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Biomedical subjects

C Putensen

Publications and source records attributed to C Putensen.

At least 37 records · Page 2Linked to original sources
PubMed2000

Prothrombin gene G20210A mutation and elevated anticardiolipin antibodies in a patient with combined portal-mesenteric vein thrombosis.

A 29-year-old man was admitted to the ICU after emergency laparotomy for portal-mesenteric vein thrombosis. Under continuous intravenous heparin therapy the portal-mesenteric shunt occluded on the first postoperative day. After thrombectomy the heparin dose was increased, and the patient remained free of symptoms (partial thromboplastin time 53 s). Two days later abdominal distension developed concomitantly with ventilatory distress due to a large retroperitoneal hematoma. The patient was mechanically ventilated and underwent the third consecutive laparotomy for the hematoma removal on the fifth day. During the surgical procedure the abdomen was packed with towels to stop multiple bleeding sites. The heparin dose was reduced, aiming for a partial thromboplastin time of 30-35 s. Initial coagulation tests revealed increased levels of anticardiolipin immunoglobulin G. After removal of the surgical towels the patient was successfully weaned from mechanical ventilation and discharged from the ICU. Two weeks later genomic testing revealed that he also had a G20210A mutation of the prothrombin gene. Both, increased levels of anticardiolipin immunoglobulin G and the G20210A mutation of the prothrombin gene predispose to thrombosis. Increased levels of anticardiolipin immunoglobulin G may also cause bleeding. Long-term anticoagulation therapy was started with a vitamin K antagonist, and 2 months later a follow-up showed that the patient had no further symptoms of portal-mesenteric vein thrombosis or bleeding. This case illustrates that the convergence of multiple risk factors, including genetic defects, must be considered in patients suffering from thrombosis in unusual sites

Adult↗
PubMed2000

Effects of mechanical ventilation on release of cytokines into systemic circulation in patients with normal pulmonary function.

BACKGROUND: Mechanical ventilation with high tidal volumes (V(T)) in contrast to mechanical ventilation with low V(T) has been shown to increase plasma levels of proinflammatory and antiinflammatory mediators in patients with acute lung injury. The authors hypothesized that, in patients without previous lung injury, a conventional potentially injurious ventilatory strategy with high V(T) and zero end-expiratory pressure (ZEEP) will not cause a cytokine release into systemic circulation. METHODS: A total of 39 patients with American Society of Anesthesiologists physical status I-II and without signs of systemic infection scheduled for elective surgery with general anesthesia were randomized to receive mechanical ventilation with either (1) V(T) = 15 ml/kg ideal body weight on ZEEP, (2) V(T) = 6 ml/kg ideal body weight on ZEEP, or (3) V(T) = 6 ml/kg ideal body weight on positive end-expiratory pressure of 10 cm H2O. Plasma levels of proinflammatory and antiinflammatory mediators tumor necrosis factor, interleukin (IL)-6, IL-10, and IL-1 receptor antagonist were determined before and 1 h after the initiation of mechanical ventilation. RESULTS: Plasma levels of all cytokines remained low in all settings. IL-6, tumor necrosis factor, and IL-1 receptor antagonist did not change significantly after 1 h of mechanical ventilation. IL-10 was below the detection limit (10 pg/ml) in 35 of 39 patients. There were no differences between groups. CONCLUSIONS: Initiation of mechanical ventilation for 1 h in patients without previous lung injury caused no consistent changes in plasma levels of studied mediators. Mechanical ventilation with high V(T) on ZEEP did not result in higher cytokine levels compared with lung-protective ventilatory strategies. Previous lunge damage seems to be mandatory to cause an increase in plasma cytokines after 1 h of high V(T) mechanical ventilation.

Adult↗
PubMed1999

Endotoxin inhibits heat shock protein 70 (HSP70) expression in peripheral blood mononuclear cells of patients with severe sepsis.

OBJECTIVE: To investigate the ex vivo endotoxin-inducible heat shock protein 70 (HSP70) expression in the peripheral blood mononuclear cells (PBMC) of patients with severe sepsis in order to assess the capacity of this potentially protective response during systemic inflammation. DESIGN: Prospective observational study in consecutive patients with severe sepsis and healthy blood donors. SETTING: Surgical intensive care unit in a university hospital. PATIENTS AND PARTICIPANTS: Eleven patients with the diagnosis of severe sepsis, one patient who had recovered from severe sepsis and 13 healthy blood donors. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: We studied the inducibility of HSP70 expression in the PBMC of patients with severe sepsis and healthy blood donors ex vivo. Human whole blood was incubated with variable lipopolysaccharide (LPS from Salmonella minnesota Re 595) concentrations (0; 0.1; 10; 100 ng/ml) for different periods of time (0.5; 2; 4; 10 h). The PBMC were separated by Ficoll density gradient and then disrupted by hypotonic lysis. HSP70 was measured by means of enzyme-linked immunosorbent assay (ELISA). We found a LPS dose- and time-dependent inhibition of ex vivo HSP70 expression in the PBMC of both patients with severe sepsis and healthy individuals. However, the levels of HSP70 expression in patients were significantly lower compared to those of healthy individuals at all LPS concentrations and incubation times. On average, HSP70 expression in the PBMC of healthy controls was 2.8 (range 1.2-3.9) times higher than in patients. HSP70 expression was inducible by thermal heat shock in the PBMC of both patients and healthy individuals. CONCLUSIONS: Endotoxin inhibits HSP70 expression in PBMC ex vivo. In vivo, the suppression of HSP70 expression induced by endotoxin and high levels of proinflammatory cytokines may contribute to the cellular dysfunction of immunocompetent cells concerning antigen presentation, phagocytosis and antibody production associated with decreased resistance to infectious insults during severe sepsis.

