Impact of Retrograde Cerebral Perfusion on Ascending Aortic and Arch Aneurysm Repair

Purpose. The effect of retrograde cerebral perfusion on the incidence of stroke and death among patients undergoing repair of aneurysms of the ascending aorta and transverse arch was determined.

Material and Methods. Between January 1991 and March 1995, 161 patients were operated on for aneurysms of the ascending aorta and transverse arch. Thirty-three of the patients (20%) had an aneurysm of the ascending aorta only and 128 (80%) had aneurysms of both the ascending aorta and the transverse arch. All the patients underwent cardiopulmonary bypass, profound hypothermia, and circulatory arrest, and 120 (74%) also underwent retrograde cerebral perfusion. Median pump time was 143 minutes (range, 21 to 461 minutes). Median circulatory arrest time was 42 minutes (range, 8 to 111 minutes), and median myocardial ischemic time was 71 minutes (range, 14 to 306 minutes).

Results. The overall 30-day mortality rate was 6% (9 patients) and the incidence of stroke was 4% (7 patients). The use of retrograde cerebral perfusion demonstrated a protective effect against stroke (3 of 120 patients, or 3%) compared with no retrograde cerebral perfusion (4 of 41 patients, or 9%; odds ratio, 0.24; confidence interval, 0.06 to 0.99; p < 0.049). This was most significant in patients more than 70 years of age; none of the 36 elderly patients who received retrograde cerebral perfusion had a stroke, compared with 3 of the 13 (23%) who did not (p < 0.003). Only pump time was associated with an increased risk of stroke (odds ratio, 1.01; 95% confidence interval, 1.00 to 1.02; p < 0.005). Pump time also was associated with increased mortality (odds ratio, 1.01; 95% confidence interval, 1.00 to 1.02; p < 0.008).

Conclusion. Retrograde cerebral perfusion decreased the incidence of stroke in patients undergoing repair of aneurysms of the ascending aorta and transverse arch.     

A double-blind, placebo-controlled trial by the sublingual route of immunotherapy with a standardized grass pollen extract

Fifty-eight patients with well-documented history of seasonal rhinoconjunctivitis caused by grass pollens were allocated randomly on a double-blind basis to receive either sublingual therapy with a solution of purified, standardized allergen preparation (Stallergenes) or a matched placebo for 17 weeks. The assessment of the effect of oral immunotherapy, done with drops of five-grass allergen extract, was on the clinical symptoms and on the medication score of the authorized rescue treatments. The actively treated patients had significantly (P<0.05 to P<0.01) fewer symptoms of rhinitis (sneezing and rhinorrhea) and of conjunctivitis (redness and tears) during the pollen season than the placebo group. Consumption of nasal solution of sodium cromoglycate and of betamethasone and dexchlorpheniramine was significantly less in the desensitized group (P<0.01). Side-effects were negligible. This study concludes that perlingual immunotherapy with grass pollen extract in grass-pollen-sensitive seasonal hay fever and conjunctivitis patients is effective, easy to perform, inexpensive, and safe.     

Genotypic analysis in large cell lymphomas expressing a restricted set of differentiation antigens

Immunophenotyping and immunogenotyping were performed in a series of 8 large cell lymphomas exhibiting anaplastic or "histiocytic" morphology and displaying an uncertain phenotype due to a restricted number of differentiation antigens. 6 cases expressed the Ki-1 antigen. 4 cases expressed one or two B-cell markers and contained rearrangements of the immunoglobulin genes. One of them also exhibited a T-cell receptor (TCR) beta gene rearrangement. 3 cases expressed a single T-cell differentiation antigen. Among them, only 1 displayed both gamma and beta TCR gene rearrangement; 1 only contained a gamma TCR gene rearrangement and 1 completely lacked clonal rearrangements. The eight cases expressed an inconclusive immunophenotype due to an abundant population of reactive cells but showed an immunoglobulin gene rearrangement. In conclusion, 5 out of the 8 unusual lymphomas studied here could be characterized by immunogenotyping. This approach was, however, inconclusive in the 3 remaining cases, whose lineage and differentiation stage remain poorly defined.     

Hypoxia stimulates the release by bovine pulmonary artery endothelial cells of an inhibitor of pulmonary artery smooth muscle cell growth

The proliferation of smooth muscle cells (SMC) seen in hypoxic pulmonary hypertension is a poorly understood phenomenon but may involve endothelial cell (EC)-SMC interaction. Using bovine pulmonary artery cells, we examined the effect of O2 tension and the role of EC or media conditioned by EC (ECCM) on SMC proliferation. We found no difference in SMC proliferation under 3%, 10%, and 20% O2. EC, co-cultured with SMC in 3% O2, inhibited SMC proliferation consistently by about 40% (versus SMC exposed to hypoxia but not to EC). In normoxia, the degree of inhibition was dependent on EC:SMC ratio. In separate experiments, media from EC exposed to 3% or 20% O2 had a mitogenic activity of 24% and 42%, respectively (compared to 100% mitogenic activity with 5% FCS), on serum-deprived SMC. On the other hand, when SMC were stimulated to grow with FCS, an inhibitory activity (IA) from ECCM on SMC proliferation was observed and was significantly greater in hypoxic versus normoxic ECCM (40% versus 21%, respectively). Amicon concentration showed that the IA was contained in the less than 10 kD fraction of ECCM. Preliminary characterization of this IA indicates that it is unlike any of the known inhibitors of SMC growth, such as lactic acid, prostaglandin derivatives, or heparan sulfate. We conclude that hypoxia causes pulmonary artery EC to release a unique inhibitor of SMC growth.     

