Heterogeneity of human albumin preparations.
Explore the source record for details and available documents.
Albumins↗
Biomedical subjects
M Heesen
Publications and source records attributed to M Heesen.
Cloning and chromosomal mapping of an orphan chemokine receptor: mouse RDC1.
Degenerate RT-PCR was used to identify a new seven-transmembrane-spanning receptor expressed in astrocytes. A receptor, termed RDC1, displaying the characteristic structural features of a chemokine receptor was cloned. The predicted 362-amino-acid sequence displayed 92% and 91% similarity to the human and dog orphan receptor RDC1, respectively. In addition, RDC1 shares 43% amino acid similarity to rabbit and mouse CXCR2. Transcripts of RDC1 were found in astrocytes, heart, kidney, the mesangial tumor line MES-13, spleen, and neutrophils by means of northern blot. Using linkage analysis of interspecies backcross mice, we localized to chromosome 1 the genes for mouse CXCR2, CXCR4, and RDC1. Mouse RDC1 is linked to and lies between the genes for the mouse CXC chemokine receptors CXCR2 and CXCR4. The combined data of chromosomal location and sequence similarity suggest that RDC1 is an orphan CXC chemokine receptor.
Amino Acid Sequence↗
Somatosensory evoked potential monitoring during positioning of the patient for posterior fossa surgery in the semisitting position.
OBJECTIVE: Midcervical flexion myelopathy is a rare but well-known complication of posterior fossa surgery. To reduce the risk, we routinely used somatosensory evoked potential (SSEP) monitoring during positioning of the patient. METHODS: Fifty-five consecutive patients were operated on for posterior fossa lesions in the semisitting position via a median (5 patients) or a lateral (50 patients) suboccipital approach. During positioning, monitoring of SSEPs by stimulation of the tibial nerve (T-SSEP) as well as by stimulation of the median nerve (M-SSEP) was established. In the case of pronounced SSEP changes, the head was repositioned. Surgery was started after SSEP recordings were unchanged as compared to the baseline investigation. RESULTS: Effective monitoring was possible in all cases. Whereas M-SSEP recordings showed no changes while placing patients in the sitting position, T-SSEP recordings were altered in 14 cases (25%). In cases using the midline approach, SSEP changes were never so pronounced to require repositioning of the head. Head flexion and rotation resulted in significant changes of T-SSEP recordings in eight patients (14.5%), requiring repositioning. In two cases, an amplitude loss was noted. In only two of these eight patients were M-SSEP recordings markedly changed. SSEP recordings after repositioning disclosed recovery of spinal cord function. In no patient were clinical signs of myelopathy observed postoperatively. CONCLUSION: We observed a high incidence of pronounced changes of T-SSEP recordings when the patient's head was flexed and rotated for lateral suboccipital craniotomy in the semisitting position. Despite the low specificity monitoring of T-SSEPs during positioning of the patient for posterior fossa surgery, the semisitting position is strongly recommended.
Adolescent↗
Use of murine CXCR-4 as a second receptor by some T-cell-tropic human immunodeficiency viruses.
The human CXCR-4 molecule serves as a second receptor for primary, T-cell-tropic, and laboratory-adapted human immunodeficiency virus type 1 (HIV-1) isolates. Here we show that murine CXCR-4 can support the entry of some of these HIV-1 isolates. Differences between mouse and human CXCR-4 in the ability to function as an HIV-1 receptor are determined by sequences in the second extracellular loop of the CXCR-4 protein.
Animals↗
Murine astrocytes express a functional chemokine receptor.
