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Biomedical subjects

D Maass

Publications and source records attributed to D Maass.

At least 19 recordsLinked to original sources
PubMed2002

Integrated L-phenylalanine separation in an E. coli fed-batch process: from laboratory to pilot scale.

Pilot-scale reactive-extraction technology for fully integrated L-phenylalanine (L-Phe) separation in Escherichia coli fed-batch fermentations was investigated in order to prevent an inhibition of microbial L-Phe production by-product accumulation. An optimal reactive-extraction system, consisting of an organic kerosene phase with the cation-selective carrier DEHPA (di-2-ethylhexyl phosphonic acid) and an aqueous stripping phase including sulphuric acid, was found particularly efficient. Using this system with two membrane contactors, mass-transfer coefficients of up to 288 x 10(-7) cm s(-1) for the aqueous/organic and 77 x 10(-7) cm s(-1) for the organic/stripping phase were derived from experimental data using a simple modelling approach. Concentration factors higher than 4 were achieved in the stripping phase as compared to the aqueous donor phase. Reactive extraction enabled a 98% cation portion of L-Phe in the stripping phase, leading to final product purity higher than 99% after L-Phe precipitation. A doubling of L-Phe/glucose yield was observed when kerosene/DEHPA was added to the fermentation solution in the bioreactor to experimentally simulate a fully integrated L-Phe separation process.

Journal Article↗
PubMed2002

Enhanced pilot-scale fed-batch L-phenylalanine production with recombinant Escherichia coli by fully integrated reactive extraction.

A fully integrated process for the microbial production and recovery of the aromatic amino acid L-phenylalanine is presented. Using a recombinant L-tyrosine (L-Tyr) auxotrophic Escherichia coli production strain, a fed-batch fermentation process was developed in a 20-l-scale bioreactor. Concentrations of glucose and L-Tyr were closed-loop-controlled in a fed-batch process. After achieving final L-phenylalanine (L-Phe) titres >30 g/l the process strategy was scaled up to 300-l pilot scale. In technical scale fermentation L-phenylalanine was continuously recovered via a fully integrated reactive extraction system achieving a maximum extraction rate of 110 g/h (final purity >99%). It was thus possible to increase L-Phe/glucose selectivity from 15 mol% without to 20.3 mol% with integrated product separation.

Journal Article↗
PubMed2001

Overexpression of cardiac I-kappaBalpha prevents endotoxin-induced myocardial dysfunction.

Nuclear factor-kappa B (NF-kappaB) is an inducible transcription factor that regulates expression of many genes, such as tumor necrosis factor-alpha (TNF-alpha), which may contribute to myocardial dysfunction. We investigated whether cardiac NF-kappaB activation is involved in the development of myocardial dysfunction after lipopolysaccharide (LPS) challenge. Mice were intraperitoneally injected with LPS, and the hearts were harvested and assayed for NF-kappaB translocation. After LPS challenge, NF-kappaB activation was detected within 30 min and remained for 8 h. In transgenic mice constitutively overexpressing a nondegradable form of I-kappaBalpha (I-kappaBalphaDeltaN) in cardiomyocytes, myocardial NF-kappaB translocation was prevented after LPS challenge. Myocytes isolated from these transgenics secreted significantly less TNF-alpha than did wild-type cardiomyocytes after LPS stimulation. When whole hearts were excised, perfused in a Langendorff preparation, and challenged with endotoxin, I-kappaBalphaDeltaN transgenic hearts displayed normal cardiac function, whereas profound contractile dysfunction was observed in wild-type hearts. These data indicate that myocardial NF-kappaB translocates within minutes after LPS administration. Inhibition of myocyte NF-kappaB activation by overexpression of myocyte I-kappaBalpha is sufficient to block cardiac TNF-alpha production and prevent cardiac dysfunction after LPS challenge.

Animals↗
PubMed2000

Nitric oxide modulation of TNF-alpha-induced cardiac contractile dysfunction is concentration dependent.