Adult↗
PubMed1999

Impaired inducibility of heat shock protein 70 in peripheral blood lymphocytes of patients with severe sepsis.

OBJECTIVE: To determine the extent of the potentially protective heat shock protein 70 response in peripheral blood lymphocytes of patients with severe sepsis after ex vivo lipopolysaccharide stimulation. DESIGN: Entry study of consecutive patients with severe sepsis, those who were critically ill or nonseptic after major surgery, and healthy blood donors. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: Ten patients with diagnoses of severe sepsis; ten critically ill, nonseptic patients after major surgery; and ten healthy blood donors. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We investigated the ex vivo endotoxin-inducible expression of heat shock protein 70 in peripheral blood lymphocytes of patients with severe sepsis by means of flow cytometry. Only negligible amounts of inducible intracellular heat shock protein 70 accumulation (<4.2% of lymphocytes) could be detected in peripheral blood lymphocytes without lipopolysaccharide stimulation. The proportion of cells accumulating heat shock protein 70 after treatment with lipopolysaccharide was distinctly lower in patients with severe sepsis (p < .05) than in critically ill, nonseptic patients after major surgery and healthy blood donors (38.3+/-3.3%, 82.2+/-4.5%, and 70.9+/-3.9%, respectively; mean +/- SEM; n = 10). Patients with clinical signs of recovery from severe sepsis showed an increase in heat shock protein 70 expression. CONCLUSIONS: Inducibility of ex vivo heat shock protein 70 was impaired in peripheral blood lymphocytes of patients with severe sepsis. The impaired expression of the potentially protective heat shock protein 70 may contribute in vivo to immune dysfunction, because intact functioning of T and B lymphocyte responses is of central importance in resisting infection in severe sepsis. Monitoring of inducible heat shock protein 70 in peripheral blood lymphocytes may contribute to the evaluation of the immune consequences of severe sepsis.

APACHE↗
PubMed1999

Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome.

Ventilation-perfusion (V A/Q) distributions were evaluated in 24 patients with acute respiratory distress syndrome (ARDS), during airway pressure release ventilation (APRV) with and without spontaneous breathing, or during pressure support ventilation (PSV). Whereas PSV provides mechanical assistance of each inspiration, APRV allows unrestricted spontaneous breathing throughout the mechanical ventilation. Patients were randomly assigned to receive APRV and PSV with equal airway pressure limits (Paw) (n = 12) or minute ventilation (V E) (n = 12). In both groups spontaneous breathing during APRV was associated with increases (p < 0.05) in right ventricular end-diastolic volume, stroke volume, cardiac index (CI), PaO2, oxygen delivery, and mixed venous oxygen tension (PvO2) and with reductions (p < 0.05) in pulmonary vascular resistance and oxygen extraction. PSV did not consistently improve CI and PaO2 when compared with APRV without spontaneous breathing. Improved V A/Q matching during spontaneous breathing with APRV was evidenced by decreases in intrapulmonary shunt (equal Paw: 33 +/- 4 to 24 +/- 4%; equal V E: 32 +/- 4 to 25 +/- 2%) (p < 0.05), dead space (equal Paw: 44 +/- 9 to 38 +/- 6%; equal V E: 44 +/- 9 to 38 +/- 6%) (p < 0.05), and the dispersions of ventilation (equal Paw: 0.96 +/- 0.23 to 0.78 +/- 0.22; equal V E: 0.92 +/- 0.23 to 0.79 +/- 0.22) (p < 0.05), and pulmonary blood flow distribution (equal Paw: 0.89 +/- 0.12 to 0.72 +/- 0.10; equal V E: 0.94 +/- 0.19 to 0.78 +/- 0.22) (p < 0.05). PSV did not improve V A/Q distributions when compared with APRV without spontaneous breathing. These findings indicate that uncoupling of spontaneous and mechanical ventilation during APRV improves V A/Q matching in ARDS presumably by recruiting nonventilated lung units. Apparently, mechanical assistance of each inspiration during PSV is not sufficient to counteract the V A/Q maldistribution caused by alveolar collapse in patients with ARDS.

Adult↗
PubMed1998

Cardiopulmonary effects of aerosolized prostaglandin E1 and nitric oxide inhalation in patients with acute respiratory distress syndrome.

