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Biomedical subjects

J Modig

Publications and source records attributed to J Modig.

At least 55 records · Page 3Linked to original sources
PubMed1986

The predictive and discriminative value of biologically active products of eosinophils, neutrophils and complement in bronchoalveolar lavage and blood in patients with adult respiratory distress syndrome.

To determine whether biologically active products of eosinophils, neutrophils and complement contribute to the development of adult respiratory distress system (ARDS) we measured eosinophil cationic protein (ECP), lactoferrin (LF) and C3a in bronchoalveolar lavage (BAL) and blood by means of radioimmunoassays. Seventeen patients served as controls. Fifteen patients were studied before and after major surgery to evaluate the influence of the surgical procedure, and 12 patients with ARDS were investigated 4-12 h after the onset of the disease. Major surgery per se significantly increased ECP in BAL, LF in serum and C3a in BAL and plasma. ECP, LF and C3a levels in BAL and blood were all significantly higher in ARDS patients as compared with levels in controls and those observed after major surgery. The higher ECP levels in BAL were associated with the more severe ARDS as was also the case for C3a in BAL and plasma and LF in serum. One out of 15 patients subjected to major surgery developed ARDS postoperatively and had very high levels of ECP, LF and C3a in BAL and blood at sampling 3 h prior to onset of ARDS, and these levels were similar to those observed in ARDS patients. One out of 12 ARDS patients died from the disease and this patient had the highest level of ECP in BAL and serum. Our results strongly support the role of activated polymorphonuclears, and notably the activated eosinophils, in the pathogenesis of ARDS. Evidence is also presented that ECP can be used as a predictor of impending ARDS.

Adult↗
PubMed1986

Effectiveness of dextran 70 versus Ringer's acetate in traumatic shock and adult respiratory distress syndrome.

During a 3-yr period, 31 adult victims of severe traumatic shock were enrolled in a prospective randomized investigation of the relative effectiveness of dextran 70 vs. Ringer's acetate to treat shock and protect against trauma-induced adult respiratory distress syndrome (ARDS). Fourteen patients were given dextran 70 and Ringer's acetate to compensate for interstitial fluid loss, and whole blood as required; the remaining 17 patients received three to four times the total fluid volume of Ringer's acetate given in the former group, and whole blood as required. Hemodynamics improved significantly more rapidly in the dextran group. In the 7 to 8-day post-trauma period, no patient in the dextran group developed ARDS, compared to five cases of ARDS in the Ringer's acetate group. Also, the cardiac index of dextran patients was significantly higher, and patients challenged with 0.5 L of dextran 70 showed a significantly higher increase in cardiac index than those challenged with 2 L of Ringer's acetate. It is concluded that in the severely traumatized patient, a fluid program based on dextran 70 is superior to Ringer's acetate alone. Furthermore, patients should continue on a fluid program containing dextran 70 to counteract unrecognized hypovolemia. Our results support the assumption that early aggressive shock treatment with dextran 70, followed by continued dextran administration in the post-trauma period might prevent complications such as ARDS.

Accidents, Traffic↗
PubMed1986

Prophylactic and delayed treatment with indomethacin in a porcine model of early adult respiratory distress syndrome induced by endotoxaemia.

The effects of prophylactic and delayed treatment with indomethacin were evaluated in a porcine model of early adult respiratory distress syndrome (ARDS) induced by endotoxaemia. Spontaneously breathing pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin (10 micrograms . h-1 . kg-1) over 6 h. Twenty animals received endotoxin without treatment. Eight animals were pretreated with indomethacin i.v., 5 mg . kg-1 in 30 min, followed by further infusion at a rate of 2 mg . h-1 . kg-1. Ten animals received the same dosage of indomethacin beginning 2 h after the start of endotoxin infusion. Pretreatment with indomethacin inhibited the endotoxin-induced impairment in pulmonary gas exchange, but did not prevent pulmonary oedema. The pulmonary hypertension was counteracted. Oxygen delivery did not improve, because of a marked reduction in cardiac output (Qt). Systemic vascular resistance (SVR) increased markedly, and mean arterial pressure (MAP) was higher. Survival was improved. Delayed indomethacin treatment prevented a further deterioration in pulmonary gas exchange and restored it towards the baseline level. The pulmonary oedema was not counteracted, while the pulmonary hypertension was reduced. O2 delivery was not restored, owing to the greater decrease in Qt compared with the untreated endotoxin group. SVR increased considerably, and MAP was better maintained. Survival was not improved. These results indicate that cyclo-oxygenase inhibitors might benefit pulmonary gas exchange in human ARDS. Drugs which interfere with arachidonate metabolism will probably be of great importance in the prophylaxis, in particular, and also in the treatment of ARDS.

