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Biomedical subjects

M Booke

Publications and source records attributed to M Booke.

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

Noradrenaline and nomega-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep.

This prospective, non-randomized, controlled experimental study looks at the effects of N(omega)-monomethyl-L-arginine (L-NMMA) on haemodynamics, oxygen transport and regional blood flow in healthy and septic sheep, and compares these effects with those of noradrenaline (NA; norepinephrine). All sheep were chronically instrumented. Six sheep received L-NMMA (7 mg.kg(-1).h(-1)), six sheep received NA, and seven sheep received the carrier alone (0.9% NaCl). The NA dosage was continuously and individually adjusted to achieve the same increase in blood pressure as observed in matched sheep of the L-NMMA group (non-septic phase). Treatment was discontinued after 3 h. Sepsis was initiated and maintained by a continuous infusion of live Pseudomonas aeruginosa. After 24 h of sepsis, the sheep were again challenged over a treatment period of 3 h with their previously assigned drug (septic phase). During the non-septic phase of the experiment, NA and L-NMMA both caused an increase in mean arterial pressure (MAP) through vasoconstriction. Ater 24 h of sepsis, all sheep developed a hyperdynamic circulatory state. While L-NMMA caused an increase in MAP through intense vasoconstriction, NA caused MAP to increase through a further elevation of the cardiac index. The NA dosage needed was significantly higher in the septic phase compared with the non-septic phase, reflecting a reduced vascular responsiveness to catecholamines during sepsis. Renal blood flow remained unchanged during either treatment in both the non-septic and the septic phases. Nevertheless, urine output increased during NA treatment in both the non-septic and the septic phases, while L-NMMA caused urine output to increase only under septic conditions.

Animals↗
PubMed1999

[Oxygen delivery in sepsis. After 10 years more questions than answers].

Object of this review is to present the physiological principles, diagnostic techniques and therapeutic options that are related to modifications of oxygen delivery in sepsis. Despite intense research activities in this area, many topics regarding oxygen transport and oxygen consumption in sepsis are still not clear. For example, the often discussed shift of the critical value of oxygen delivery to higher values in sepsis has not been proven, yet. Beside an impaired regional perfusion also disturbances in the cellular oxygen utilization may be responsible for organ failure in sepsis. Until now, it was not shown, whether the increase of oxygen delivery to supranormal levels reduces mortality in septic patients. It is also unknown, which catecholamine and which infusion solution is suitable for the treatment of septic patients. In future further research is necessary to solve the problems associated with sepsis therapy.

Fluid Therapy↗
PubMed1999

[Venous paradoxical air embolism].

Paradoxical air embolism may occur with any venous air embolism. Air may either enter the systemic circulation through a patent foramen ovale or through transpulmonary passage of air. While small venous air emboli are mostly well tolerated, even the smallest paradoxical air emboli can have fatal consequences in the systemic circulation. Therapy and prophylaxis of paradoxical air embolism equal those of venous air embolism. This is especially true, since paradoxical air embolism may not become obvious under general anesthesia. More specific therapeutic regiments, such as hyperbaric oxygenation and the infusion of perfluorocarbons, are still in an experimental stage.

Embolism, Air↗
PubMed1999

Inhaled vasodilator therapy for treatment of acute lung injury.

In randomized controlled trials, inhaled nitric oxide failed to provide significant clinical benefit in patients with acute lung injury. Despite temporary improvement in oxygenation, inhaled nitric oxide neither improved survival, nor decreased length of mechanical ventilation. Thus, with the exception of severe hypoxaemia refractory to conventional therapy, inhaled nitric oxide is not indicated in patients with acute lung injury. Inhalation of prostacyclin and prostaglandin E1, respectively, has been associated with an improvement in oxygenation and a decrease in pulmonary artery pressure. Prospective randomized trials are warranted to assess the impact of inhaled prostaglandins on the outcome of patients with acute lung injury.

Journal Article↗
PubMed1999

Selective inhibition of inducible nitric oxide synthase: effects on hemodynamics and regional blood flow in healthy and septic sheep.

