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Biomedical subjects

M Ritter

Publications and source records attributed to M Ritter.

At least 127 records · Page 7Linked to original sources
PubMed1994

Persistent root abscess after emergency repair with an aortic homograft.

A fifty eight year old man with Marfan's syndrome and an aortic composite graft with a Björk-Shiley mechanical prosthesis presented with a large aortic root abscess caused by Staphylococcus aureus endocarditis. Despite extensive surgical debridement and implantation of an aortic homograft as a composite graft, early postoperative transoesophageal echocardiography continued to demonstrate a large aortic root abscess and the patient died in a septic shock.

Abscess↗
PubMed1994

Helicobacter heilmannii (formerly Gastrospirillum hominis) gastritis: an infection transmitted by animals?

BACKGROUND: The source of infection with Helicobacter heilmannii (formerly Gastrospirillum hominis), a relatively rare causative agent of gastritis in humans, is not clear. It has long been known that this organism occurs in the stomach of domestic animals and pets. METHODS: By performing an epidemiologic investigation on possible contact of patients with Helicobacter heilmannii gastritis with such animals, we made an attempt to gain further information about the source of infection. RESULTS: Of 125 patients with confirmed H. heilmannii infection, 111 provided us with information about contact with animals. Some 70.3% of the patients had contact with one or more animals (as compared with 37% in the 'normal' population); 73% were males, and 1.6% had concomitant infection with H. pylori. CONCLUSIONS: Our analysis indicates that H. heilmannii gastritis is due to its transmission to humans by domestic animals or pets. Concomitant infections by H. heilmannii and H. pylori are very rare, and it is possible that H. heilmannii might protect from infection with H. pylori. However, the results of our retrospective analysis will have to be tested against those of a prospective study investigating the day-to-day situation of the individual patients in greater detail and also be compared with patients not infected with H. heilmannii.

Adolescent↗
PubMed1994

Lytic susceptibility of target cells to cytotoxic T cells is determined by their constitutive major histocompatibility complex class I antigen expression and cytokine-induced activation status.

Cytotoxic T-cell lines (TCL) were raised in vitro using stimulator cells with a defined major histocompatibility complex (MHC) mismatch and tested in a cytotoxic chromium-release assay against haemopoietic and non-haemopoietic target cells from the original stimulator. Monoclonal antibody (mAb)-blocking experiments and simultaneous determination of MHC class I, class II, lymphocyte function-associated antigen-1 (LFA-1) and intracellular adhesion molecule-1 (ICAM-1) density by quantitative radioimmunometric methods and flow cytometry on target cells demonstrated that lysis was restricted by MHC class I and dependent upon the constitutive MHC class I antigen expression. Measurements showed a high constitutive expression of class I MHC antigens on peripheral blood mononuclear cells (PBMC), but a low one on keratinocytes (K). Also, PBMC were more susceptible to lysis by TCL than K. Interferon-gamma (IFN-gamma) treatment of K resulted in increased MHC class I antigen expression and enhanced lytic susceptibility to TCL. IFN-alpha and tumour necrosis factor-alpha (TNF-alpha) treatment, which did not modulate MHC class I antigen expression on K, did not influence the amount of K lysis either. None of the cytokines tested in this analysis, however, increased the expression of MHC class I, class II, ICAM-1 and LFA-1 on PBMC. Only IFN-gamma pretreatment showed a minimal, statistically significant increase in MHC class I antigen expression. In spite of the minimal effect of IFN-gamma and no effect of IFN-alpha on class I MHC expression, pretreatment of target cells with both cytokines considerably increased their lytic susceptibility. The mechanism of cytokine-induced enhanced lytic susceptibility to TCL was not explained by increased MHC class I, LFA-1 or ICAM-1 expression, since no correlation was found between surface expression of these molecules and lytic susceptibility to TCL. These data demonstrate that: (1) the constitutive density of MHC class I antigens determines the extent of TCL lysis; (2) IFN-gamma, and not IFN-alpha or TNF-alpha controls the amount of K target cell lysis by increasing their MHC class I antigen expression; and (3) IFN-gamma and IFN-alpha control the amount of PBMC target cell lysis by a mechanism independent of MHC class I, ICAM-1 or LFA-1 expression.