Whereas previous studies suggest that tumor necrosis factor-alpha (TNF-alpha) induces cardiac contraction-relaxation deficits, the mechanisms remain unclear. Our recent studies have implicated cardiac-derived nitric oxide (NO). This study examined the detrimental and protective effects of NO donors S-nitroso-N-acetyl-penicillamine (SNAP) or (Z)-1- [N-(3-ammonio-propyl)-N-(n-propyl)amino]diazen-1-ium- 1,2diolate (PAPA/NO) on TNF-alpha-related changes in cardiac contractile function (Langendorff), cellular injury, and intracellular myocyte Ca(2+) concentration ([Ca(2+)](i)). Myocytes were incubated in the presence/absence of TNF-alpha (200-500 pg/ml x 10(5) cells) for 3 h; subsets of myocytes were incubated with one of several concentrations of SNAP or PAPA/NO (0.1, 0.3, 0.5, and 1.5 mM) for 15 min before TNF-alpha challenge. Supernatant creatine kinase (CK), cell viability (Trypan blue dye exclusion), and myocyte [Ca(2+)](i) (fura 2-acetoxymethyl ester) were measured. In parallel experiments, cardiac function (Langendorff) was examined after TNF-alpha challenge in the presence or absence of SNAP or PAPA/NO (0.1 and 1.5 mM). TNF-alpha in the absence of an NO donor impaired cardiac contraction and relaxation and produced cardiomyocyte injury. Pretreating perfused hearts or isolated cardiomyocytes with a low concentration of either SNAP or PAPA/NO decreased TNF-alpha-mediated cardiac injury and improved contractile dysfunction, whereas high concentrations of NO donor exacerbated TNF-alpha-mediated cardiac effects. These data provide one explanation for the conflicting reports of beneficial versus detrimental effects of NO in the face of inflammation and suggest that the effects of NO on organ function are concentration dependent; low concentrations of NO are cardioprotective, whereas high concentrations of NO are deleterious.

Animals↗
PubMed2000

Increased cardiomyocyte intracellular calcium during endotoxin-induced cardiac dysfunction in guinea pigs.

Septic shock is a complex pathophysiologic state characterized by circulatory insufficiency, multiple system organ dysfunction, and frequent mortality. Although profound cardiac dysfunction occurs during sepsis, the pathogenesis of this dysfunction remains poorly understood. To determine whether abnormalities in intramyocyte calcium accumulation might contribute to the development of cardiac dysfunction, we measured myocyte intracellular calcium during peak cardiac dysfunction after an endotoxin challenge. Intraperitoneal administration of Escherichia coli lipopolysaccharide 4 mg/kg to adult guinea pigs resulted in significantly impaired cardiac performance (Langendorff preparation) 18 h after challenge compared with control. This included diminished left ventricular pressure development (56 +/- 7 versus 95 +/- 4 mm Hg, p < 0.05), maximal rate of left ventricular pressure rise (998 +/- 171 versus 1784 +/- 94 mm Hg/s, p < 0.05) and left ventricular pressure fall (1014 +/- 189 versus 1621 +/- 138 mm Hg/s, p < 0.05). Assay of intracellular calcium in fura-2AM-loaded cardiac myocytes demonstrated increased intracellular calcium concentration in myocytes obtained from lipopolysaccharide-challenged animals compared with controls (234 +/- 18 versus 151 +/- 6 nM, p < 0.05). Inhibition of calcium-release channel (ryanodine receptor) opening by administration of dantrolene prevented the increase in intracytoplasmic calcium (159 +/- 8 versus 234 +/- 18 nM, p < 0.05) and partially ameliorated systolic and diastolic ventricular dysfunction. These data indicate that abnormalities of intracellular calcium contribute to the development of endotoxin-induced myocardial dysfunction.

Animals↗
PubMed1999

Calcium antagonists improve cardiac mechanical performance after thermal trauma.