OBJECTIVES: To investigate the effects of S-ethylisothiourea (S-EITU) on hemodynamics, oxygen transport, and regional blood flow in healthy and septic sheep. DESIGN: Prospective, randomized, controlled experimental study with repeated measures. SETTING: Investigational intensive care unit at a university medical center. SUBJECTS: Eleven healthy, female adult sheep of the Merino breed, divided into a control group (n = 5) and into a group treated with S-EITU (n = 6). INTERVENTIONS: All sheep were chronically instrumented. After a 5-day recovery period, they were randomly assigned to either control or S-EITU groups. While control sheep received only saline, S-EITU was administered in increasing doses of 1, 3, and 9 mg/kg/hr over 1 hr each (nonseptic phase). After 2 days of recovery, a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) was started in all sheep and maintained for the remainder of the experiment. After 24 hrs of sepsis, the sheep again received their assigned treatment (septic phase). In both the nonseptic and septic phases, the sheep received colored microspheres through a left atrial catheter to allow analysis of regional blood flows. All animals were autopsied at the end of the experiments, and organ probes were removed for blood flow analyses. MEASUREMENTS AND MAIN RESULTS: The administration of S-EITU caused a dose-dependent vasoconstriction in the nonseptic phase. After 24 hrs of Pseudomonas infusion, all sheep developed a hyperdynamic circulatory state, with increased cardiac indices and reduced arterial pressures and systemic vascular resistances. Oxygen extraction decreased significantly, preventing an increase in oxygen consumption, despite an increased oxygen delivery. The hyperdynamic circulation was dose dependently reversed by S-EITU, causing an increase in arterial pressure by peripheral vasoconstriction. Sheep in the control group showed a continuation of the hyperdynamic circulation. The effects of S-EITU on hemodynamics and regional blood flows were comparable under septic and nonseptic conditions. CONCLUSIONS: With the inducible form of nitric oxide synthase expressed under septic, but not under nonseptic conditions, S-EITU was expected to have vasoconstrictive properties only in the septic phase. It produced a comparable vasoconstriction during the nonseptic phase of the experiment. Thus, either S-EITU does not selectively block the inducible nitric oxide synthase in sheep, or other vasodilators besides nitric oxide play an important role in septic vasodilation.

Animals↗
PubMed1999

Role of nitric oxide in sepsis-associated pulmonary edema.

Transient pulmonary hypertension after inhibition of nitric oxide synthase (NOS) does not alter pulmonary reflection coefficients or lymph flows in endotoxemic sheep. To test the effects of persistent pulmonary hypertension induced by N omega-nitro-L-arginine methylester (L-NAME) and of inhaled NO on pulmonary edema, 18 sheep (three groups) were chronically instrumented with pulmonary artery catheters, femoral arterial fiberoptic thermistor catheters, and tracheostomy. The awake, spontaneously breathing animals received Salmonella typhi endotoxin (lipopolysaccharide; LPS) (10 ng/kg/ min) for 28 h. After 24 h, an airflow of 6 L/min was delivered through the tracheostomy. One group of animals (L-NAME/air) received L-NAME intravenously (25 mg/kg + 5 mg/kg/h) and breathed air. The second group (L-NAME/NO) was given L-NAME and NO (40 ppm) was added to the airflow. The third group was given NaCl 0.9% and breathed air (NaCl/air). Extravascular lung water was measured through the double-indicator dilution technique. Endotoxemia caused pulmonary edema, which was aggravated by L-NAME. Breathing of NO normalized pulmonary artery pressure (Ppa) and ameliorated pulmonary edema. Inhalation of NO may therefore be a therapeutic option for pulmonary edema associated with pulmonary hypertension.

Administration, Inhalation↗
PubMed1999

The hemodynamic effects of cell-free hemoglobin during general and epidural anesthesia.

UNLABELLED: Although hemoglobin-based oxygen carriers (HBOC) are now being investigated, the effects of HBOC solutions during regional anesthesia have never been analyzed. Therefore, we investigated the hemodynamic changes after HBOC infusion during general anesthesia and thoracic epidural anesthesia. Sheep were assigned to three different groups: a) a control group with six unanesthetized sheep; b) six sheep with a halothane anesthesia (2.0 vol.% in oxygen); and c) six awake sheep with a thoracic epidural anesthesia with bupivacaine. After a period of stabilization, all 18 animals received 100 mg/kg of the HBOC pyridoxalated hemoglobin polyoxyethylene conjugate. The infusion of the HBOC caused a significant increase in mean arterial pressure and pulmonary artery pressure in both the control and epidural anesthesia groups. Anesthesia with halothane reduced the effects of the HBOC-solution on mean arterial pressure but did not abolish the increase in pulmonary artery pressure. Our results demonstrate that vasoconstriction caused by HBOC solutions is not abolished by epidural anesthesia, but halothane anesthesia may alter the hemodynamic effects of HBOC solutions. IMPLICATIONS: We evaluated the effects of epidural anesthesia and halothane anesthesia on the vasoconstrictive properties of a cell-free hemoglobin solution. The vasoconstriction caused by a cell-free hemoglobin solution was similar in unanesthetized sheep and sheep with thoracic epidural anesthesia and was reduced in sheep with halothane anesthesia.

Anesthesia, Epidural↗
PubMed1998

Arterio-venous carboxyhemoglobin difference suggests carbon monoxide production by human lungs.

Carbon monoxide is hypothesized to be produced by the enzyme heme oxygenase predominantly in liver and spleen, bound to hemoglobin, and excreted by the lungs. Thus, venous carboxyhemoglobin is expected to be higher or equal to arterial carboxyhemoglobin. Unspecific inflammatory stimuli have been shown to induce heme oxygenase in lung tissue possibly leading to pulmonary carbon monoxide production. Arterial and central venous carboxyhemoglobin levels were measured in critically ill patients on the third day of ICU stay (n = 59) as well as in otherwise healthy humans prior to orthopedic surgery (n = 29). Arterial and central venous carboxyhemoglobin were higher in ICU patients than in healthy humans, respectively. In both groups, arterial carboxyhemoglobin was significantly higher than central venous carboxyhemoglobin. The arteriovenous carboxyhemoglobin differences were similar in both groups. The data suggest (a) increased CO-generation in critical illness and (b) pulmonary CO-production in healthy and critically ill humans.

