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Biomedical subjects

O Elmér

Publications and source records attributed to O Elmér.

At least 19 recordsLinked to original sources
PubMed1989

Polymorphonuclear leucocyte sequestration in the lungs and liver following soft-tissue trauma: an in vivo study.

Neutrophils are thought to sequestrate in the lungs and the liver in association with shock. Indications for this have previously been demonstrated in different in vitro studies. In this experiment an in vivo technique for dynamic studies of pulmonary and liver neutrophil sequestration (PNT and LNT, respectively) is described. Autologous neutrophils from ten pigs were labelled with 111Indium-oxine. The pigs were placed under a scintillation camera for continuous recording of the activity distribution in the pigs during 105 minutes. Following a steady-state period of 15 minutes seven pigs were subjected to a standardized soft-tissue trauma. Three pigs were used as controls and not traumatized. Within 1-3 minutes after trauma the radioactivity over the lungs increased dramatically, indicating PNT. This was followed by a fast decrease but 90 minutes after trauma PNT levels were still significantly elevated. LNT showed a similar pattern, although the immediate increase was less dramatic. This study shows that PNT and LNT occur immediately after soft-tissue trauma and can be studied dynamically in vivo.

Animals↗
PubMed1989

Different effects of bleeding and soft-tissue trauma on pulmonary platelet trapping in pigs.

Immediate reactions to different types of trauma have been the object of several studies recently. It has been shown that pulmonary platelet trapping (PPT) occurs within minutes after both septic shock and soft-tissue trauma. The purpose of this study was to investigate whether hypovolemia induced by hypoperfusion might trigger platelet trapping in the lungs in the same way as soft-tissue trauma. Platelets labelled with indium-oxine were reinfused in anesthetized and mechanically ventilated pigs 4 hours before either induction of standardized hypovolemia caused by bleeding to the amount of 20% of the estimated blood volume (n = 6) or a standardized soft-tissue trauma to the hind limbs (n = 7). Platelet sequestration in the lungs was recorded dynamically by means of scintigraphy for 15 minutes before and 90 min after the start of the trauma and bleeding episodes. Central hemodynamics were recorded using a Swan-Ganz catheter. Soft-tissue trauma induced a marked PPT; in the animals subjected to bleeding alone there was no such effect despite a hemodynamic deterioration of greater magnitude than in the trauma group. The PPT was accompanied by a reduction in the number of platelets and leukocytes in peripheral blood. Our results indicate that immediate trapping of platelets in the lungs after trauma occurs as a response to factors other than those related to simple hypovolemic hypoperfusion.

Animals↗
PubMed1988

Effect of epidural analgesia on immediate posttraumatic cardiovascular hemodynamics and pulmonary platelet trapping.

Immediate reactions to different types of trauma have been the object of several studies recently. Thus, it has been shown that pulmonary platelet trapping (PPT) occurs within minutes after both septic and traumatic shock following soft tissue trauma. To study whether block of the nervous supply to the traumatized tissue had any effect on PPT, 40 mg of mepivacaine was injected through an epidural catheter inserted between the second and third lumbar vertebrae in pigs. After a period of stabilization the animals were subjected to a standardized soft tissue trauma to the hind limbs. A group of animals without an epidural catheter served as control. The trauma induced a profound decrease in cardiac output and mean arterial pressure. Pulmonary platelet trapping was recorded dynamically by labelling platelets with radioactive indium. Trapping of platelets in the lungs occurred immediately after the trauma, and there was no difference in animals pretreated with epidural block compared with the control animals. Our findings indicate that the trapping of platelets after soft tissue trauma is triggered at the trauma site and not affected by a block of the nervous supply to the trauma sites, including the peripheral sympathetic outflow.

Analgesia↗
PubMed1987

Early post-traumatic changes in hemodynamics and pulmonary ventilation in alcohol-pretreated pigs.