Cell Adhesion Molecules↗
PubMed1994

Dissection of the descending thoracic aorta extending into the ascending aorta. A therapeutic challenge.

Proper management of dissections of the descending thoracic aorta with intimal disruption close to the left subclavian artery and retrograde extension of the dissection into the aortic arch or the ascending aorta is controversial, because the standard approach for ascending aortic aneurysms is surgical repair, which is difficult to achieve through a median sternotomy if the predominant aortic lesion is located in its descending part. Sixteen patients with descending thoracic aortic dissection, intimal disruption close to the subclavian artery, and extension of the dissection into the aortic arch or the ascending aorta are described here: Eleven patients underwent surgical repair including 9 emergency (82%) and 2 elective (18%) procedures. Retrograde aortic dissection included the aortic arch in 11 of 11 patients (100%) and the ascending aorta in 7 of 11 (63%). Pericardial effusion was present in 1 of 11 patients (9%) and mild aortic regurgitation was found in 1 of 11 (9%). Repair of the ascending aorta and arch with transaortic closure of the entrance tear in the descending thoracic aorta was performed in 4 of 11 patients (36%) via a median sternotomy. In 6 of 11 patients (55%) a lateral thoracotomy was used for repair of the descending thoracic aorta and closure of the entrance tear. Hospital mortality occurred in 1 of 11 patients (9%) and there was 1 late death. Paraplegia occurred in 1 of 11 patients (9%). Five patients with descending thoracic aortic dissection, intimal disruption close to the subclavian artery, and extension into the ascending aorta but without ascending aortic aneurysm (diameter 4.2 +/- 0.2 cm), pericardial effusion, or aortic incompetence were treated medically without early mortality. These results are compared with those achieved in 120 patients operated on during the same period for type A (89/120) and type B (31/120) aortic dissections. Considering the technical difficulties of simultaneous repair of dissections of the ascending and the descending thoracic aorta, we recommend that descending thoracic aortic dissection extending into the arch or the ascending aorta be managed in accordance with the site of the predominant lesion. Replacement of the arch with a varying portion of ascending aorta via a median sternotomy is recommended in patients with enlarged aortic diameter, pericardial effusion, and/or aortic insufficiency. Predominantly distal dissections with dilated descending thoracic aorta and/or distal complications are best approached via a lateral thoracotomy.

Adolescent↗
PubMed1994

Cytoskeletal reorganization in NIH 3T3 fibroblasts expressing the ras oncogene.

Expression of the Ha-ras oncogene in NIH 3T3 fibroblasts leads to a set point shift of cell volume regulation and causes an increase in cell volume by activation of Na+/H+ exchange and Na+, K+, 2Cl- cotransport. Since both ion transport systems are thought to be governed by the cytoskeleton, the aim of this study was to examine the alterations in growth characteristics and cytoskeletal organization due to the expression of the oncogene. The experiments were performed on NIH 3T3 fibroblasts transfected with a transforming Ha-ras MMTV-LTR construct and expressing the oncogene after treatment with low serum medium and 1 mumol/l dexamethasone (+ras cells). Transfected cells not expressing the oncogene (-ras cells) and treated with low serum medium, but without the addition of dexamethasone, served as controls. The growth characteristics were examined and the cytoskeletal architecture was visualized by indirect immunofluorescence microscopy using specific antibodies and fluorescent dyes. Expression of the ras oncogene was accompanied by a significant and serum-independent increase in proliferative activity irrespective from the coating of the dishes with attachment factors (poly-L-lysine, collagen type I). Both, -ras and +ras cells, proliferated slower on substrates coated with poly-L-lysine than on tissue culture plastic or collagen type I. Expression of the ras oncogene also resulted in a significant increase in cell volume which was independent from the substrate. +ras Cells became more elongated, exhibited long cytoplasmic protrusions and tended to detach when compared with -ras cells. Examination of the cytoskeletal architecture in +ras and -ras cells revealed marked differences such as a depolymerization of the stress fiber network to strongly fluorescent "focals" as well as the absence of vinculin-containing attachment plaques (focal contacts), a disorganization of non-muscle myosin and of cell surface fibronectin in +ras cells. In addition, a retraction of microtubules and vimentin filaments to the perinuclear region was also observed in +ras cells. For comparison, NIH 3T3 fibroblasts which were not transfected with the ras oncogene (0ras cells) and which were also subjected to the experimental conditions described above (low serum medium +/- dexamethasone), did not exhibit the cytoskeletal alterations as observed for +ras cells. The results demonstrate that the expression of ras oncogene causes not only profound alterations in the proliferative activity, cell volume and cell morphology, but also a marked reorganization of cytoskeletal architecture, which may participate in the altered regulation of volume-regulatory ion transporters in the cell membrane.