Burn trauma initiates a pathophysiologic cascade, which includes cardiac dysfunction and intramyocyte calcium accumulation. This study examined the hypothesis that therapeutic interventions which limit intracellular cardiac Ca(2+) accumulation after burn trauma will improve cardiac function. Guinea pigs were anesthetized (methoxyflurane), burned over 43% of total body surface area, and fluid resuscitated (FR) for 24 h. Burn guinea pigs were randomly divided into three groups: Group 1, FR alone, Group 2, FR plus dantrolene (10 mg/kg body wt, IV, 30 min, 8 and 22 h postburn), a drug which inhibits the Ca(2+) release channel (ryanodine receptor) of the cardiac sarcoplasmic reticulum, and Group 3, FR plus diltiazem (0.20-0.22 mg/kg given IV as a slow infusion over 6 h postburn), a drug which specifically blocks Ca(2+) slow channels; sham burn guinea pigs were given vehicle (Group 4), dantrolene (Group 5), or diltiazem (Group 6) as described above (respective controls). Cardiac dysfunction was impaired in fluid-treated burns (Group 1) compared to sham burns (Group 4) as indicated by reduced developed left ventricular pressure (LVP) (86 +/- 2 vs 52 +/- 3 mm Hg, P < 0.05), rate of LVP rise, (+dP/dt max, 1379 +/- 64 vs 909 +/- 44 mm Hg/s, P < 0.05), and LVP fall (-dP/dt max, 1184 +/- 31 vs 881 +/- 40 mm Hg/s, P < 0.05), and time to peak pressure (110 +/- 2 vs 102 +/- 2 ms, P < 0.05). In addition, [Ca(2+)](i) rose in cardiomyocytes harvested from fluid-treated burns (Group 1, 307 +/- 29 nM) compared to vehicle-treated controls (Group 4, 152 +/- 6 nM, P < 0.05). Neither calcium antagonist altered ventricular function or [Ca(2+)](i) in sham burns (Groups 5 and 6). In contrast, antagonists given after burn injury reduced cardiomyocyte [Ca(2+)](i) (Group 2, dantrolene-treated burns: 196 +/- 8 nM, and Group 3, diltiazem treated burns: 216 +/- 8 nM) and improved cardiac performance compared to that measured in burns given FR alone. Our data suggest that calcium antagonists given after burn trauma restored intracellular Ca(2+) homeostasis, decreased cardiac cell injury, and improved cardiac contractile function.

Animals↗
PubMed1998

Digital 3D image reconstruction of ventriculocapillary communication as revealed in one case after transmyocardial laser revascularization.

TMR (Transmyocardial Laserrevascularization) was performed on the partially dyskinetic left ventricular anterior wall with stenotic coronary blood supply in a 61 year old woman with a history of angina and myocardial infarction. As an ischemic aneurysm developed in the anteroapical region of the TMR treated area, it became clear that TMR did not provide a substitute for coronary blood supply in this very heart region. The aneurysm was removed surgically 7 months after TMR and showed histopathologic features of an acute aneurysm. Three-dimensional image analysis helped prove the presence of linear tracks through several serial sections which were not easily visible in routine histology sections. Also, three-dimensional vessel reconstruction showed a connection between a small endocardial pit on one serial section with the capillary network in the adjacent serial sections. The results should not be generalized, as currently aneurysmectomy is an end point not reached by the majority of TMR-treated patients.

Capillaries↗
PubMed1998

Protein kinase C inhibition improves ventricular function after thermal trauma.