Elevated levels of chemokines have been observed in various diseases of the CNS. Little is known, however, about how these chemokines affect parenchymal cells of the CNS. The current studies examine astrocyte chemotaxis to the mouse chemokine macrophage inflammatory protein-1alpha (MIP-1alpha). Murine astrocytes demonstrate directed migration along a chemical gradient in response to 10(-10)-10(-8) M MIP-1alpha. Peak chemotactic responses are noted at 10(-9) M. MIP-1alpha-induced astrocyte migration is specifically inhibitable with pertussis toxin, suggesting a role for Galphai proteins in the signaling process. RT-PCR and in situ hybridization were used to identify expression of the murine CCR1 MIP-1alpha receptor on astrocytes. Astrocytes contain mRNA for CCR1, but messages for CCR4 and the orphan chemokine receptor MIP-1alphaR-like#1 were not detected. The combined results suggest that a functional chemokine receptor is expressed on resident cells of the CNS. We speculate that the interactions of chemokines with astrocytes are involved in inflammatory reactions of the CNS.
Animals↗
Functional expression of the CXC-chemokine receptor-4/fusin on mouse microglial cells and astrocytes.
The mRNA for the seven-transmembrane-spanning G protein-coupled receptor fusin/CXCR-4 is expressed in primary mouse astrocyte cultures and the transformed mouse microglial cell line, N9. Cell surface expression of fusin in these cells was confirmed by staining with a polyclonal anti-fusin Ab. The functional capacity of this chemokine receptor was examined by evaluating the calcium responses following stimulation of glial cells with the CXC-chemokine, stromal-derived cell factor-1alpha (SDF-1alpha). Both astrocytes and microglial cells mobilized calcium following stimulation with chemically synthesized SDF-1alpha. SDF-1alpha- and carbachol-mediated calcium responses of astrocytes were partially inhibited by treatment with pertussis toxin (PTx), suggesting receptor coupling to a combination of G alpha(i) and other G proteins. In contrast, the calcium responses of microglial cells to SDF-1alpha were completely PTx sensitive, while responses to carbachol stimulation were PTx resistant. The ability of SDF-1alpha to induce glial cell migration was also examined. Synthetic SDF-1alpha was a potent chemoattractant for mouse microglial cells at ligand concentrations of 10 to 500 ng/ml; peak responses were noted at 100 ng/ml. In contrast, astrocytes did not migrate toward a gradient of SDF-1alpha. The failure of SDF-1alpha to induce astrocyte migration was specific, as another chemokine, macrophage inflammatory protein-1alpha, triggered astrocyte chemotaxis.
Animals↗
Alternate splicing of mouse fusin/CXC chemokine receptor-4: stromal cell-derived factor-1alpha is a ligand for both CXC chemokine receptor-4 isoforms.
Inspection of the intron splice junction of the mouse chemokine receptor fusin/CXC chemokine receptor R-4 (CXCR-4) revealed a potential in-frame alternative splice site in the region encoding the N-terminal ectodomain of the receptor. Both predicted splice products were detected by reverse transcriptase-PCR. Cell lines of T lymphocyte, B lymphocyte, and macrophage lineage, plus populations of elicited peritoneal exudate cells, thymocytes, and astrocytes coexpressed mRNA for both isoforms. The full length cDNA of the shorter alternate splice product, termed CXCR-4B, was cloned from peritoneal exudate cell RNA. Chinese hamster ovary cells transfected with either isoform, CXCR-4A or CXCR-4B, responded to stromal cell-derived factor-1alpha with a rise in intracellular calcium. Both alternate splice products are therefore functional stromal cell-derived factor-1 alpha receptors.
Alternative Splicing↗
What the neurosurgeon needs to know about the coagulation system.
Intracranial surgery is often complicated by thromboembolic events including the life-threatening pulmonary embolism. After head trauma and in patients with brain tumors disseminated intravascular coagulation (DIC) can occur, characterized by the triggering of the coagulation cascade and the depletion of coagulation factors which ultimately leads to bleeding. The identification of patients at high risk as well as the early diagnosis of hemostatic problems uses routine laboratory parameters such as partial thromboplastin time and prothrombin time reflecting the intrinsic and the extrinsic pathway of the coagulation respectively. Thrombin antithrombin III complexes (TAT) and prothrombin fragment 1 + 2 (F1 + 2) are further indicators of an activation of the coagulation whereas fibrinogen degradation products (FDP) refer to the fibrinolytic system. The basic principles of coagulation and fibrinolysis are summarized as well as the changes of laboratory parameters accompanying DIC, hypercoagulability and hyperfibrinolysis.
