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Biomedical subjects

G Ricard

Publications and source records attributed to G Ricard.

11 recordsLinked to original sources
PubMed2005

[1/1 nodo-ventricular conduction atrial flutter with amiodarone].

1/1 atrial flutter is a regularly described complication of class I anti-arrhythmics. It is, however, very rarely encountered with class III anti-arrhythmics because prolongation of the atrio-ventricular node refractory period prevents 1/1 nodo-ventricular conduction. There have only been seven cases of 1/1 atrial flutter with amiodarone reported in the literature. Here we describe a new case of 1/1 atrial flutter with amiodarone. Our case clearly illustrates not only the different pro-arrhythmic effects of amiodarone (prolongation of the flutter cycle, and infra-Hissian block) but also the pathophysiological mechanisms possible with 1/1 conduction (prolongation of the flutter cycle, considerable permeability of the AV node). It demonstrates the difficulties of diagnosing such a rhythm disturbance, and that it is sometimes poorly tolerated, as well as underlining the importance of early diagnosis (in this case by oesophageal recording). Preventive treatment of 1/1 flutter can include amiodarone, digitalis, a betablocker or a bradycardic calcium inhibitor.

Aged↗
PubMed2003

[Antenatal diagnosis of congenital left ventricular aneurysm].

Congenital aneurysm of the left ventricle is a rare condition of unknown origin, the main differential diagnosis of which is the diverticulum. The natural history of this pathology is well known in adults and adolescents, contrary to those forms diagnosed by foetal echocardiography. Based on a case of congenital left ventricular aneurysm diagnosed ante-natally and a review of the literature, the authors propose echocardiographic prognostic factors useful for prenatal management. Thus, early antenatal diagnosis, size and progression of the aneurysm, signs of antenatal cardiac failure, are poor prognostic factors and should be discussed during parent counselling.

Adult↗
PubMed2003

[Myocardial infarction revealing an antiphospholipid syndrome in a 27-year-old woman].

We report the case of a 27 year old woman, with no vascular risk factors other than moderate smoking, admitted for a first acute anterior myocardial infarction. Emergency coronarography detected an isolated thrombosis, localised at the level of the middle section of the anterior inter-ventricular artery in an otherwise normal coronary network. Angioplasty of the artery with direct stenting was performed successfully and the follow up was uncomplicated. The diagnosis of primary antiphospholipid syndrome was made on the association of a raised level of anti-cardiolipin antibodies and the absence of elements in favour of an associated connective tissue disorder.

Adult↗
PubMed2000

Nitric oxide, prostaglandins, and impaired cerebral blood flow autoregulation in group B streptococcal neonatal meningitis.

Impaired autoregulation of cerebral blood flow (CBF) contributes to CNS damage during neonatal meningitis. We tested (i) the hypothesis that cerebrovascular autoregulation is impaired during early onset group B streptococcal (GBS) meningitis, (ii) whether this impairment is regulated by vasoactive mediators such as prostaglandins and (or) nitric oxide (NO), and (iii) whether this impairment is preventable by specific and (or) nonspecific inhibitors: dexamethasone, ibuprofen, and Nomega-nitro-L-arginine, a NO inhibitor. Sterile saline or 10(9) colony-forming units (cfu) of heat-killed GBS was injected into the cerebral ventricle of newborn piglets. CBF autoregulation was determined by altering cerebral perfusion pressure (CPP) with balloon-tipped catheters placed in the aorta. GBS produced a narrow range of CBF autoregulation due to an impairment at the upper limit of CPP. We report that in vivo in the early stages (first 2 h) of induced GBS inflammation (i) GBS impairs the upper limit of cerebrovascular autoregulation; (ii) ibuprofen, dexamethasone, and Nomega-nitro-L-arginine not only prevent this GBS-induced autoregulatory impairment but improve the range of cerebrovascular autoregulation; (iii) these autoregulatory changes do not involve circulating cerebral prostanoids; and (iv) the observed changes correlate with the induction of NO synthase gene expression. Thus, acute early onset GBS-induced impairment of the upper limit of CBF autoregulation can be correlated with increases of NO synthase production, suggesting that NO is a vasoactive mediator of CBF.

Animals↗
PubMed1999

Deregulation of cyclooxygenase and nitric oxide synthase gene expression in the inflammatory cascade triggered by experimental group B streptococcal meningitis in the newborn brain and cerebral microvessels.