OBJECTIVE: To examine the effect of protein kinase C (PKC) inhibition on cardiac performance and intracellular Ca2+ homeostasis. DESIGN: Previous studies have shown that trauma impairs cardiac mechanical function, and recent studies suggest that PKC activation and subsequent perturbations in Ca2+ sequestration/release contribute to this cardiac dysfunction. In this study, anesthetized guinea pigs were given third-degree scald burns over 43 +/- 1% of the total body surface area and resuscitated with lactated Ringer's solution (LR) 4 mL/kg per percent of burn, Parkland formula. Animals with sham burns served as controls (n = 18). Burns were randomly divided into two groups: LR alone (N = 18) or LR + PKC inhibitor, calphostin C (0.1 mg/kg, intravenous bolus), given 30 minutes and 3, 6, and 21 hours after burn (n = 18). MATERIALS AND METHODS: Cardiac function was assessed by Langendorff preparation 24 hours after burn in 8 to 12 animals per group. Intracellular calcium concentration ([Ca2+]i) was measured in cardiac myocytes (collagenase digestion) from additional animals in each experimental group (n = 5-9 per group) after Fura-2 AM loading of myocytes; fluorescence ratios were measured with a Hitachi spectrofluorometer. RESULTS: Cardiac dysfunction occurred 24 hours after burn in LR burns as indicated by lower left ventricular pressure and a reduced rate of left ventricular pressure rise and fall, +/-dP/dt (61 +/- 3 mm Hg, 1,109 +/- 44 mm Hg/s, and 880 +/- 40 mm Hg/s, respectively) compared with values measured in sham-burned animals (86 +/- 2 mm Hg, 1365 +/- 43 mm Hg/s, and 1183 +/- 30 mm Hg/s, respectively; p < 0.05). Ventricular function curves confirmed significant postburn contractile depression despite aggressive fluid resuscitation. Cardiac injury in burned animals was indicated by an increase in perfusate creatine kinase and lactate dehydrogenase, and Ca2+ dyshomeostasis was confirmed by increased myocyte [Ca2+]i (sham 151 +/- 6 vs. burn 307 +/- 20 nmol/L, p < 0.05). PKC inhibition improved all indices of cardiac performance, producing left ventricular pressure (82 +/- 3 mm Hg), +/-dP/dt (1,441 +/- 48 and 1,294 +/- 32 mm Hg/s), and left ventricular function curves that were comparable with those of sham-burned animals. In addition, [Ca2+]i in calphostin-treated burned animals (154 +/- 11 nmol/L) was identical to values in sham-burned animals. CONCLUSION: Our data suggest that PKC may serve as a final common pathway in signal transduction events mediating postburn cardiac dysfunction.

Animals↗
PubMed1998

Burn trauma and tumor necrosis factor alpha alter calcium handling by cardiomyocytes.

It is well recognized that burn trauma induces an inflammatory cascade and the release of cytokines including tumor necrosis factor (TNF)-alpha. The negative inotropic effects of TNF-alpha on the heart are well recognized, but the cellular mechanisms remain unclear. To examine one aspect of cellular function, we exposed cardiac myocytes isolated from NZW rabbits (collagenase digestion) to either TNF-alpha (200, 400, or 1000 U/mL) or sham or burn plasma (10% by volume) for 3 to 4 h and measured calcium transient ratios in the isolated, contracting myocytes using the fluorescent indicator Fura-2-acetoxymethyl (1.2 microM); myocytes treated with media alone served as controls. Cells were placed in a perfusion chamber on the stage of an inverted Nikon microscope and superfused with buffer at 37 degrees C and stimulated at 1 Hz. A Tracor Northern Fluoroplex 1000 microspectrofluorometer and camera system, set to provide excitation of 340 and 380 nm with emission at 450-580 nm, was used to measure Ca2+ transients during systole-diastole. [Ca2+]i was reported as a fluorescence ratio (F340/F380) to minimize effects of different cell thickness and motion artifacts. After recording diastolic/systolic [Ca2+]i, cells were stimulated with isoproterenol, and [Ca2+]i was again measured. TNF-alpha produced diastolic and systolic [Ca2+]i values (1.067 +/- .023/1.301 +/- .017) that were similar to values seen after myocyte exposure to burn plasma (1.099 +/- .024/1.307 +/- .028) and significantly greater than values measured in controls (.857 +/- .017/1.077 +/- .015, p < .05). Our data confirm that burn trauma and TNF-alpha alter calcium handling by cardiomyocytes. The possible contribution of altered intracellular calcium dynamics to cardiac contractile abnormalities after burn trauma and TNF-alpha administration warrants further study.