Blood Coagulation↗
Coagulation alterations in patients undergoing elective craniotomy.
BACKGROUND: Thromboembolism remains a major problem in patients scheduled for craniotomy. The present study examined parameters of coagulation and fibrinolysis in 15 patients undergoing elective craniotomy in the perioperative period. METHODS: Plasma concentrations of thrombin antithrombin III complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), and d-dimer were measured before and after induction of anesthesia, 60 minutes and 180 minutes after the beginning of surgery, and on the first postoperative morning. RESULTS: TAT, a marker of activation of coagulation, increased significantly (p < 0.05) from the preoperative measurements to the data obtained 60 minutes after beginning the surgery, reaching a maximum of 180 minutes after the start of surgery. F1 + 2, also indicating activation, showed a similar concentration time course with an intraoperative maximum. D-dimer, a marker of fibrinolysis, tended to increase slightly beginning 180 minutes after surgery with a maximum on the morning after surgery. Statistical significance for F1 + 2 and d-dimer was not found. CONCLUSIONS: This study showed a transient activation of coagulation with an intraoperative maximum in patients undergoing craniotomy. This result could be due to a liberation of thromboplastin from brain tissue.
Adult↗
Does age influence circulating adhesion molecules in the critically ill?
OBJECTIVE: Soluble adhesion molecules are regarded to be markers of inflammation, endothelial activation, or damage. The influence of age on plasma concentrations of circulating adhesion molecules should be serially studied in critically ill intensive care patients. DESIGN: Prospective and descriptive study over 5 days. SETTING: Clinical investigation in a surgical intensive care unit of a university hospital. PATIENTS: Thirty critically ill patients (Acute Physiology and Chronic Health Evaluation [APACHE] II score of > 15 points), with sepsis secondary to postoperative complications, were included in this study. Fifteen consecutive patients aged < 50 yrs and 15 consecutive patients aged > 70 yrs were prospectively studied. INTERVENTIONS: All patients were treated by the standard protocols of our intensive care unit, which did not differ between the groups. The patients received continuous analgesia-sedation and mechanical ventilation. Intensivists caring for the patients were not involved in the study and were blinded to data analysis. MEASUREMENTS AND MAIN RESULTS: Hemodynamic parameters were extensively monitored in all patients. From arterial blood samples, plasma concentrations of soluble adhesion molecules (endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, granule membrane protein-140) were measured on the day of admission (i.e., baseline values) and during the following 5 days. Three of the younger patients and six of the elderly patients died during the study period (p < .05). Oxygen delivery and consumption, and the other hemodynamic data, were without group differences throughout the study. Plasma concentrations of all adhesion molecules were beyond normal at baseline in both groups. These concentrations increased further during the first 2 to 3 days in both groups, with a significantly higher increase in the elderly patients (endothelial leukocyte adhesion molecule-1 to 179 +/- 32 ng/mL; intercellular adhesion molecule-1 to 1695 +/- 158 ng/mL; vascular cell adhesion molecule-1 to 1395 +/- 212 ng/mL; and granule membrane protein-140 to 888 +/- 119 ng/mL). In the younger patients, concentrations of soluble adhesion molecules decreased later in the study and almost reached baseline values on day 5. In the elderly patients, these concentrations remained significantly higher until the end of the study. CONCLUSIONS: The higher plasma concentrations of the measured adhesion molecules in elderly critically ill patients indicate that elderly patients are more prone than younger patients to a more pronounced activation or even damage of the endothelium. Further work needs to be done to determine the prognostic importance and to define the role of soluble adhesion molecules, particularly in the elderly critically ill patient.
Adult↗
Cloning of the mouse fusin gene, homologue to a human HIV-1 co-factor.