Group B Streptococcus (GBS) is the most common cause of neonatal sepsis and meningitis. Despite antibiotics, GBS in the newborn initiates a cascade of molecular and biological events leading to altered cerebral perfusion, blood-brain barrier disruption, cerebral edema, intracranial hypertension, neurological damage, and even death. Having previously shown that GBS infection impairs cerebral blood flow autoregulation and increases prostaglandin (PG) levels, we examined the regulation of some crucial inflammatory mediators (PGs, nitric oxide (NO), tumor necrosis factor-a) in the brain and cerebral microvessels (MVs) from newborn piglets. Cyclooxygenase (COX), the key enzyme in PG biosynthesis, exists in two isoforms, COX-1 and COX-2. Both may be directly induced by NO in a model of renal inflammation. Besides its neurotransmitter role, NO is a potent vasorelaxant whose production is catalyzed by at least three distinct nitric oxide synthases (NOS) (bNOS, ecNOS, iNOS). Western blot analyses showed that the newborn (4 day old) brain expressed lower levels of COX-1 (8-fold), COX-2 (20-fold), bNOS (12-fold), and ecNOS (5-fold) than in the 1 day old. MV showed approximately equal levels of COX-2, lower levels of COX-1 (4-fold), bNOS (5-fold), and higher levels of ecNOS (20-fold) in comparison to 4-day-old cerebral MV. A 4-day-old brain expressed lower levels of bNOS (5-fold), ecNOS (10-fold), and COX-1 (2-fold) than the 6-week-old pig. COX-2 protein was undetected in a 4-day-old pig brain, but present in great excess in MV. Purified MV showed lower ecNOS (14-fold), COX-1 (2-fold), and about equal levels of bNOS and COX-2 in comparison with MV from 6-week-old pigs. Reverse transcription polymerase chain reaction analyses confirmed these results. Treatment with noo-nitro-L-arginine (LNA), a NOS inhibitor, downregulated COX-1 expression in the newborn brain and both COX-1 and COX-2 cerebral MV expression. GBS infection (10(9) colony-forming units, 0.5 mL intracerebroventricular) of sedated newborn piglets induced the expression of tumor necrosis factor-alpha in the cerebrospinal fluid after 2 hours, upregulated bNOS expression in both brain and MVs, upregulated ecNOS in MVs, and downregulated COX-1, COX-2, and ecNOS in the brain. GBS did not trigger the expression of iNOS. Our data suggest that there is a net deficiency of NOS isoforms in the immature brain and microvasculature of the 4-day-old piglet and that the differences in expression lead to the immature control of NO and PG production, rendering newborns particularly susceptible to neurological damage because of the undeveloped nature of their response mechanisms. Moreover, the GBS-induced cascade deregulates the gene expression of interacting inflammatory mediators and may cause a net vasoconstrictor/vasodilator imbalance, leading to cerebral hypertension and edema in the early stages of infection. Pharmacological manipulations of the inflammatory cascade could lead to novel therapeutic approaches for the treatment of GBS meningitis.

Animals↗
PubMed1998

Plasmodium yoelii: identification of rhoptry proteins using monoclonal antibodies.

Thirteen monoclonal antibodies, obtained after immunization of mice with Plasmodium yoelii schizonts, were selected using immunofluorescence assay: they all presented typical fluorescence patterns of rhoptries. This antigen localization was confirmed by immunoelectron microscopy. The molecular weights of the recognized antigens are 68, 80, 105, 130 and 140 kDa as determined by immunoprecipitation and immunoblot under reducing and nonreducing conditions. These values are very similar to these of the low and high molecular weight complex components of Plasmodium falciparum. Furthermore, these antigens are soluble like P. falciparum rhoptry proteins. Interestingly, our monoclonal antibodies also reacted with two other Plasmodium species (Plasmodium berghei NKK173 strain and P. yoelii nigeriensis 798 VK strain), giving sometimes more complex labeling with apical, membranous, nuclear, or/and cytoplasmic localizations. Finally, none of the monoclonal antibodies stained the rhoptries of P. falciparum FCCE-1/Niger strain.

Animals↗
PubMed1995

Biochemical mediators of meningeal inflammatory response to group B streptococcus in the newborn piglet model.