Anesthesia, General↗
PubMed1986

Pulmonary function, extravascular lung water and chest radiography in a porcine model of adult respiratory distress syndrome.

To study the pathophysiology and the value of chest radiography in the diagnosis of early adult respiratory distress syndrome spontaneously air-breathing pigs under ketamine anaesthesia were investigated. Five control animals received physiological saline and showed no notable changes in physiological or radiological data. Eleven animals were infused i.v. with E. coli endotoxin over 6 h. The pulmonary dysfunction in the endotoxin animals was characterized by an early increase in venous admixture with hypoxaemia and a peak increase in pulmonary vascular resistance at 0.5 h after start of endotoxin infusion. Subsequently there was a tendency towards a restitution to baseline physiology, but from 3 h onwards a "second wave" of pulmonary dysfunction developed in addition to an increase in extravascular lung water. No significant correlation (r = 0.44) existed between the increase in extravascular lung water and venous admixture. The increase in calculated pulmonary microvascular pressure correlated significantly (r = 0.77) with the increase in extravascular lung water. Radiographic signs of pulmonary oedema were sparse. Thus, only three of 11 animals displayed increased density on chest radiography indicative of pulmonary oedema.

Animals↗
PubMed1986

Adult respiratory distress syndrome after renal transplantation. A case report.

A potentially lethal case of "air-borne" adult respiratory distress syndrome, most likely consequent to cytomegalovirus (CMV) pneumonitis, is described in a kidney transplant patient. It was characterized by confluent densities on both lung fields with peripheral zones of normal radiographic pattern and with one of the highest values of extravascular lung water reported in the literature, in the presence of a normal pulmonary capillary wedge pressure. When specific conservative therapy for curing a potentially lethal CMV pneumonitis after kidney transplantation fails, we suggest that transplantectomy should be considered.

Adult↗
PubMed1986

Adult respiratory distress syndrome. Pathogenesis and treatment.

ARDS is a complication of septic and traumatic shock. It ranges from slight pulmonary dysfunction to forms so severe as to be incompatible with life. There seem to be initial pathogenic differences between sepsis-induced and trauma-induced ARDS, in that activation of granulocytes is primarily involved in the former and activation of the clotting system during a fibrinolysis-inhibition phase in the latter. In the later course the granulocyte-mediated and the coagulation-mediated injury can potentially amplify each other's effects in several positive feedback systems. In the end stage the two forms involve similar pathogenic mechanisms which may include production of oxygen radicals. Therapy aims primarily to eradicate the initiating event. Firm data support shock treatment with dextran-70 and early or prophylactic ventilator treatment using positive end-expiratory pressure. Despite lack of conclusive evidence, high-dose corticosteroids in one or two doses should be given very early, at least in sepsis-induced ARDS. Other agents which may be tried early in the course of ARDS include prostaglandin E1, cyclooxygenase inhibitors and oxygen radical scavengers.

Adrenal Cortex Hormones↗
PubMed1986

Lung mechanics with relation to pulmonary haemodynamics, gas exchange and extravascular lung water in mechanically ventilated endotoxaemic pigs.

In a porcine model employing a continuous i.v. infusion of E. coli endotoxin the pathophysiology of early adult respiratory distress syndrome was studied with main emphasis on the early changes in lung mechanics and their relation to changes in pulmonary haemodynamics, gas exchange and extravascular lung water in intermittent positive pressure ventilated (IPPV) pigs under ketamine anaesthesia. Six animals served as controls and revealed no major physiological changes. Nine animals received endotoxin and developed significant changes in lung mechanics with increases in end-inspiratory pressure (32%), expiratory resistance (29%) and decrease in total dynamic lung compliance (27%). Changes in dynamic compliance and pulmonary haemodynamics displayed a 2-phase reaction. Venous admixture showed a rapid increase at with the increase in mean pulmonary arterial pressure (r = -0.8) and with the increase in venous admixture (r = -0.7). Extravascular lung water did not increase significantly. The decrease in dynamic compliance is most likely explained by peripheral airway constriction. A contributory factor might be pulmonary microvascular constriction with vascular stasis and mechanical compression of small airways. The increased venous admixture is best explained by a bronchiolar and microvascular constriction, i.e. a "dry" ventilation/perfusion inequality and not consequent to oedema. IPPV seems to counteract the increase in extravascular lung water.