3T3 Cells↗
PubMed1993

[Late pericardial tamponade: a dangerous complication of postoperative anticoagulation following heart surgery].

Late cardiac tamponade is a condition that presents with subtle signs and symptoms within days or weeks after cardiac surgery. During a one-year period, 16 patients, operated in our institution, developed this complication, mostly due to overdosage of anticoagulants. Diagnosis can be difficult and is best confirmed by echocardiography. The incidence of this dangerous complication is reportedly between 0.3 and 1%. The treatment consists in sub-xyphoid drainage when ever possible. In case of loculated or posterior tamponade, re-sternotomy might be necessary to assume complete decompression of the heart.

Aged↗
PubMed1993

[Problems of non-invasive diagnosis of congenital heart defects in adulthood].

Non-invasive assessment of adult congenital heart disease comprises Doppler echocardiography and magnetic resonance imaging (MRI). Doppler echocardiography represents the modality of choice to perform serial follow-up and MRI is used as supplementary method in the diagnosis of congenital heart disease in adults. The spectrum of congenital heart disease in adults encompasses (a) uncorrected and newly detected defects; (b) palliatively corrected and totally corrected defects. In general, diagnostic modalities must be able to fulfill the following requirements: (a) sequential morphologic analysis; (b) assessment of hemodynamics. Sequential morphologic analysis using 2-dimensional echocardiography includes determination of the situs of the atria, atrio-ventricular and ventriculo-arterial connections. Non-invasive assessment of hemodynamics is performed with the Doppler technique and comprises diagnosis and quantitation of (a) (residual) shunt lesions, (b) valvular regurgitation and (c) valvular, subvalvular, supravalvular and infundibular stenosis as well as pressure gradients across anastomoses and intracavitary or intercavitary gradients, respectively. Pulmonary vascular resistance cannot be assessed quantitatively by Doppler. However, the determination of the end-diastolic gradient between the pulmonary artery and the right ventricle in the presence of pulmonic regurgitation allows estimation of the diastolic pulmonary artery pressure.

Adult↗
PubMed1993

[Role of heart transplantation in the treatment of complex congenital malformations in adolescents and adults].

The number of pediatric heart transplants for complex congenital heart disease has increased in recent years, but little experience has been reported in the adolescent and adult population. Between 1987 and 1992, 6 patients (mean age 24 years, range 14 to 42) underwent transplant in our institution because of structural congenital heart disease with or without prior palliative operation or definitive repair. The diagnose covered: congenitally corrected transposition of the great vessels, late systemic ventricular failure after surgically corrected transposition of the great arteries, left superior vena cava, and tricuspid atresia with right ventricular hypoplasia. The palliative repairs included modified Blalock-Taussig shunt, cavo-pulmonary Glenn shunt, two aorto-pulmonary Waterstone shunts, two Blalock-Hanlon atrioseptectomies and one pulmonary valvotomy by the method of Brock. One patient had undergone pulmonary artery banding, in two patients atrial repair by Senning's technique had been performed for definitive repair of transposition of the great arteries. Donor cardiectomy was modified to remove complete inflow and outflow tissue and transplantation was performed without prosthetic material in all patients, in no case was deep hypothermic arrest necessary. There was no early or late mortality after a mean follow-up of 28 months. Postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results. There was no early or late mortality after a mean follow-up of 28 months. Postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results. Adult patients with complex congenital cardiac diseases can be transplanted with a very low perioperative risk, even after several prior operative procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[Right ventricular dysplasia (right ventricular cardiomyopathy). Clinical aspects, diagnosis and course in 15 patients from the Zurich area].