Previous studies have demonstrated that mouse cells do not become infected with HIV-1 despite transfection with human CD4. Recently, a human protein termed "fusin" with characteristics of a seven-transmembrane-spanning receptor was found to be a co-factor required for the entry and fusion of HIV-1 with human CD4-bearing lymphocytes. Thus, cloning of the murine homologue of the human fusin (also termed CXCR-4) gene could provide an important comparative tool for identification of the structures crucial for fusin function. Using degenerate PCR, the mouse homologue of human fusin was cloned from a peritoneal exudate cell cDNA library. The predicted amino acid sequence is 91% identical to human fusin. Twenty-eight of the 37 amino acid differences between mouse and human fusin are located in the ectodomains, suggesting that the intracytoplasmic components that mediate G protein binding and signaling are highly conserved. Northern blot analysis showed a message of 2.2 kb in thymus, spleen, neutrophils, and primary astrocyte cultures. Lymphoid and monocyte cell lines also expressed message for fusin. The coding regions of most chemokine receptors lack introns. In contrast, cloning of genomic DNA for mouse fusin revealed the presence of a 2.3-Kb intron separating the first seven amino acids from the remaining 352 residues. Therefore, the mouse fusin gene has a unique genomic organization compared with other chemokine receptors.
Amino Acid Sequence↗
Mouse astrocytes respond to the chemokines MCP-1 and KC, but reverse transcriptase-polymerase chain reaction does not detect mRNA for the KC or new MCP-1 receptor.
Previous studies demonstrated the involvement of astrocytes in the development of astrogliosis, a condition in which these cells undergo proliferation and hypertrophy. To examine whether astrocytes could migrate into lesions, we tested the influence of the murine chemokines MCP-1, KC, TCA3, and MIP-1 beta on migration of cultured neonatal mouse astrocytes. Subnanomolar concentrations of MCP-1 and KC were active chemoattractants indicating that these molecules were effective at physiologic concentrations. Specificity of MCP-1 was demonstrated by antibody inhibition and by the finding that the chemokine MIP-1 beta failed to induce astrocyte migration. The migratory responses were sensitive to pertussis toxin; this finding is consistent with involvement of G protein-coupled receptors. To examine the receptors for these chemokines further, we cloned the mouse homolog of the human MCP-1 receptor from a mouse peritoneal exudate cell cDNA library. The gene had 78% nucleotide sequence homology with the human MCP-1 receptor (the nucleotide sequence of clone 1 encoding the mouse MCP-1 receptor can be obtained from the GenBank database, accession number U56819). However, reverse transcriptase-polymerase chain reaction (RT-PCR) failed to detect message for either the MCP-1 or KC receptors in astrocytes. The combined data suggest that mouse astrocytes use novel receptors to recognize these chemokines.
Animals↗
Increase of interleukin-6 plasma levels after elective craniotomy: influence of interleukin-10 and catecholamines.
Accidental and operative trauma are able to induce a systemic reaction of the organism characterized by fever, leukocytosis, catabolism, and an activation of the coagulation system. Interleukin-6 (IL-6) has been found to be an important mediator of this acute-phase response. In this study the influence of elective craniotomy on IL-6 plasma levels was evaluated. Blood samples were obtained from 20 patients undergoing elective craniotomy for vascular or tumorous diseases of the brain. IL-6 increased significantly (p < 0.05) from the pre-operative (0(0-5.4) pg/ml) to the intraoperative (180 min after beginning of surgery) time-point (10.6 (0-18.5) pg/ml). The maximum was reached on the first postoperative morning (13.9(4.3-45.0) pg/ml). Interleukin-10 (IL-10) is an anti-inflammatory cytokine which suppresses IL-6 synthesis in vitro in various cell lines. IL-10 plasma concentrations showed no alterations throughout the study period. Epinephrine plasma concentrations increased significantly from pre-operative values (15 (0-74) pg/ml) to the postoperative time-point (57(9-459) pg/ml). A 4.5-fold increase (p < 0.05) of norepinephrine plasma concentrations was found when comparing the data obtained 60 min after beginning of surgery with the data of the first postoperative morning. In monocytes, which are a major source of plasma IL-6, an elevation of intracellular cAMP stimulates the IL-6 synthesis. The postoperative maximum of IL-6 in plasma could be due to a release of catecholamines. In conclusion this study demonstrated an elevation of IL-6 plasma concentrations during and after elective craniotomy. Increased plasma catecholamine concentrations as well as a damage in the blood-brain barrier due to the surgical trauma with a spill-over of IL-6 from brain tissue into plasma could have contributed to this result.