Animals↗
PubMed1998

Arginine in burn injury improves cardiac performance and prevents bacterial translocation.

This study examined the effects of arginine supplement of fluid resuscitation from burn injury on cardiac contractile performance and bacterial translocation after a third-degree burn comprising 43% of the total body surface area in adult rats. Before burn injury, rats were instrumented to measure blood pressure; after burn (or sham injury), paired groups of sham-burned and burned rats were given vehicle (saline), L-arginine, D-arginine, or N-methyl-L-arginine (300 mg/kg in 0.3 ml of saline 30 min, 6 h, and 23 h postburn) plus fluid resuscitation; sham-burned rats received drug only. Twenty-four hours after burn trauma, hemodynamics were measured; the animals were then killed and randomly assigned to Langendorff heart studies or to studies examining translocation of gut bacteria. Burn rats treated with vehicle, D-arginine, or N-methyl-L-arginine had well-defined cardiocirculatory responses that included hypotension, tachycardia, respiratory compensation for metabolic acidosis, hypocalcemia, cardiac contractile depression, and significant bacterial translocation. Compared with values measured in vehicle-treated burn rats, L-arginine given after burn improved blood pressure, prevented tachycardia, reduced serum lactate levels, improved cardiac performance, and significantly reduced bacteria translocation, confirming that L-arginine administration after burn injury provided significant cardiac and gastrointestinal protection. Circulating neutrophil counts fell after burn trauma and serum glucagon levels rose, but these changes were not altered by pharmacological intervention. Our finding of significantly higher coronary perfusate guanosine 3',5'-cyclic monophosphate concentration in L-arginine-treated burn rats suggests that the beneficial effects of L-arginine were mediated by nitric oxide production.

Animals↗
PubMed1997

[Transmyocardial laser revascularization. Histopathology of laser channels in 10 postoperatively deceased patients 1 to 18 days after treatment with a CO2 laser].

TMLR (Transmyocardial laser revascularization) is a disputed cardiosurgical technique available in Europe since 1994 that aims to deliver additional blood flow to ischemic myocardium from the left heart chamber. Goal of our study is morphological examination of laser channels in human hearts to answer the questions: Are there patent laser channels with communication to the left chamber and to intramural vessels? We examined hearts of 10 patients who died during the first 18 days after TMLR. Channels were examined in histological serial sections under the light microscope. Laser channels in the first days postoperatively have a lumen diameter of about 1 mm and are surrounded by coagulation necrosis about 500 microns thick. Despite phagocytic removal of necrotic tissue the lumen diameter decreases during the following two weeks. Open intramyocardial channels can be shown in all patients. These channels communicate with intramural vessels, but in no instance with chamber lumen. Our results suggest that clinical benefits are based on improved distribution of coronary blood. Additional blood is not delivered from left chamber lumen to the myocardium. However, our patients represent the small subgroup of the decreased. If similar observations can be made in the majority of patients living symptom free after TMLR remains open.

Angina Pectoris↗
PubMed1997

End stage coronary disease treated with the transmyocardial CO2 laser revascularization: a chance for the 'inoperable' patient.