Effect of sensory stimulus on striatal dopamine release in humans and cats: a [(11)C]raclopride PET study

BACKGROUND: Sensory stimulation of the forelimb extremities constitutes a well-established experimental model that has consistently shown to activate dopamine (DA) neurotransmission in the mammals' forebrain. OBJECTIVES: To visualize in vivo this modification of striatal DA release in healthy human volunteers using Positron Emission Tomography (PET) and [(11)C]raclopride. Experiments in humans were paralleled by experiments in anesthetized cats. Changes in endogenous DA release were assessed through its competition with [(11)C]raclopride binding (BP(raclo)), a radioligand probing DA D2-receptors. RESULTS: In humans no significant difference of BP(raclo) in caudate (with sensory stimulation: 2.0 +/- 0.3 versus without sensory stimulation: 2.2 +/- 0.3; P = 0.3) or putamen (2.6 +/- 0.3 versus 2.6 +/- 0.2; P = 0.9) ipsilateral to the stimulus was disclosed as a result of sensory stimulation. Similarly, no change of BP(raclo) was observed contralaterally to the stimulation in the caudate nucleus (with sensory stimulation: 2.0 +/- 0.4 versus without sensory stimulation: 2.1 +/- 0.2; P = 0.5) and the putamen (2.5 +/- 0.4 versus 2.6 +/- 0.2; P = 0.4). In cats the same results were obtained in the ipsilateral to stimulation striatum (with sensory stimulation: 2.5 +/- 0.03 versus without sensory stimulation: 2.4 +/- 0.05; P = 0.7). No change was also observed contralaterally to the stimulation (2.4 +/- 0.04 versus 2.5 +/- 0.06; P = 0.6). The [(11)C]raclopride binding remained unchanged by sensory stimuli in both humans and cats. CONCLUSION: This suggests that the DA release induced by sensory stimulus is mostly extrasynaptic whereas the synaptic DA release is probably small, which fits well with the absence of [(11)C]raclopride displacement. The mechanism of this extrasynaptic DA release could be related to a local action of glutamate on dopaminergic terminals via a thalamo-cortico-striatal loop. Present results also underline homology between cat and human responses to sensory stimuli and validate the use of cat brain to find physiological concepts in humans.     

Rearrangement of the beta T-cell receptor gene in a monocytoid B-cell lymphoma

We describe an unusual case of monocytoid lymphoma displaying a rearrangement of the T-cell receptor beta-chain gene associated with a rearrangement of the immunoglobulin heavy-chain gene, and of the lambda light-chain gene. This lymphoma was morphologically similar to previous cases in the literature, and was clinically of low grade. The lymphoma expressed the lambda light chain, HLA-DR, CD21, and CD22. Though the B-cell lineage of this lymphoma seems very likely, the genotypic profile raises a cautionary note regarding the supposed high stage of differentiation of monocytoid lymphomas.     

Variation in the histological pattern of nodal involvement by gamma/delta T-cell lymphoma

AIMS: Gamma-delta (gammadelta) T-cell non-Hodgkin's lymphomas (NHLs) usually present with liver, spleen and marrow infiltration. Lymph node involvement by gammadelta T-cell NHL has been rarely documented so far; its histological pattern needs to be further defined. METHODS AND RESULTS: Two cases of nodal gammadelta T-cell NHL are reported: case 1, a 44-year-old man, presented with cytomegalovirus retinitis and superficial lymphadenopathies. Histological analysis of an inguinal lymph node showed complete destruction by a diffuse pleomorphic lymphoid proliferation, which was positive for CD2, CD3, CD43, CD45, TIA-1 and granzyme B, and displayed a gammadelta phenotype (deltaTCR1+, Vdelta1+, Vdelta2-, Vdelta3-, betaF1-). Bone marrow was normal. Case 2, a male 24-year-old patient with a history of renal transplantation, presented with hepatosplenomegaly and supraclavicular lymph node enlargement. Lymph node architecture was globally preserved. Peripheral sinuses contained scattered nests of medium-sized irregular lymphoid cells. Bone-marrow was infiltrated. Phenotype showed positivity for CD2, CD3, CD45 and TIA1 and expression of gammadelta TCR (deltaTCR1+, deltaV1+, deltaV2-, deltaV3-, betaF1-). Both patients died a short time after diagnosis. CONCLUSIONS: These observations suggest that at least two forms of nodal gammadelta T-cell NHL may be encountered: one mimicking classical alphabeta T-cell NHL, with diffuse pleomorphic cell proliferation, and one displaying sinusoidal neoplastic infiltration suggesting a close relationship with hepatosplenic gammadelta T-cell NHL.