Fifteen patients (8 men, 7 women) with right ventricular dysplasia (RVS) from the greater Zürich area are described. Two thirds of these patients were younger than 30 years at first manifestation. 12 presented with ventricular tachycardia of left bundle branch block type. Other forms of arrhythmia (supraventricular tachycardia, sinus node dysfunction) or condition disturbances were documented in 9 subjects. 6 patients had additional symptoms of congestive heart failure; in 3 of them this was the only symptom. 12-lead ECG at rest showed precordial T-negativity (1 pacemaker ECG not interpretable) in 14/15 subjects. Signal averaged ECG revealed late potentials as well as spectral turbulence in the Y or Z leads. Echocardiography yielded typical local abnormalities in the whole study cohort and all but 2 patients showed decreased right ventricular ejection fraction and right heart dilatation. Moreover, left ventricular ejection fraction was concomitantly impaired in 6 subjects. 4 of these 6 individuals suffered from further impairment of left ventricular function within a time period of 19 to 47 months. Recurrent ventricular tachycardia was documented in 11 patients. 2 subjects underwent heart transplantation because of severe progressive right heart failure. One subject died shortly after diagnosis and autopsy confirmed nearly total absence of right ventricular myocardium. This extreme form of right ventricular dysplasia corresponds to Uhl's anomaly. Thus, recurrent ventricular arrhythmias, in particular ventricular tachycardia of left bundle branch block type, together with precordial T-negativity without signs of ischemic heart disease, is highly suggestive of RVD. Echocardiography allows reliable diagnosis. Concomitant left ventricular involvement is frequent. Considering that the etiology and pathogenesis of this disease are unknown, the term right ventricular cardiomyopathy, rather than right ventricular dysplasia, seems more accurate.

Adult↗
PubMed1993

Effects of HOE 694--a novel inhibitor of Na+/H+ exchange--on NIH 3T3 fibroblasts expressing the RAS oncogene.

Among the sequelae of ras oncogene expression are intracellular alkalinization and increase of cell volume, both phenomena attributed at least in part to activation of the Na+/H+ exchanger. The present study was performed to elucidate the effects of HOE 694--a novel inhibitor of the Na+/H+ exchanger--on intracellular pH, cell volume, cytoarchitecture and cell proliferation of ras oncogene expressing NIH 3T3 fibroblasts. Following transient exposure of the cells to 20 mmol/l NH3/NH4+, intracellular pH decreases sharply. The following slow realkalinization is completely blocked by 10 mumol/1 HOE 694. Half-maximal inhibition is achieved by 100 nmol/l HOE 694. Cell proliferation is inhibited by HOE 694 with similar potency, whereas the increase in cell volume and cytoskeletal transformation are not prevented, even by 10 mumol/l HOE 694.

3T3 Cells↗
PubMed1993

The role of calcium in cell shrinkage and intracellular alkalinization by bradykinin in Ha-ras oncogene expressing cells.