Acute-Phase Reaction↗
Influence of different volume therapies on platelet function in the critically ill.
OBJECTIVE: Both albumin and synthetic colloids such as hydroxyethyl starch (HES) solution are used to optimize hemodynamics in the critically ill. The influence of different long-term infusion regimes on platelet function was studied. DESIGN: Prospective, randomized study. SETTING: Clinical investigation on a university hospital surgical intensive care unit. PATIENTS: Twenty-eight consecutive trauma patients (injury severity score > 15 points) and 28 consecutive nontraumatized surgical patients with sepsis. INTERVENTIONS: The patients received either 20% human albumin (HA trauma, n = 14; HA sepsis, n = 14) or 10% low-molecular-weight HES solution HES 200/0.5 (HES trauma, n = 14; HES sepsis; n = 14) for 5 days to maintain central venous pressure and/or pulmonary capillary wedge pressure between 12 and 16 mmHg. MEASUREMENTS AND RESULTS: Platelet function was assessed by aggregometry (= turbidimetric technique) using adenosine diphosphate 2.0 mumol/l, collagen 4 microliters/ml, and epinephrine 25 mumol/l as inductors. Arterial blood was sampled on the day of admission or the day of diagnosis of sepsis (= baseline value) and over the next 5 days. Standard coagulation parameters (antithrombin III, fibrinogen, partial thromboplastin time) were also measured. Total use of HES by the 5th day totalled 4870 +/- 990 ml in the trauma and 3260 +/- 790 ml in the sepsis patients (HA trauma: 1850 +/- 380 ml; HA sepsis: 1790 +/- 400 ml). Maximum platelet aggregation decreased significantly during the first 2-3 days after baseline in all groups. At the end of the investigation period, platelet aggregation variables had recovered and reached (or even exceeded) baseline values. Within the entire investigation period, the course of platelet aggregation variables did not differ significantly between HA and HES-treated patients irrespective of whether they were trauma or sepsis patients. CONCLUSIONS: Alterations in hemostasis may occur for several reasons in the critically ill. Human albumin is the preferred first-line volume therapy in patients at risk for coagulation disorders. With respect to platelet function, volume replacement with (lower-priced) low-molecular-weight HES solutions can be recommended in this situation without any risk.
Adult↗
The effects of pentoxifylline on circulating adhesion molecules in critically ill patients with acute renal failure treated by continuous veno-venous hemofiltration.