OBJECTIVE: The aim of this study is to evaluate the short and mid-term efficacy of the Transmyocardial High Power CO2 Laser Revascularisation (TMLR) as a last resource method for end-stage coronary disease patients. METHOD AND PATIENTS: The High Power CO2 Laser 800 W Heart Laser (PLC Medical Systems) was used since February 1994 to treat 268 patients. In 52% of the cases (140) the indication for TMLR treatment was virtual inoperability by the classical bypass revascularisation. In the other 128 patients (48%), where only an incomplete revascularisation was expected, the TMLR was combined with a feasible bypass revascularisation (CABG). Of all patients, 71% were operated on 1-5 times before and or treated by several percutaneous transluminal coronary angioplasty (PTCA). All patients were sufferers of angina pectoris and most were classified Canadian Cardiac Society (CCS) 3-4, despite the maximal medical treatment. The ejection fraction was normal in 13% of patients only, and in 47% of them it was below 40% (10-68%). RESULTS: The operation itself was generally well tolerated. We lost only one patient at the table. The hospital survival was 89.2%; 88.2% in the combined group and 90.3% in the TMLR only group. After the routine follow up screening 3, 6 and 12 months postoperatively (262 patients--131 TMLR and 131 TMRL/CABG), 40% of the TMLR patients upgraded into the functional class CCS 0-1; the combined group of patients scored up even in 84%. All considering their quality of life to be 'better than years ago'. The ergometry stress test, impossible for most of them before, became feasible and better in 80% of the patients. In the follow up period of the combined group, another 6 (4.7%), and in the TMLR only group, 12 (9.4%) patients died. CONCLUSION: The short and middle term results of this--until now the largest single institution series of TMLR treated patients--were that patients almost without exception were refused for any kind of surgery by several other centres; this shows an acceptable survival rate and a surprising level of pain relief, increased activity and better quality of life then ever expected. In our experience, TMLR is a suitable method for treatment of end stage coronary disease, if all standard measures, medical therapy, PTCA and redo coronary revascularisation possibilities are exhausted. The favourable results imply the question as to whether this method will become an alternative for a second bypass operation in the future. The TMLR as an alternative for heart transplant is already a reality for some of our patients.

Cohort Studies↗
PubMed1990

[Extracorporeal circulatory assistance with centrifugal pumps in postcardiotomy low-output syndrome].

From 6/86 to 5/89 seven out of 1700 (0.4%) open heart patients had to be assisted with centrifugal pumps for postcardiotomy low cardiac output syndrome. In 4 cases a left ventricular assist device (LVAD) was used, one case each had a right ventricular assist device (RVAD), an extracorporeal membrane oxygenation (ECMO) and a biventricular assist device (BVAD) with ECMO and ultrafiltration. The last 3 patients were assisted non-pulsatile without intraaortic balloon counterpulsation (IABP) and no impairment of vital organ function was observed. Four out of 7 patients could be weaned from the assist device after a mean of 30 hours (0.5-48). Three patients became long-term survivors with 2 assisted non-pulsatile. Transesophageal echocardiography (TEE) was used to determine the timing for wean off and was found to be an important adjunct to the monitoring of filling--and systemic pressure.

Adult↗
PubMed1989

Initial clinical experience with an endoluminal spiral prosthesis for treating complicated venous thrombosis and preventing pulmonary embolism.

Fourteen patients with complicated venous thrombosis or recurrent pulmonary embolism were treated by implantation of an endoluminal spiral prosthesis subsequent to balloon angioplasty, surgical thrombectomy or embolectomy, a combination of these, or, in 2 cases, no other treatment. The patients were divided into 2 groups, based on their primary diagnosis and the purpose of the prosthesis. Group I included 8 patients with extensive iliofemoral or caval thrombosis, caused by congenital caval stenosis (1 case) or extravascular compression or retraction (7 cases); 7 of these patients had had previous operations, and the remaining patient had undergone thrombolysis, which failed. The current treatment consisted of balloon angioplasty and surgical thrombectomy or embolectomy, and implantation of an endoluminal spiral stent to prevent elastic recoil of the vessel. In 4 cases, an arteriovenous fistula was constructed and was taken down 3 months later; in 1 additional patient, a bilateral arteriovenous fistula was created. Group II comprised 6 patients with recurrent pulmonary embolism (4 cases), massive pulmonary embolism (1 case), or paradoxical bilateral carotid artery embolism (1 case). Four of these patients underwent surgical thrombectomy or embolectomy, while 2 had no treatment other than filter implantation. All 6 underwent transluminal implantation of a helix caval filter (a modification of the endoluminal spiral stent). All but 1 implantation was accomplished by means of either a transfemoral or a transjugular cutdown; the remaining implantation was performed transatrially after a pulmonary embolectomy. The only device-related complication was a retroperitoneal hematoma in Group I, resulting from perforation of the inferior vena cava by the guidewire during device implantation. This complication necessitated an emergency laparotomy and takedown of the arteriovenous fistula, which resulted in rethrombosis of the left iliofemoral vein. The other 7 stented veins were patent at early phlebographic follow-up, as were all 5 of those studied later. One Group-I patient died 4 months after surgery, due to tumor progression and without signs of caval restenosis. Twelve months postoperatively, 1 Group-II patient died of urosepsis without a recurrence of pulmonary embolism. Four of the 6 Group-II patients were studied late postoperatively, and all of their stented vessels were patent. There was no operative mortality or postoperative embolism. On the basis of these results, we conclude that endoluminal stenting with an expandable spiral prosthesis is a promising method for remote venous reconstruction. Moreover, it appears that the modified stent, or helix caval filter, compares favorably with commercially available filters.