In ras oncogene expressing cells, bradykinin leads to intracellular alkalinization by activation of the Na+/H+ exchanger. This effect is paralleled by oscillatory increase of intracellular calcium activity and cell shrinkage. Staurosporine (1 mumol/l) is not sufficient to prevent bradykinin induced intracellular alkalinization, thus pointing to a protein kinase C independent pathway for the activation of Na+/H+ exchange. The present study has been performed to elucidate, whether the increase of intracellular calcium contributes to cell shrinkage and activation of the Na+/H+ exchanger. To this end, the effects of the calcium ionophore ionomycin have been tested. Ionomycin leads to a dose dependent increase of intracellular calcium activity. At 100 nmol/l ionomycin intracellular calcium is increased from 114 +/- 17 nmol/l to 342 +/- 24 nmol/l (n = 9), a value within the range of intracellular calcium concentrations following application of bradykinin. The calcium increase is paralleled by a decrease of cell volume by 12 +/- 2% (n = 5) and an increase of intracellular pH from 6.78 +/- 0.02 to 6.90 +/- 0.03 (n = 11), values similar to those following application of bradykinin. The alkalinizing effect of ionomycin is completely abolished in the presence of the novel Na+/H+ exchange inhibitor HOE 694 (10 mumol/l), but is not inhibited by 1 mumol/l staurosporine. Inhibition of K+ and Cl- channels by barium (5 mmol/l) and ochratoxin-A (5 mumol/l) prevents both ionomycin induced cell shrinkage and protein kinase C independent intracellular alkalinization. It is concluded that bradykinin leads to intracellular alkalinization mainly by increasing intracellular calcium concentration. Calcium triggers calcium sensitive K+ channels, and presumably Cl- channels, the subsequent loss of cellular KCl leads to cell shrinkage which, in turn, activates Na+/H+ exchange.

3T3 Cells↗
PubMed1993

Correlation of minor histocompatibility antigen-specific cytotoxic T lymphocytes with graft-versus-host disease status and analyses of tissue distribution of their target antigens.

Peripheral blood mononuclear cells (PBMC) from 17 patients receiving HLA-identical sibling bone marrow grafts were stimulated with host pretransplant PBMC. Cytotoxic T-cell lines (TCL) with specificity for host pretransplant PBMC were obtained from 9 of these patients, all presenting with severe graft-versus-host disease (GVHD), but from none of the remaining cases lacking evidence of disease. Cytotoxic TCL were specific for host targets and failed to lyse donor cells. Monoclonal antibodies (MoAbs) blocking experiments and donor population screening analyses demonstrated that minor histocompatibility antigen (MiHA)-specific lysis of host targets was restricted by class I major histocompatibility complex (MHC) determinants. Whereas hematopoietic cells such as phytohemagglutinin (PHA) blasts or lymphoblastoid cell lines were susceptible to lysis by MiHA-specific TCL, keratinocytes (K) representing the natural targets of GVHD were quite resistant. Quantitative radioimmunometric measurements indicated very low constitutive expression of class I MHC antigens on K targets, which was readily increased by treatment with interferon-gamma (IFN-gamma). IFN-gamma treatment at the same time rendered these cells susceptible to lysis by MiHA-specific TCL. Host leukemic cells of 3 patients were recognized by MiHA-specific TCL in a chromium release assay and in one experiment host leukemic cells were effectively killed and their growth specifically inhibited in a leukemia colony assay by a clone. These data demonstrate that (1) host-specific cytotoxic TCL are detected exclusively in the PB of patients with acute GVHD grades II through IV after allogeneic matched bone marrow transplantation, and (2) their target antigens are simultaneously expressed on several host cell lines, including lymphoblastoid cell lines, PHA blasts, leukemic cells, and K. We also extend previous findings by showing that, besides the expression of the nominal MiHA, the density of the restricting class I MHC elements also crucially determines the extent of TCL lysis. Because of its capacity to enhance class I MHC antigen expression, IFN-gamma represents a key cytokine for determining the susceptibility of MiHA targets for lysis by TCL and clones, and in one patient an MiHA-specific clone recognized host leukemic cells and also inhibited host leukemic cell growth in a colony inhibition assay.

Bone Marrow Transplantation↗
PubMed1993

Hydroperoxide metabolism in rat liver. K+ channel activation, cell volume changes and eicosanoid formation.