Animals↗
PubMed1986

Treatment with prostaglandin E1 in a porcine model of early adult respiratory distress syndrome.

The effects of treatment with PGE1 were evaluated in a porcine model of early adult respiratory distress syndrome induced by endotoxaemia. Spontaneously breathing pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin (10 micrograms X kg-1 X h-1) for 6 h. Thirteen pigs were given endotoxin, and 11 pigs were treated with a continuous infusion of PGE1, 0.25 microgram X kg-1 X min-1 for 4 h, beginning 2 h after start of endotoxin and established lung injury. Four pigs served as controls and receiving only PGE1 (0.25 microgram X kg-1 X min-1) during the whole observation period of 6 h. PGE1 treatment did not influence the decline in platelet and polymorphonuclear cell counts, whereas it markedly decreased the pulmonary hypertension induced by endotoxaemia. The increased extravascular lung water returned towards baseline after institution of PGE1. The increased venous admixture was not significantly influenced by PGE1. Treatment with PGE1 induced an exacerbated hypotensive state in the endotoxaemic animals primarily due to vasodilation. The decline in cardiac output and oxygen delivery noted in endotoxaemic pigs were not influenced by PGE1 and survival was not improved. Although one should be extremely careful in extrapolating these data to the clinical situation the results from the present study suggest the need for optimum volume replacement when starting PGE1 infusion in endotoxin-induced ARDS.

Alprostadil↗
PubMed1985

The role of polymorphonuclear leucocytes in the pulmonary dysfunction induced by complement activation.

To determine the role of polymorphonuclear leucocytes (PMNs) in the pulmonary reaction induced by complement activation, pigs were infused with complement-activated plasma (CAP), cell-free supernatant from PMNs activated in vitro, or washed PMN aggregates produced in vitro. Infusion of CAP resulted in transient peripheral leucopenia, a reversible rise in pulmonary vascular resistance (PVR) and decreased arterial oxygen tension (PaO2). Indomethacin did not influence the CAP-induced drop in PMN count or the accumulation of PMNs in the lung, but significantly counteracted the rise in PVR and fall in PaO2. Antihistamines did not prevent the cellular or pulmonary reactions to CAP infusion. Methylprednisolone did not inhibit the decrease in PMN count, but modified the pulmonary reaction to CAP, although it did not prevent the rise in PVR to the same extent as indomethacin; it counteracted the fall in PaO2. Infusion of supernatant from activated PMNs did not influence the PMN count, but caused a reversible increase in PVR and a drop in PaO2. Indomethacin counteracted the pulmonary reaction to this infusion. Infusion of washed PMN aggregates did not result in any cellular or physiological changes. These findings suggest that the pulmonary reaction induced by complement activation is mediated by humoral components generated and/or released during activation of PMNs. Arachidonic acid metabolites play an important role and it is likely that substance(s) released from activated PMNs trigger prostanoid synthesis in other cells. It is conceivable, however, that PMNs exposed to activated complement factors also directly synthesize and release arachidonic acid metabolites.

Animals↗
PubMed1985

Potential anti-thrombotic effects of local anaesthetics due to their inhibition of platelet aggregation.

The aim was to study the possible anti-aggregating effects of local anaesthetics on platelets stimulated by physiological doses of adenosine-diphosphate and collagen. Platelet-rich plasma was therefore incubated in an aggregometer with lidocaine, bupivacaine or tocainide in various concentrations and for different incubation times. It was found that of the local anaesthetics tested, lidocaine was the most effective anti-aggregating compound. Furthermore, the longer the incubation time with the different local anaesthetics, the more efficient the anti-aggregating effect. These results may have clinical implications, and they may be one of the explanations for the lower incidence of thromboembolism in patients operated on under lumbar epidural anaesthesia.

Adenosine Diphosphate↗
PubMed1985

A porcine model of early adult respiratory distress syndrome induced by endotoxaemia.