OBJECTIVE: Circulating adhesion molecules appear to be excellent markers of endothelial activation in critically ill patients. Pentoxifylline (PTX) may limit sequelae of inflammation and subsequent endothelial activation by various mechanisms. The influence of PTX on the plasma levels of soluble adhesion molecules in critically ill patients undergoing continuous veno-venous hemofiltration (CVVH) was studied. DESIGN: Prospective, randomized, blinded study. SETTING: Clinical investigation in the surgical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: Fourteen consecutive patients suffering from acute renal failure (ARF) with postoperative complications who received continuous pentoxifylline (CVVH-PTX) i.v. were compared with 14 patients with ARF who did not receive PTX (CVVH control group). INTERVENTIONS: Pump-driven CVVH was carried out with a blood flow ranging from 120 to 150 ml/min. All patients received fentanyl and midazolam continuously and were on mechanical ventilation. PTX (300 mg) was given as a loading dose, followed by continuous infusion of 1.2 mg/kg per h for the next 5 days. MEASUREMENTS AND RESULTS: From arterial blood samples, plasma levels of soluble adhesion molecules (endothelial leukocyte adhesion molecules [sELAM-1], and intercellular adhesion molecule-1 [sICAM-1], vascular cell adhesion molecule-1 [sVCAM-1], and P-selectin granule membrane protein [sGMP-140] were measured using enzyme-linked immuno-sorbent assays (ELISA). Measurements were carried out before the start of CVVH to establish baseline values and continued during the next 5 days. MAIN RESULTS: Eleven of the CVVH-PTX patients and 8 of the CVVH control patients survived during the investigation period. In the CVVH-PTX patients 2.4 +/- 0.3 g/day of PTX was given. At baseline, plasma levels of sELAM-1, sICAM-1, and sVCAM-1 were markedly higher than normal in both groups. In the CVVH control patients, all measured soluble adhesion molecules increased further during the study period (sELAM-1 from 90 +/- 22 to 134 +/- 30 ng/ml; sICAM-1 from 958 +/- 173 to 1460 +/- 209 ng/ml; sVCAM-1 from 1100 +/- 188 to 1804 ng/ml; sGM-140 from 499 +/- 102 to 688 +/- 121 ng/ml) (p < 0.05), whereas in the PTX-treated CVVH patients, plasma levels of all soluble adhesion molecules remained almost unchanged. The PaO2/FIO2 increased in the PTX-treated patients (from 209 +/- 67 to 282 +/- 58 mmHg) and remained almost unchanged in the CVVH control patients. CONCLUSION: Leukocyte/endothelial interactions play an important role in the inflammatory process. Circulating adhesion molecules may serve as markers of the extent of inflammation. Continuous i.v. administration of PTX was successful in blunting the increase of soluble adhesion molecules in critically ill patients undergoing CVVH. Whether these effects result from improved circulation at the microcirculatory level or from (direct or indirect) beneficial effects on endothelial cells warrants further controlled studies.
Acute Kidney Injury↗
Does long-term continuous administration of pentoxifylline affect platelet function in the critically ill patient?
OBJECTIVE: The methylxanthine derivative pentoxifylline (PTX) is one of those promising substances which are under current investigation to modify or limit inflammatory response. Anti-aggregation activity has also been described that may contribute to the beneficial effects of this substance. Long-term effects on platelet function have not been elucidated yet. DESIGN: Prospective, randomized study. SETTING: Clinical investigation on a surgical intensive care unit of a university hospital. PATIENTS: 26 trauma patients and 26 patients suffering from sepsis secondary to major operations were consecutively studied. INTERVENTIONS: The patients prospectively received either 1.5 mg/kg per h pentoxifylline continuously for 5 days (after a loading dose of 600 mg) (trauma-PTX, n = 13; sepsis-PTX, n = 13) or saline solution as placebo (trauma-control; n = 13; sepsis-control, n = 13). MEASUREMENTS: On the day of admission (trauma patients) or day of the diagnosis of sepsis and at 12:00 p.m. during the next 5 days, platelet aggregation induced by adenosine diphosphate (ADP 2.0 mumol/l), collagen (4 microliters/ml), and epinephrine (25 mumol/l) was determined by a turbidimetric method from arterial blood samples. Standard coagulation screen was also monitored. MAIN RESULTS: In untreated trauma and sepsis patients, maximum platelet aggregation induced by all three agonists decreased during the first few days after inclusion in the study [trauma: ADP - 17.1 +/- 8.0 rel% (% change from baseline); sepsis: ADP -26.1 +/- 5.6 rel%]. In due course, maximum platelet aggregation recovered, reaching the baseline value or even exceeding it (trauma patients). In the PTX-treated patients, platelet aggregation was significantly less impaired (sepsis group: ADP -4.4 +/- 3.3 rel%) or even increased beyond baseline values in the first few days of the study (trauma group: ADP 16.1 +/- 8.0 rel%). Fibrinogen plasma levels were lower in the non-treated control groups (p < 0.05) than in the PTX groups. CONCLUSIONS: Continuous infusion of PTX for 5 days did not impair platelet function in critically ill patients. In both trauma and sepsis patients, the usual deterioration in platelet function was even attenuated, which may be due to the effects of PTX on cytokine release (e.g., reduction in tumor necrosis factor and interleukin-1), improvement in microcirculation, or additional fibrinolytic effects.