Addition of t-butylhydroperoxide (0.2 mM) to isolated perfused rat liver led to a net K+ release of 7.2 +/- 0.2 mumol/g within 8 min and a net K+ reuptake of 6.6 +/- 0.4 mumol/g following withdrawal of the hydroperoxide, in line with earlier findings by Sies et al. [Sies, H., Gerstenecker, C., Summer, K. H., Menzel, H. & Flohé, R. (1974) in Glutathione (Flohé, L., Benöhr, C., Sies, H., Waller, H. D., eds) pp. 261-276, G. Thieme Publ. Stuttgart]. Net K+ release roughly paralleled the amount of GSSG released from the liver under the influence of the hydroperoxide. The t-butylhydroperoxide-induced K+ efflux was inhibited by approximately 70% in the presence of Ba2+ (1 mM), by 30% in Ca(2+)-free perfusions and was decreased by 50-60% when the intracellular Ca2+ stores were simultaneously depleted by repeated additions of phenylephrine. t-Butylhydroperoxide-induced K+ efflux was accompanied by a decrease of the intracellular water space by 58 +/- 14 microliter/g (n = 4), corresponding to a 10% cell shrinkage. The effect of t-butylhydroperoxide on cell volume was inhibited by 70-80% in the presence of Ba2+. In isolated rat hepatocytes treatment with t-butylhydroperoxide led to a slight hyperpolarization of the membrane at concentrations of 100 nM, but marked hyperpolarization occurred at t-butylhydroperoxide concentrations above 10 microM. t-Butylhydroperoxide (0.2 mM) transiently increased the portal-perfusion pressure by 3.3 +/- 0.6 cm H2O (n = 18), due to a slight stimulation of prostaglandin-D2 release under the influence of the hydroperoxide. In the presence of Ba2+ (1 mM), t-butylhydroperoxide increased the perfusion pressure by 12.7 +/- 1.2 cm H2O (n = 9) and produced an approximately tenfold increase of prostaglandin-D2 and thromboxane-B2 release. Under these conditions, glucose output from the liver rose from 0.9 +/- 0.03 to 2.9 +/- 0.7 mumol.g-1.min-1 (n = 4) with a time course roughly resembling that of portal-pressure increase and prostaglandin-D2 overflow. These effects were largely abolished in the presence of ibuprofen or the thromboxane-receptor-antagonist BM 13.177. The t-butylhydroperoxide effects on perfusion pressure, glucose and eicosanoid output were also enhanced in the presence of insulin or during hypotonic exposure; i.e. conditions known to swell hepatocytes, but not during hyperosmotic exposure. The data suggest that t-butylhydroperoxide induces liver-cell shrinkage and hyperpolarization of the plasma membrane due to activation of Ba(2+)-sensitive K+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Prognostic factors in medullary thyroid carcinoma: evaluation of 741 patients from the German Medullary Thyroid Carcinoma Register.

A retrospective study of 741 patients with medullary thyroid carcinoma diagnosed between 1967 and 1991 was carried out by members of the German Medullary Thyroid Carcinoma Study Group to evaluate prognostic factors. A total of 559 patients (75%) were considered to have sporadic disease, and 182 (25%) had the familial type. The sex ratio (male to female) was 1:1.4 in sporadic disease patients, and the mean age at diagnosis was 45.9 years (range 5-81 years). For familial disease patients the sex ratio was 1:1.1, and the mean age at diagnosis was 33.4 (range 5-77 years). The follow-up time for 630 patients ranged from 1 month to 20.8 years (mean 13.0 years). The overall adjusted survival rate was 86.7% at 5 years and 64.2% at 10 years. In a univariate analysis the stage of disease at diagnosis, age, sex, and type of disease (sporadic, familial) were relevant prognostic factors, with a better prognosis for young female patients with familial disease and diagnosed at an early stage. In a multivariate proportional hazards analysis, the difference in the survival rate of patients with familial disease versus those with the sporadic form disappeared, while prognostic information provided by age and sex was still significant. The poorer prognosis of patients with sporadic medullary thyroid carcinoma may be related to the patients' older age at detection and more advanced tumor stage at diagnosis. There seems to be no difference in biological behavior between tumors of the sporadic and those of the familial type.

Adolescent↗
PubMed1993

Cell shrinkage stimulates bradykinin-induced cell membrane potential oscillations in NIH 3T3 fibroblasts expressing the ras-oncogene.

In NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ ras) bradykinin leads to sustained oscillations of cell membrane potential due to oscillations of intracellular Ca2+ with subsequent activation of Ca(2+)-sensitive K+ channels. In cells not expressing the oncogene (-ras), bradykinin leads only to a single transient hyperpolarization of the cell membrane. The present study has been performed to elucidate the possible interaction of cell volume, intracellular pH and bradykinin-induced oscillations of the cell membrane potential. Bradykinin leads to cell shrinkage and intracellular alkalinization of both + ras cells and -ras cells. Inhibition of Na+/H+ exchanger by HOE 694 abolishes the bradykinin-induced alkalinization but does not significantly interfere with the bradykinin-induced oscillations of cell membrane potential. In contrast, prevention of bradykinin-induced cell shrinkage by simultaneous reduction of extracellular osmolarity blunts the oscillations. Thus, cell shrinkage stimulates bradykinin-induced oscillations of cell membrane potential. On the other hand, cell shrinkage alone does not elicit oscillations unless, in addition, Ca2+ entry is stimulated by ionomycin.

3T3 Cells↗
PubMed1993

Retrograde ascending aortic dissection: a diagnostic and therapeutic challenge.

Aortic dissection with an entrance tear in the transverse aorta is generally considered to have the highest acute fatality rate of any type of dissection and the direction of its extension is the most difficult to predict. In a prospective study, we evaluated 61 consecutive patients (mean age 56.7 years, ranging from 21 to 75 years), presenting with ascending aortic dissection during a 36-month-period and tried to clarify the incidence of retrograde ascending aortic dissection. In 49 patients (80.3%), the intimal tear was located in the ascending aorta, whereas the dissection originated in the transverse aorta in 12 patients (19.7%); in this latter group, extension was strictly retrograde in 5 patients and in both directions in 7 patients. Three patients died before operation; 58 patients underwent aortic replacement/repair under moderate hypothermia; if the primary tear extended into the transverse aorta or was not found in the ascending aorta, the aortic arch was explored during a brief period of deep hypothermic circulatory arrest. The overall operative mortality was 12.1% (7/58); it was 10.4% (5/48) in ascending aortic dissection and 20% (2/10) in dissection of the transverse aorta. Age (P < 0.005), concomitant coronary artery disease (P < 0.01) and the site of intimal tear (P < 0.01) were significant predictive factors of operative risk. A tear in the transverse aorta is almost always associated with retrograde dissection and may simulate dissection with the entrance tear in the ascending aorta. Localization of the entrance tear remains a diagnostic challenge in aortic dissection but Doppler-echocardiography had a high sensitivity in this series (96.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Association of mononuclear cells and eosinophils with airway resistance and responsiveness in rat pulmonary inflammatory responses.

To evaluate the association of various leukocytes with pulmonary resistance and methacholine responsiveness, we induced pulmonary eosinophil-rich inflammation in IgE-sensitized (ovalbumin) Sprague Dawley rats. Sensitized rats were challenged with either relevant (OA) or irrelevant antigen by tracheal insufflation a) with no other treatment, b) in conjunction with intravenous Sephadex beads pretreatment, or c) with antigen coupled covalently to Sepharose beads. About 24 h after antigen challenge, respiratory system resistance (Rrs), response to aerosolized methacholine, and pulmonary histopathology were evaluated. Challenge with OA, insufflation with Sepharose, and treatment with i.v. Sephadex all independently increased inflammatory cell infiltrates, but the combination of OA with the other agents did not significantly enhance the inflammatory response over OA alone. Interactive stepwise regression techniques were utilized to identify correlates for Rrs and methacholine responsiveness. Mononuclear cell score was a significant predictor (p < .01) for Rrs, and insufflation of Sepharose had a significant independent effect on Rrs (p = .01) above that predicted by mononuclear cell infiltrates. Conversely, eosinophil score and neutrophil score were not significant predictors for Rrs, and challenges with antigen or Sephadex had no significant independent effect on Rrs beyond that predicted from mononuclear cell infiltrates. Eosinophil score was the only significant histological predictor for methacholine responsiveness (p < .0001). Challenges with Sephadex, antigen and Sepharose did not significantly change methacholine responsiveness independently of the changes associated with eosinophil infiltrates. These findings suggest that mononuclear cells and eosinophils contribute to increases in airway resistance and responsiveness, respectively, following the induction of pulmonary inflammation by both allergic and non-allergic stimuli.

Airway Resistance↗