To study the pathophysiology of early adult respiratory distress syndrome (ARDS) induced by sepsis, spontaneously breathing pigs under ketamine anaesthesia were investigated. Twenty animals were infused i.v. with E. coli endotoxin (10 micrograms . h-1 . kg-1) over 6 h, and ten control animals received physiological saline. In the controls, cardiac output (Qt) and O2 delivery decreased slightly. There were no changes in pulmonary gas exchange, pulmonary haemodynamics or extravascular lung water (EVLW). The polymorphonuclear (PMN) leucocyte count gradually increased, while the platelet count decreased slightly. Endotoxin infusion caused profound deterioration of pulmonary gas exchange, a marked rise in pulmonary vascular resistance (PVR) and a moderate increase in EVLW. The pulmonary dysfunction was not attributable to the pulmonary oedema per se, whereas a "dry" ventilation/perfusion inequality played an important role. The "responders" (peak venous admixture greater than 20%; n = 14) were characterized by higher Qt and lower PVR than the "non-responders". Qt declined progressively, especially in non-survivors. O2 delivery decreased considerably. Metabolic acidosis probably indicated oxygen deficit. Eleven of 20 animals died during the observation period. Mortality was related more to the imbalance between O2 delivery and oxygen demand than to the deterioration in pulmonary gas exchange. The PMN count decreased markedly while the gradual decline in platelet count was similar to that in the controls. Lung microscopy revealed PMN accumulation in the microvasculature, moderate interstitial oedema and microvascular blood stasis. Our porcine model, which closely mimics early ARDS in man, will be useful in further studies of the pathophysiological pathways and the treatment of this syndrome.

Acid-Base Equilibrium↗
PubMed1985

Prophylactic and delayed treatment with high-dose methylprednisolone in a porcine model of early ARDS induced by endotoxaemia.

The effects of prophylactic and delayed treatment with high-dose methylprednisolone were evaluated in a porcine model of early adult respiratory distress syndrome induced by endotoxaemia. Spontaneously breathing pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin (10 micrograms . h-1 . kg-1) over 6h. Twenty animals received endotoxin without treatment. Eight animals were pretreated with methylprednisolone i.v., 60 mg . kg-1, followed by an i.v. infusion at a rate of 10 mg . h-1 . kg-1. Ten animals received the same dosage of methylprednisolone beginning 2 h after the start of endotoxin infusion. Pretreatment with methylprednisolone prevented the endotoxin-induced impairment in pulmonary gas exchange and the development of pulmonary oedema. The pulmonary hypertension was counteracted. Cardiac output (Qt) and O2 delivery were improved. Mean arterial blood pressure (MAP) increased and was higher than in the untreated endotoxin group. The profound fall in PMN count was inhibited, while the accumulation of these cells in the lung was still substantial. Survival was improved. Delayed methylprednisolone treatment prevented further deterioration in pulmonary gas exchange and tended to restore it towards baseline. The pulmonary oedema and pulmonary hypertension were reduced. Qt and O2 delivery did not improve. MAP was higher than in the untreated endotoxin group towards the end of the observation period. The decline in PMN count and the pulmonary accumulation of these cells were not significantly influenced. Survival was improved. These results indicate that high-dose methylprednisolone, when given early in the course of sepsis, might be of clinical value in prevention of the devastating pulmonary and circulatory complications of this disease.

Animals↗
PubMed1985

Determinants of early adult respiratory distress syndrome. A retrospective study of 220 patients with major fractures.

The records of 220 consecutive trauma patients admitted to intensive care in the period 1974 through 1982 were reviewed in an attempt to find determinants of early adult respiratory distress syndrome (ARDS). All the patients were considered to be at risk of ARDS and had major fractures without concomitant severe injuries to brain, chest or abdomen. No patient died. ARDS developed in 27 patients (12.3%), on average in the second day post-trauma. The clinical determinants of post-traumatic ARDS were high fracture index, implying severe tissue trauma, and shock on admission. Fluid overload was not found to cause ARDS. Conventional signs of disseminated intravascular coagulation (DIC) were not predictive or diagnostic of ARDS, but were related to the transfused amount of stored blood. Chest radiography was indicative of ARDS in 21 cases, but in six it was normal despite hypoxaemia. In the cases with radiographic signs of ARDS there was generally good chronologic correspondence with hypoxaemia. Ventilation with positive end-expiratory pressure may prevent the classic radiographic picture of ARDS with alveolar densities.

Adolescent↗
PubMed1985

Positive effects of prophylactic ventilator treatment on gas exchange and extravascular lung water in a porcine model of adult respiratory distress syndrome induced by endotoxaemia.