Arteries↗
PubMed1998

Comparison of the haemodynamic effects of nitric oxide synthase inhibition and nitric oxide scavenging in endotoxaemic sheep.

OBJECTIVE: The present study compared the effects of nitric oxide (NO) synthase inhibition and NO scavenging with haemoglobin in endotoxaemic sheep. DESIGN: 12 sheep were instrumented for chronic study. Six sheep received LG-nitro-arginine-methylester (L-NAME, 2.5 mg/kg bolus followed by a continuous infusion of 0.5 mg/kg per h), the other 6 sheep received pyridoxalated haemoglobin polyoxyethylene conjugate (PHP, 100 mg/kg bolus followed by a continuous infusion of 20 mg/kg per h). MEASUREMENTS AND RESULTS: Haemodynamic and oxygenation parameters were measured in healthy sheep, after infusion of Salmonella typhosa endotoxin (10 ng/kg per min) for 24 h and after infusion of L-NAME or PHP. The infusion of endotoxin resulted in a hypotensive, hyperdynamic circulation. Infusion of L-NAME increased mean arterial pressure (MAP) from 76.1 +/- 4.2 mmHg to normal values of 95.8 +/- 5.7 mmHg (p < 0.05). PHP increased MAP from 73.0 +/- 3.0 to 88.6 +/- 4.7 mmHg (p < 0.05). This increase in MAP was associated in the L-NAME group with a more prominent drop in cardiac index (from 10.2 +/- 0.4 to 7.0 +/- 0.51.min-1.m-2; p < 0.05) than in the PHP group (from 10.7 +/- 0.2 to 9.3 +/- 0.61.min-1.m-2). During the first 90 min of infusion, cardiac index remained lower in the L-NAME group than in the PHP group. The increase in pulmonary vascular resistance was also higher in the L-NAME group. CONCLUSION: These results suggest, that at the doses used in the experiment, NO scavenging with PHP has smaller effects on cardiac index and pulmonary vascular resistance than NO synthase inhibition with L-NAME. Therefore, the concept of NO scavenging in hyperdynamic sepsis should be further evaluated.

Animals↗
PubMed1998

Thoracic epidural anesthesia does not affect functional recovery from myocardial stunning in sevoflurane-anesthetized dogs.

OBJECTIVE: A beneficial effect of thoracic epidural anesthesia (TEA) on recovery from myocardial stunning was previously shown in awake dogs. The aim of this study was to investigate the effects of TEA on recovery from myocardial stunning in sevoflurane-anesthetized dogs. DESIGN: Randomized animal study. SETTING: Animal laboratory of a university hospital. PARTICIPANTS: Chronically instrumented mongrel dogs. INTERVENTIONS: Six dogs were chronically instrumented for measurement of hemodynamics and myocardial wall thickening fraction (WTF). The following experiments were performed on separate days in a crossover fashion: (1) 10 minutes of ischemia of the left anterior descending (LAD) coronary artery during sevoflurane anesthesia without TEA and (2) 10 minutes of ischemia during sevoflurane anesthesia with TEA. MEASUREMENTS AND MAIN RESULTS: WTF was measured awake (baseline) and at predetermined time points until complete recovery of myocardial function occurred. Induction of anesthesia led to a decrease of WTF compared with baseline. Induction of ischemia led to a further decrease of WTF to negative values, which returned to positive values within the first minute of reperfusion. There were no differences between the two experimental conditions at any of the time points measured. In awake dogs, TEA improved the recovery from myocardial stunning compared with the control experiment. There was no difference between conscious dogs with TEA or sevoflurane-anesthetized dogs with or without TEA. CONCLUSION: TEA has no additional protective effect on the recovery of WTF during sevoflurane anesthesia.

Anesthesia, Epidural↗
PubMed1998

Inhaled prostaglandin E1 for treatment of acute lung injury in severe multiple organ failure.

UNLABELLED: Acute lung injury is characterized by hypoxemia due to pulmonary ventilation/perfusion-mismatching. I.v. administered prostaglandin E1 (PGE1), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and prostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. In the present study, PGE1 inhalation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as PaO2/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE1 inhalation in addition to standard intensive care. The drug was continuously delivered via a pneumatic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE1 was administered for 103 +/- 17 h at a dose of 41 +/- 2 microg/h. The PaO2/FIO2 ratio increased from 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE1 inhalation decreases in mean pulmonary artery pressure and central venous pressure were not statistically significant. Mean arterial pressure, pulmonary capillary wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that inhaled PGE1 is an effective therapeutic option for improving oxygenation in patients with acute lung injury. Whether inhaled PGE1 will increase survival in acute lung injury should be investigated in a controlled prospective trial. IMPLICATIONS: In patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E1 improved oxygenation and decreased venous admixture without affecting systemic hemodynamic variables. Controlled clinical trials are warranted.

APACHE↗