Time relations among trauma, pulmonary and systemic circulation, and lung function were studied in pigs. Eleven animals (b.w. 25-30 kg) were investigated under balanced anesthesia. Ventilation was mechanically controlled. Hemodynamics, pulmonary ventilation, and gas exchange were serially recorded. Seven animals were pretreated with 40% ethanol in saline and four with saline only. Ninety minutes after the ingestion of alcohol or saline, the animals were subjected to a standardized soft-tissue trauma. Cardiac output decreased significantly 2 minutes after trauma and remained low in both groups throughout the observation period of 30 minutes. Pulmonary vascular resistance was significantly increased in the alcohol-pretreated group but was virtually unchanged in the control animals. Systemic vascular resistance was similarly reduced in the two groups. Total compliance was somewhat lower in alcohol-pretreated animals and 10 minutes after the trauma arterial oxygen tension was significantly lower in the alcohol group than in control animals. Carbon dioxide elimination was reduced after trauma in both groups. It is concluded that pulmonary vascular response increased and that total pulmonary compliance is somewhat decreased shortly after trauma in the alcohol group while gas exchange is almost unchanged. The results indicate a negative interaction between alcohol and trauma.

Alcoholic Intoxication↗
PubMed1987

Central hemodynamics and pulmonary ventilation after trauma: effect of portacaval transposition.

Immediate reaction to traumatic shock involves, among other factors, trapping of platelets in the lungs. It has previously been shown that this trapping is associated with an increase in pulmonary vascular resistance (PVR). To elucidate whether this increase in PVR was due to cellular sequestration or other factors, we performed a portacaval transposition in a group of pigs (n = 9), making the liver the first receiving capillary bed for blood from the lower extremities. One week later, these animals and a control group (n = 6) were subjected to a standardized soft tissue trauma to the hind limbs. Following trauma, there was an immediate increase in PVR in the control group but not in the operated animals. This increase in PVR was accompanied by a fall in alveolar ventilation that was significantly lower in the control group than in the operated animals. There were no differences in blood gases, probably because of high FiO2 during the experiment. Our findings indicate that the early response in pulmonary circulation following trauma is due to cellular sequestration from the trauma sites.

Animals↗
PubMed1987

Outcome of inguinal hernia surgery.

A consecutive series of 584 patients, operated for 635 groin hernias, was clinically evaluated at a median of 6 years after surgery. The cumulative recurrence rate was 16%, established by clinical examination and in uncertain cases with herniography; for primary hernias 14.6% and for recurrent hernias 20.7%. The recurrence rate for indirect hernias was 12.9% and for direct hernias 25%. The direct type of hernia was more frequent among recurrent hernias than among primary hernias (p less than 0.005), indicating that they were overlooked at or caused by the primary operation. The recurrences were noted by the patients themselves in 71% but only 58% had taken the initiative towards another repair. Considering the great number of hernia operations performed and the presented poor long-term results, the need for more research and interest focused on hernia surgery is indicated.

Adolescent↗
PubMed1986

Early posttraumatic pulmonary platelet trapping and its potentiation by oral pretreatment with alcohol.

Soft tissue trauma is associated with platelet aggregation and sequestration in the lungs. This is believed to be an early step in the later development of adult respiratory distress syndrome. In the present experiment using a new method for in vivo dynamic studies of platelet sequestration, we wanted to evaluate the effect of soft tissue trauma on pulmonary platelet trapping in pigs and the influence of acute alcohol intoxication. The results show that significant pulmonary platelet trapping is registered within minutes of trauma and that alcohol significantly increases platelet sequestration in the lungs. This indicates an increased risk for posttraumatic pulmonary problems in alcohol-intoxicated trauma victims.

Administration, Oral↗
PubMed1986

Herniography: a diagnostic tool in groin symptoms following hernial surgery.

The diagnostic value of herniography for groin symptoms after hernial surgery was evaluated in 106 patients. When clinical examination indicated recurrent hernia, herniography was positive in 32 of 40 cases (80%). When no hernia was palpable, herniography revealed recurrence in 28 of 66 cases (42%). A narrow hernial neck was found in 33% of recurrent direct inguinal hernias. Preoperative herniographic findings were confirmed at subsequent surgery in 51 of 53 cases (96%). Postoperative herniography in symptomatic patients without palpable hernial recurrence increased the number of diagnosed recurrences by 44%. Herniography significantly adds to the reliability of clinical diagnosis, with specific information concerning type of recurrent hernia and appearance of the hernial neck.

Adult↗
PubMed1985

Influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma.

The influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma was investigated in a prospective study. Alcohol was found in the blood in 35 of the 69 patients, with mean level 136 +/- 13 mg/100 ml. The patients were admitted to hospital 29.5 +/- 2 min after the injury and had mean ISS 25 +/- 2. In the patients with alcohol in the blood, the blood pressure and PCO2 on arrival were lower than in the other patients. When the alcohol level exceeded 100 mg/100 ml, the blood pressure and PCO2 were lower than in the sober patients despite significantly shorter time between injury and admission to hospital. The hospital stay and mortality were similar in the alcohol and the control group. The greater hypovolemia in the patients with alcohol in the blood indicates that alcohol may be a negative factor for the traumatized patient if resuscitation is delayed, and it underlines the need for rapid and adequate fluid resuscitation of these patients.

Accidents, Traffic↗
PubMed1985

Herniography in the diagnosis of obscure groin pain.

Obscure groin pain was investigated in 250 consecutive patients (including 171 males) with no palpable hernia or previous hernia operation. Herniography revealed nonpalpable but symptomatic hernia in 51% of the male and 21% of the female patients. Among the hernia patients with bilateral pain, 40% had unilateral hernia. Direct-type hernia was most commonly found. Of the surgically treated patients, 87% were free from groin pain postoperatively. Further clinical investigations with a broad diagnostic approach gave a treatable diagnosis in 70% of the patients without hernia surgery. Spontaneous improvement occurred during the investigation in 25%, and the cause of groin pain remained unclear in 5% of the patients. Herniography is a valuable diagnostic tool in obscure groin pain and its use is justified at an early stage of investigation. "Blind" exploration can thus be avoided.

Bone Diseases↗
PubMed1984

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↗
PubMed1983

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↗
PubMed1983

Acute alcohol intoxication and traumatic shock. An experimental study on circulating microaggregates and survival.

The reaction to a standardized soft tissue trauma was investigated in pigs pretreated with gastric administration of saline or 40% ethanol. Circulating microaggregates in vena cava, vena portae and aorta were determined with screen filtration pressure (SFP). Using Swan-Ganz thermistor catheters changes in central hemodynamics were recorded. 1 min after trauma, pulmonary capillary wedge pressure (PCW) increased over pretrauma values in alcohol-intoxicated pigs while cardiac output (CO) and mean arterial pressure (MAP) decreased. In control animals, CO and MAP were reduced. 30 min after trauma the control animals had restored their circulatory parameters while intoxicated animals had not. SFP increased in alcohol-intoxicated animals before trauma and more so after trauma except for in aorta. The standardized trauma was nonlethal to control animals while 6 out of 7 pigs, pretreated with alcohol, died within 65 min of the trauma. The data indicate that alcohol intoxication decreases survival after traumatic shock and that alcohol and trauma induced a significant increase in circulating microaggregates.

Alcoholic Intoxication↗
PubMed1981

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↗
PubMed1980

Circulating microaggregates after gastric administration of ethanol in the pig.

Earlier in vitro experiments have shown microaggregate formation in pig and rabbit blood after addition of ethanol. In this study ethanol was given to pigs resulting in ethanol concentrations of 30-40 mmol/l 2-4 h after administration. As would be expected ethanol concentration was higher in the portal vein than in the hepatic vein, caval vein or aorta. Microaggregates in circulating blood were measured with screen filtration pressure (SFP). SFP rose to more than double the initial value in ethanol-intoxicated pigs whereas it remained unchanged in controls. The ethanol-intoxicated pigs developed hemoconcentration and metabolic acidosis. Our results indicate that microaggregates probably made up of aggregated platelets are formed in pig blood during acute ethanol intoxication.

Acidosis↗
PubMed1979

Effect of acute and chronic ethanol intake on metastasis formation in rat liver.

The effect of acute ethanol intoxication and prolonged intake of ethanol on metastasis formation in the liver was studied in the rat. The tumour cells used were derived from a pharmacologically induced colon carcinoma (NGW 1) and were injected intraportally. Acute ethanol intoxication at the time of injection was associated with a liver weight of 13.29 +/- 0.89 gm two weeks later, compared to 8.43 +/- 0.51 gm in controls. Daily intake of ethanol for eight weeks resulted in a mild reduction of platelets. The liver weight in two groups was 7.31 +/- 0.50 gm and 12.19 +/- 1.40 gm three weeks after intraportal injection of cancer cells as compared to 9.53 +/- 1.11 gm and 19.63 +/- 1.67 gm in controls. The results indirectly supported the hypothesis that acute ethanol intoxication causes increased platelet activity and confirmed earlier results showing the importance of platelets for metastasis formation.

Alcoholic Intoxication↗