The influence of prophylactic ventilator treatment was evaluated in a porcine model of early adult respiratory distress syndrome (ARDS) induced by endotoxaemia. Sixteen animals, controls, under continuous i.v. ketamine anaesthesia were either mechanically ventilated using intermittent positive pressure ventilation (IPPV; n = 6) with air or breathed air spontaneously (n = 10). Twenty animals under continuous i.v. ketamine anaesthesia and spontaneously breathing air were infused i.v. with E. coli endotoxin (10 micrograms X kg-1 X h-1) over 6 h. Fifteen animals under continuous i.v. ketamine anaesthesia were given IPPV with air and were infused i.v. with E. coli endotoxin in the same dosage regimen. In the controls, cardiac output decreased slightly. Otherwise there were no changes in pulmonary gas exchange, pulmonary haemodynamics or extravascular lung water. In spontaneously breathing and IPPV animals given endotoxin there was a profound deterioration in pulmonary gas exchange, a marked rise in pulmonary vascular resistance and a moderate increase in extravascular lung water. Animals given IPPV showed a significantly less pronounced impairment in pulmonary gas exchange and a significantly smaller increase in extravascular lung water than in animals breathing spontaneously, whereas the changes in pulmonary haemodynamics were fairly similar in both groups. Animals with IPPV also had an improved survival rate. The beneficial effects of mechanical ventilation on pulmonary gas exchange are not due to changes in extravascular lung water, but are caused by its influence in counteracting terminal airway and alveolar closure. These results indicate that mechanical ventilation, when instituted early in the course of human ARDS induced by septicaemia, might be of potential value in the prevention of severe pulmonary failure and death.

Animals↗
PubMed1985

High-dose methylprednisolone in a porcine model of ARDS induced by endotoxemia.

Using a continuous i.v. infusion of E. coli endotoxin in spontaneously breathing pigs under ketamine anesthesia we have developed a lung injury model which closely mimics the pathophysiological and morphological changes of early ARDS induced by sepsis in man. Pretreatment with high doses of methylprednisolone largely prevented the pulmonary, cardiovascular and morphological features induced by the endotoxin. Methylprednisolone treatment initiated 2 h after starting the endotoxin abolished further derangements in pulmonary and cardiovascular functions and there was a restoration towards normal values. Both pretreatment and delayed treatment with methylprednisolone improved survival. Although one should be extremely cautious in extrapolating these data to the more complex clinical situation, the implications are that high doses of methylprednisolone, given early in the course of sepsis in man, may help to prevent both the pulmonary and cardiovascular derangements of this disease.

Animals↗
PubMed1985

The role of lumbar epidural anaesthesia as antithrombotic prophylaxis in total hip replacement.

A review of a series of clinical and experimental investigations established that the incidence of deep venous thrombosis and of pulmonary embolism after total hip replacement surgery was lower in patients given continuous lumbar epidural anaesthesia than in others with general anaesthesia. The thromboprophylactic effect of continuous lumbar epidural anaesthesia is explained by its beneficial influence on all factors of the triad proposed by Virchow, viz. blood flow, factors within the blood itself, and the vascular endothelium. Continuous lumbar epidural anaesthesia is associated with hyperkinetic blood flow in the major vessels of the lower limbs, lessened tendency to coagulation of the blood and better preservation of fibrinolysis function. Other characteristics include an inhibitory action on platelet aggregation and stabilizing effect on leukocytes and endothelial cells--effects exerted by the local anaesthetics per se. The smaller blood loss and thus the lower transfusion requirements during continuous lumbar epidural anaesthesia may also play a beneficial role as a thromboprophylactic factor.

Anesthesia, Epidural↗
PubMed1984

Signs of neutrophil and eosinophil activation in adult respiratory distress syndrome.

Circulating levels of lactoferrin, a specific granule protein of neutrophilic leukocytes, and eosinophil cationic protein (ECP), a specific granule protein of eosinophilic leukocytes, were serially measured in 19 patients at risk for adult respiratory distress syndrome (ARDS). Those patients who developed ARDS had significantly higher concentrations of both proteins than the patients without signs of ARDS. High ECP levels were observed in spite of peripheral eosinopenia. The lactoferrin levels were also increased in relation to circulating numbers of neutrophils. These findings are consistent with an enhanced turnover and/or activity of eosinophils and neutrophils in ARDS and thereby support other clinical and experimental observations suggesting a central pathophysiologic role for granulocytes in ARDS. No relation was found between ARDS or serum concentrations of lactoferrin or ECP and degree of complement consumption, suggesting that other mechanisms besides complement activation may underlie granulocyte activation in ARDS.

Adolescent↗