Adult↗
[The in vitro effect of alpha-2 agonists on thrombocyte function and density of thrombocyte alpha-2 receptors].
UNLABELLED: alpha 2-Agonists are being used increasingly in anaesthesia and intensive care medicine because of their antihypertensive, analgesic and sedative properties. Platelets bear alpha 2-receptors on the cell surface. Stimulation of these receptors by agonists induces platelet aggregation. The present study examined whether in vitro incubation of blood with the alpha 2-agonists clonidine and dexmedetomidine decreases alpha 2-receptor density and hereby influences platelet aggregation. METHODS: Whole blood of 20 healthy volunteers was incubated over 24 h at 37 degrees C with 1 ng/ml clonidine or 1 or 10 ng/ml dexmedetomidine. Induced platelet aggregation was determined by means of turbidometry. Epinephrine (22 mumol/l) or collagen (20 mg/l) served as inductors. The density of alpha 2-receptors was measured in radioligand assays with 3H-Yohimbine. Phentolamine was used to assess unspecific binding. The data were analyzed with an analysis of variance. RESULTS: Neither 1 ng/ml clonidine nor 1 ng/ml dexmedetomidine altered platelet aggregation or alpha 2-receptor density in comparison with the control sample. As a major result we found that 10 ng/ml dexmedetomidine caused a significant (P < 0.05) reduction in epinephrine-induced platelet aggregation (16.0 +/- 5.4%, n = 20, mean +/- SEM) compared with the control (46.0 +/- 1.3%, n = 20). alpha 2-Receptor density was not any different from the control. CONCLUSIONS: This in vitro study showed that clinically relevant concentrations of 1 ng/ml clonidine or dexmedetomidine did not alter platelet aggregation or alpha 2-receptor density, even after 24 h exposure. However, 10 ng/ml dexmedetomidine was found to diminish significantly epinephrine-induced platelet aggregation, but did not change alpha 2-receptor density. This result showed that desensitization of platelet aggregation can occur without quantitative changes in alpha 2-receptors.
Adrenergic alpha-2 Receptor Agonists↗
Volume replacement with gelatin or hydroxyethylstarch solutions does not impair somatosensory evoked potential monitoring: a haemodilution study in conscious volunteers.
The influence of haemodilution with colloids on somatosensory evoked potentials in non-premedicated volunteers is reported. In seven volunteers (randomized crossover design), blood (20 mL kg-1 within 30 min) was removed and simultaneously replaced by gelatin 3% or hydroxyethylstarch 6%. After 30 min, blood was retransfused within 30 min. Median and posterior tibial nerve somatosensory evoked potentials were recorded from the cortex, second cervical vertebra, Erb's point and 1st lumbar vertebra, respectively. One volunteer experienced a severe allergic reaction to gelatin, therefore only six gelatin trials were evaluated. Haemodilution decreased the haematocrit from 39.8 +/- 1.6% (mean +/- SD) to 31.1 +/- 2.0% (gelatin) and from 40.7 +/- 1.7% to 29.8 +/- 1.5 % (hydroxyethylstarch), respectively. Retransfusion increased haematocrit to 34.4 +/- 0.9% (gelatin) and to 34.2 +/- 1.3% (hydroxyethylstarch). Neither haemodilution with gelatin nor haemodilution with hydroxyethylstarch or retransfusion influenced evoked potentials. In conclusion, the treatment of blood loss up to 30% of estimated blood volume with gelatin or hydroxyethylstarch will not affect somatosensory evoked potential monitoring provided normovolaemic conditions are maintained.
Adult↗