Journal Article↗
PubMed1989

Topology of the non-structural rotavirus receptor glycoprotein NS28 in the rough endoplasmic reticulum.

The rotavirus non-structural glycoprotein (NS28), the receptor for the virus core during budding into the lumen of the rough endoplasmic reticulum (RER), is 175 amino acids long and possesses an uncleaved signal sequence and two amino-terminal glycosylation sites. Utilizing one of three potential hydrophobic domains, the protein spans the membrane only once, with the glycosylated amino-terminal region oriented to the luminal side of the ER and the carboxy-terminal region to the cytoplasmic side. To localize sequences involved in translocation of NS28, we constructed a series of mutations in the coding regions for the hydrophobic domains of the protein. Mutant protein products were studied by in vitro translation and by transfection in vivo. In transfected cells, all mutant forms localize to the ER, and none are secreted. In vitro, each of the three hydrophobic domains is able to associate with microsomes. However, glycosylation and proteolysis of wild-type and mutant forms of NS28 indicates that the wild-type protein is anchored in the membrane only by the second hydrophobic domain, leaving approximately 131 residues exposed on the cytoplasmic side for receptor - ligand interaction.

Amino Acid Sequence↗
PubMed1987

[Successful post-bypass extracorporeal circulatory assistance with the centrifugal pump].

Patients with reduced left ventricular function do have an increased risk of inability to be weaned off bypass after open heart surgery despite maximal pharmacologic support and intraaortic balloon counter-pulsation. Centrifugal pumps used for extracorporeal circulatory assist can maintain a patient in low cardiac output up to days without anticoagulation. We used a centrifugal pump in 3 patients: as a left ventricular assist device (LVAD) in 2 patients and right ventricular assist device (RVAD) in 1 patient. One LVAD-patient became a long-term survivor after 20 h of assist, another was bridged successfully to an open heart procedure for 2 h after papillary muscle rupture. One RVAD patient died on the operating table due to massive tracheal bleeding probably caused by pulmonary hypertension.

Assisted Circulation↗
PubMed1987

Successful post-bypass ventricular assist with a centrifugal pump.

A 56 year old male with massive anterior wall infarction and development of a large aneurysm underwent aneurysmectomy and aorto-coronary bypass grafting to the RCA. Preoperative ejection fraction was 20%, LVedP was 30 mm Hg. During induction of anesthesia the patient sustained ventricular fibrillation and was successfully resuscitated. With the patient in progressive cardiogenic shock the operation was performed under emergency conditions. Despite adequate myocardial protection and cross-clamp time as well as prolonged reperfusion and balloon counterpulsation the patient could not be weaned off cardiopulmonary bypass. In this situation a centrifugal pump system was connected between the left atrium and the ascending aorta. With a pump flow of 5 l/min the patient was taken off cardiopulmonary bypass. After 20 hours of extracorporeal support without anticoagulation the device could be removed: explantation of the IABP followed 48 hours later. The patient gradually recovered and finally was discharged home in fair condition.

Assisted Circulation↗