sympathectomy also increased blood loss as compared to controls, but there was no difference when compared with sham operation. Adenosine diphosphate and collagen induced platelet aggregation was not inhibited in all animals as compared to controls. The results indicate that primary hemostasis was not seriously affected, but that hepatic blood flow was augmented after sympathetic block.

Anesthesia, Epidural↗

Effect of latex-stimulated granulocytes on platelet aggregation in man.

The effect of granulocytes on human platelet aggregation was investigated in vitro. Platelet function was assayed by photometric technique. Incubation of platelets with latex-stimulated granulocytes for 1 h at room temperature resulted in total inhibition of arachidonic acid-induced platelet aggregation. ADP-induced platelet aggregation was suppressed, lacked secondary wave and was pursued by swift disaggregation. Platelet aggregates induced by collagen dispersed faster under the influence of stimulated granulocytes. The present results indicate that granulocytes may play a role in the hemostatic mechanism in man.

Adenosine Diphosphate↗

Significant bleeding at kidney resection after experimental denervation.

The effects of microsurgical denervation of the kidney on blood loss, bleeding time, platelet count and APT time in standardized kidney resection were studied in rats. The renal nerves running alongside the blood vessels were stained, identified and resected with a microsurgical technique. One week after the denervation, the blood loss and bleeding time at kidney resection were significantly greater than in control rats (without denervation). The bleeding resulted in reduced haemoglobin and haematocrit values, but the platelet count and APT time were unchanged. Platelet aggregation was not influenced by the denervation procedure. The increased bleeding at parenchymal kidney resection in the denervated rats was regarded as a consequence of interrupted nerve supply to the kidney. The effects on bleeding may have implications for renal surgery in humans.

Animals↗

Colloid-induced changes in bleeding following liver resection in the rat.

The effect of preoperative infusion of Ringer's solution, Ringer's acetate solution, dextran 70, dextran 40, degraded gelatin and hydroxyethyl starch on haemostasis after standardized liver resection was studied in the rat. Ringer's and Ringer's acetate solutions did not affect haemostasis more than expected from haemodilution. Dextrans, degraded gelatin and hydroxyethyl starch caused a significant increase in bleeding time and blood loss. APT time was significantly increased after infusion of hydroxyethyl starch. Dextran and hydroxyethyl starch impaired ADP- and collagen-induced aggregation. Platelet aggregation was not affected by the infusion of Ringer's solution or Ringer's acetate solution as compared to non-treated controls.

Animals↗

Comparative evaluation of local hemostatic agents in experimental liver trauma: a study in the rat.

The efficacy of gelatin foam, oxidized regenerated cellulose, collagen fleece, and microcrystalline collagen as hemostatic agents was tested after standardized liver trauma in the rat. Experiments were divided into two series. In the first series all the above local hemostatic agents were tested on normal animals. Animals in which surgical gauze was applied to the traumatized surface served as controls. Nontreated animals bled profusely. Microcrystalline collagen and collagen fleece were more effective than gauze. In the second series collagen preparations were tested on animals with hemostatic disorders caused by administration of acetylsalicylic acid, ethanol intoxication, or infusion of bensylpenicillin. Collagen preparations were as effective as gauze in diminishing bleeding time and blood loss after liver trauma.

Animals↗

Impairment of primary hemostasis and platelet function after alcohol ingestion in man.

The effect of alcohol ingestion on primary hemostasis was investigated in fasting healthy humans. Primary hemostasis was measured with the template bleeding time and platelet aggregation assayed with the turbidometric method. Blood was collected to study coagulation and fibrinolysis. 1 h after ingestion of 2 ml/kg body weight of 40% alcohol the plasma alcohol concentration was 19.3 +/- 1.6 mmol/l. At this time there was a significant prolongation of the bleeding time accompanied by an impairment of platelet responsiveness to both collagen and ADP. A prolongation of the bleeding time and impairment of platelet function was also found 2 h after alcohol ingestion. Ingestion of this amount of alcohol did not affect parameters of coagulation or fibrinolysis. The data indicate that primary hemostasis is impaired in man after ingestion of moderate amounts of alcohol. This may explain the favorable effect of moderate alcohol consumption on ischemic heart disease but indicates an increased risk for patients with bleeding.

Adenosine Diphosphate↗

Effects of ethanol on platelet aggregation: an in vitro study.

Alcohol ingestion results in the formation of circulating microaggregates in the pig. To investigate the underlying mechanism, the effects of alcohol on platelet aggregation using a Born-aggregometer, was investigated. After incubating unstirred platelet rich plasma (PRP) with moderate concentrations of alcohol (175 mmol/l) the aggregation induced by collagen was reduced. This was probably due to platelet refractoriness caused by platelet ADP release. We could also demonstrate that high concentrations of alcohol (630 mmol/l) caused platelet release in stirred PRP. Release of ADP from red cells, after incubating unstirred whole blood with low concentrations of alcohol (17 mmol/l), was the probable explanation to the observed platelet refractoriness to ADP and collagen. Alcohol causing release of ADP from red cells is likely the cause of platelet aggregation in circulating blood and is probably the mechanism in formation of circulating platelet aggregates after alcohol ingestion.

Adenosine Diphosphate↗

Effect of acute ethanol intoxication on primary haemostasis, coagulation factors and fibrinolytic activity.

The effect of ethanol intoxication on haemostasis was studied by transection of mesenteric microvessels and liver resection in the rat. Plasma concentrations of alcohol were within the range of those found in ethanol intoxication in man. Bleeding time and blood loss were increased 1 h after ethanol administration, regardless of the utilized technique. A significant positive correlation existed between bleeding time following liver resection and bleeding time after simultaneous transection of a mesenteric arteriole and venule. Coagulation mechanisms, assayed by whole blood clotting time, APT time, one-stage prothrombin time, recalcification time, thrombin time, Owren's P & P test and determination of plasma factor V and fibrinogen levels, were not significantly changed in ethanol-intoxicated animals. Administration of alcohol did not affect fibrinolytic activity, while it inhibited significantly ADP and collagen-induced platelet aggregation in the rat.

Alcoholic Intoxication↗

In vitro effect of ethanol on ADP and collagen-induced platelet aggregation.

Platelet aggregation was measured by Born's method. Plasma from Sprague-Dawley rats and inbred albino rabbits was used. 20% ethanol in 0.9% (w/v) NaCl was added to plasma at final concentrations of 56.5 mM, 85.9 mM 171.5 mM and 343.1 mM or to whole blood at final concentrations of 8.7 mM, 17.4 mM, 52.5 mM, 171.5 mM and 343.1 mM. Experiments using 0.9% NaCl volumes equivalent to the added ethanol volume were also conducted. Dose-response aggregation tests showed that a decrease in ADP- and collagen-induced aggregation existed when ethanol was mixed with rat or rabbit blood prior to the preparation of platelet-rich plasma. There was no effect on ADP-induced platelet aggregation when ethanol was mixed with rat or rabbit plasma. Collagen-induced aggregation was impaired only in rat plasma when ethanol concentration reached 343.1 mM. These results suggested that ethanol modified platelet function possibly via red cells.

Adenosine Diphosphate↗