The meningeal inflammatory response to a heat-killed mutant unencapsulated strain of type III group B Streptococcus (GBS) was studied in a newborn piglet model. GBS (10(9) colony-forming unit equivalents) or saline (control) was inoculated intraventricularly. Serial cerebrospinal fluid measurements were done at baseline and over the course of the next 24 h for cytochemical changes and production of tumor necrosis factor (TNF) and prostaglandins. In separate experiments, we defined the time course of early changes during the first 6 h and dose response relationship over a range of inocula 10(6) to 10(9) colony-forming unit equivalents. The intraventricular inoculation of the heat-killed unencapsulated GBS induced marked leukocytosis and increased protein by 6 h. These changes were preceded by a several hundredfold increase in TNF (maximum at 2 h) and prostaglandins (maximum at 2-4 h). The early and sharp rise in TNF suggests its pivotal role in initiating the inflammatory cascade. The magnitude of the inflammatory response increased with increasing bacterial dose over the range studied. To study the effect of encapsulation of GBS in the induction of meningeal inflammation, we compared the response to the unencapsulated mutant strain with that to the encapsulated parent strain. The encapsulated strain produced much smaller inflammatory changes, and only with high doses of bacteria. The GBS cell wall appeared to be the primary bacterial product triggering inflammation. Intraventricular injection of the heat-killed unencapsulated GBS with exposed cell wall can serve as a valid model for studying neonatal meningitis.

Animals↗
PubMed1991

[Mastication and the electromyographic silent period in denture wearers].

The purpose of this study is to compare the masticatory efficiency and the physiological activity of masticatory muscles among patients with removable partial dentures (R.P.D.) and patients with natural dentition. The masticatory efficiency is assessed from the duration of chewing sequences for various foods, from the first masticatory cycle to the swallowing. The physiological activity is tested by the duration of the inhibition reflex called the "silent period" (S.P.) obtained upon each muscle examined: 29 subjects are examined, 24 of them had a R.P.D.; they were divided into four groups according to the extent of their edentation; 5 control subjects have full natural dentition. The study is performed using global electromyography of the two masseter muscles and the two anterior temporal muscles. The mastication of the control subjects appears to have a regular alternance of working potential and periods of rest. The duration of the chewing sequences is determined by the nature of the food, brief for soft food, long for hard food. The mastication of patients with R.P.D. appears more irregular with a lengthening of active phases. The duration of chewing sequences is significantly longer for the control subjects. The duration of the S.P. is 19-21 milliseconds for the masseter muscles of the patients with dentures and the control patients, and 20-22 milliseconds for the temporal muscles for the same individuals. The differences of the S.P. durations between control subjects and patients with R.P.D. is never significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Augmentation cystoplasty in rats: development of an animal model.

An animal model of the Long-Evans species of rats was developed to study the short-term and long-term effects of enterocystoplasty. Various enterocystoplasties were performed in 39 rats, including ileal in 29, colonic in 5 and gastric in 5. The followup period was 3 months. Frequency and pattern of voiding, 24-hour urinary collection for mucus production, and blood and urinary electrolytes were analyzed. All voiding parameters, renal function and biochemical studies remained normal. Mucus production was higher in the gastrocystoplasty and colocystoplasty than in ileocystoplasty cases. Postmortem histopathological examination of the enteropatch was performed, which showed urothelialization of the graft with native transitional epithelium extending over the junctional margin of the graft and covering the enteropatch mucosa. The enteropatch muscle orientation was maintained in all 3 types of grafts. We believe that the Long-Evans species of rats is a good model for the study of enterocystoplasty.

Animals↗
PubMed1977

Back stabilization during knee strengthening exercise.

Twenty normal women were tested for maximal isometric contraction of the right knee extensor muscles. The knee was positioned in 60 degrees of extension and the hip at 120 degrees of extension, with and without a backrest. The purpose of the study was to determine whether the use of a backrest resulted in greater force than when not using a backrest when the angle of back inclination was held constant and the support was varied. The results indicated that the addition of a backrest, when the body assumes an optimal position, enables the knee extensors to generate greater force then when no backrest is used. A backrest adds to the comfort and support of the subject performing resistive knee exercise and should be incorporated into the design of knee exercise units.

Adult↗