Ten patients with acute respiratory distress syndrome (ARDS) received in random order nitric oxide (NO) inhalation, aerosolized prostaglandin E1 (PGE1), infusion of PGE1, or no intervention. Inhalation of either aerosolized PGE1 (10 +/- 1 ng/kg/min) or NO (7 +/- 1 ppm) reduced pulmonary vascular resistance (PVR) from 158 +/- 14 to 95 +/- 11 dyn . s/cm5/m2 (NO) and 100 +/- 12 dyn . s/cm5/m2 (aerosolized PGE1), and improved PaO2 from 78 +/- 3 to 96 +/- 5 mm Hg (NO) and 95 +/- 4 mm Hg (aerosolized PGE1) (p < 0.05), venous admixture (Q VA/Q T) from 45 +/- 2 to 36 +/- 2% (NO), and 36 +/- 2% (aerosolized PGE1) (p < 0.05), oxygen delivery (DO2) from 711 +/- 34 to 762 +/- 45 ml/min/m2 (NO) and 780 +/- 46 ml/min/m2 (aerosolized PGE1) (p < 0.05), and right ventricular ejection fraction (RVEF) from 32 +/- 6 to 37 +/- 5% (NO), and 36 +/- 4% (aerosolized PGE1) (p < 0.05) at a constant cardiac index (CI). Although infusion of PGE1 (12 +/- 1 ng/kg/min) caused a similar reduction in PVR as aerosolized PGE1 and NO inhalation, it improved RVEF and increased CI but decreased Q VA/Q T and PaO2. These results suggest that in ARDS patients inhalation of aerosolized PGE1 or NO in low concentrations equally improves PVR and gas exchange by selective vasodilation in ventilated areas.

Administration, Inhalation↗
PubMed1995

Method of delivering constant nitric oxide concentrations during full and partial ventilatory support.

OBJECTIVE: The objective of our study was to evaluate the precision and safety of administering nitric oxide (NO) during full and partial ventilatory support. METHODS: NO was administered either using a microprocessor-controlled servo ventilator, substituting an NO-N2 mixture for the ventilator's usual air supply or by adding an NO-N2 mixture with a constant flow at the proximal end of the tracheal tube. NO, nitrogen dioxide (NO2), and nitrous and nitric acid (HNOx) was quantified selectively with a sequential, selective, hollow tube preconcentration and chemiluminescence analysis in a respiratory system model during various modes of full and partial ventilatory support. RESULTS: The servo valve system of the ventilator provided accurate NO concentrations during full and partial ventilatory support. Interaction of spontaneous and mechanical ventilation during partial ventilatory support resulted in irregular inspiratory flow patterns and a difference of 3.6% to 44.1% between the desired and measured inspiratory NO concentrations when NO was administered at a constant flow to the proximal end of the tracheal tube. NO2 was not detected. Small amounts of 0.6 to 0.8 ppm HNOx were detected when 80 ppm NO was administered in a humid gas mixture of 37 degrees C in the presence of 90% oxygen. CONCLUSIONS: NO can be administered accurately without formation of NO2 during full and partial ventilatory support with the electronically controlled valve system of the ventilator. Formation of HNOx is a potential problem at high NO and O2 concentrations in the presence of moisture.

Administration, Inhalation↗
PubMed1995

Improvement in VA/Q distributions during inhalation of nitric oxide in pigs with methacholine-induced bronchoconstriction.

Effects of nitric oxide (NO) and aerosolized terbutaline inhalation on ventilation-perfusion (VA/Q) distributions were determined during methacholine-induced bronchoconstriction in nine mechanically ventilated pigs. Animals inhaled, in random order, zero, 20, and 80 parts per million (ppm) of NO or aerosolized terbutaline. Inhalation of either 20 ppm NO or terbutaline produced similar reduction in pulmonary resistance and increase in lung compliance. Bronchodilation was most pronounced during inhalation of 80 ppm NO. NO inhalation increased PaO2 from 65 +/- 4 to 90 +/- 5 (20 ppm NO) and 104 +/- 6 mm Hg (80 ppm NO) (p < 0.05), and oxygen delivery (DO2) from 484 +/- 49 to 565 +/- 25 (20 ppm NO) and 619 +/- 43 ml/kg/min (80 ppm NO) (p < 0.05) compared with control. Aerosolized terbutaline did not increase PaO2 and DO2. NO inhalation accounted for a decrease in blood flow to shunt units (20 ppm NO: 14 +/- 1%, 80 ppm NO: 19 +/- 2%; p < 0.05) and an increase in the perfusion of normal VA/Q units (20 ppm NO: 12 +/- 1%, 80 ppm NO: 18 +/- 1%; p < 0.05). Perfusion of shunt and normal VA/Q units was similar in the absence of NO inhalation with and without aerosolized terbutaline. Pulmonary vascular resistance decreased from 510 +/- 55 to 332 +/- 22 dyn.s/cm5 with 20 ppm NO (p < 0.05) and to 329 +/- 41 dyn.s/cm5 with 80 ppm NO (p < 0.05) but did not change with terbutaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