Jean-Claude Pourny

Detection of the fluorescence of GI vessels in rats using a CCD camera or a near-infrared video endoscope

BACKGROUND Choroidal near-infrared fluorescent angiography can detect vessels in the eye with high resolution. Observation of fluorescent gastrointestinal (GI) vessels by endoscopy may be useful in portal hypertension and bleeding ulcer. We here describe a technique for the detection of fluorescent GI vessels with a CCD camera or a near-infrared video endoscope. METHODS Laparotomy was performed on rats. A tissue target was excited by means of a laser diode. We took pictures of tissue under both white and near-infrared light, both before and after intravenous injection of indocyanine green. Fluorescent light was selected by means of filters placed in front of the lens of a CCD camera or a near-infrared video endoscope. RESULTS Under near-infrared light and after dye injection, we observed fluorescent vessels in real time and distinguished arterial from venous fluorescence. CONCLUSIONS This device permits visualization of GI vessels, which could be useful for diagnosis of vascular abnormalities during endoscopy and surgery.

Effect of beta adrenoceptors and thyroid hormones on velocity and acceleration of peripheral arterial flow in hyperthyroidism.

Brachial artery flow patterns were studied in 10 hyperthyroid and 10 normal subjects. Mean blood velocity and flow were evaluated by pulsed Doppler, and peak systolic acceleration was calculated by computer-assisted digitization of the instantaneous velocity curve. Compared to control subjects, hyperthyroid patients had higher velocity and flow (p less than 0.01, p less than 0.02) and higher peak systolic acceleration (p less than 0.01). In hyperthyroid patients, measurements were repeated after (1) mechanical exclusion of the hand from brachial circulation, (2) short-term beta-blocker treatment and (3) inducement of the euthyroid state. Exclusion of the hand reduced velocity and flow (p less than 0.001) but did not change peak systolic acceleration. Beta blockade induced disparate changes of velocity and flow but reduced peak systolic acceleration (p less than 0.05). In the euthyroid state, decreased blood velocity (p less than 0.01), flow (p less than 0.02) and acceleration (p less than 0.02) were observed. A hyperkinetic arterial circulation consisting of an increase in both velocity and acceleration is thus observable in hyperthyroidism. Hand exclusion showed that velocity seems to be influenced by peripheral factors while beta blockade suggests that acceleration is dependent of beta 1 adrenoceptors. Comparison between euthyroidism and hyperthyroidism indicates that both mean blood velocity and peak systolic acceleration are influenced by thyroid hormones.

Influence of dietary polyunsaturated fatty acids on contractility, lusitropy and compliance of isolated rat myocardium

Two groups of 15 rats were fed for 4 weeks with diets containing 15% by weight of fat varying in polyunsaturated fatty acids (PUFA) content and type. Diet C18:2 (n-6) contained 20% of total fatty acids as linoleic acid and small amount of (n-3) PUFA (0.4% of the total fatty acids). Diet LC (n-3) contained the same amount of 18:2 (n-6) and of long chain (n-3) C20 and C22 PUFA (10% of the total fatty acids). Contents of both saturated fatty acids and amount of total PUFA were kept constant in the two diets. Left ventricular papillary muscle mechanics were studied blind at Lmax and over the entire load-continuum, in terms of inotropy, characteristics of the force-velocity relationship, relaxation and compliance. Inotropy, force-velocity relationships and muscle compliance were similar in both groups. There was a trend towards a lower peak lengthening velocity at preload in the LC (n-3) group (P = 0.10) together with an unchanged peak rate of isometric force decline. This resulted in a significant impairment of the two mechanical indexes testing the load dependence of myocardial relaxation (P = 0.019 and P = 0.002). In conclusion, short-term differences in PUFA regimen were associated with an unchanged myocardial contractility and economy of force generation. The decreased load dependence of relaxation together with unchanged myocardial compliance strongly favored a physiological relevance of the previously reported modifications of sarcoplasmic reticulum phospholipid composition and calcium transport under (n-3) PUFA regimen.

Lusitropic effect and modifications of contraction-relaxation coupling induced by α-adrenergic stimulation in rat left ventricular papillary muscle

Phenylephrine (PE) and metaraminol (MR) were studied alone at 2 x 10(-5) M and at 4 x 10(-5) M respectively. These drugs were also used both in the presence of either propranolol (PR) at 4 x 10(-7) M (PE/PR and MR/PR groups) or prazosin (PZ) at 2 x 10(-7) M (PE/PZ and MR/PZ groups). Specific alpha-adrenergic stimulation (AS) was induced in the PE/PR and MR/PR groups. These AS were evaluated in isotonic and isometric conditions on rat left ventricular papillary muscle. Peak shortening velocity (Vcmax) and peak lengthening velocity (Vrmax) were calculated from the twitch with preload only. Positive (+dF/dtmax) and negative (-dF/dtmax) peak derivative forces were calculated from the isometric twitch. Two coefficients R1 and R2 were used to measure the coupling between contraction and relaxation at low and heavy load, respectively: R1 = Vcmax/Vrmax and R2 = (+dF/dtmax)/(-dF/dtmax). In all groups, there was a significant positive inotropic effect. As compared to control values before AS, R1 significantly decreased in all groups, (PE/PR: -15%; MR/PR: -18%; PE/PZ: -8%; MR/PZ: -23%; PE: -19%; MR: -32%). On the other hand, R2 significantly decreased only in three groups (PE/PZ: -5.4%; MR/PZ: -16.5%; MR: -12.0%) whereas it did not significantly change in the three other groups (PE/PR; MR/PR; PE). In all groups, and at low load, Vrmax increased more than Vcmax (positive relaxant effect i.e. R1 decreased). At heavy load, despite the positive inotropic effect, there was no significant relaxant effect after predominent alpha-AS. These results indicate that alpha-AS modified the coupling between contraction and relaxation differently, depending on the level of load.

The effects of gadolinium, a stretch-sensitive channel blocker, on diaphragm muscle

Stretch-activated channels (SAC) have been identified in many cell types including striated muscles. In diaphragm muscle, the influence of SAC on the length-active tension relationship remains unknown. Patch clamp experiments were performed on single fibres (n = 10). In isolated diaphragm muscle from adult hamsters, the effects of gadolinium (Gd3+), the most potent inhibitor of SAC blocker, on tension response to stretch at baseline were studied (n = 10), after pretreatment of the muscle with 1 nmol isoproterenol (n = 10), 0.5 micromol forskolin (n = 6), or 0.1 mmol dibutyryl cyclic adenosine monophosphate (cAMP) (n = 10). Results were compared to those obtained in low [Na+]e (n = 10), Ca2+-free medium (n = 6) or after 5 micromol nifedipine (n = 8). Gd3+ reduced active tension measured over a range of initial muscle lengths in a concentration-dependent manner (10 and 50 micromol). In isolated fibres, mechanical stretch generated a membrane current that was sensitive to Gd3+. In muscles, lowering [Na+]e mimicked the effects of Gd3+, while no change in the length-tension relationship was observed in Ca2+-free medium or after nifedipine. Drugs which increase cAMP prevented the effects of Gd3+ on active tension. In the diaphragm, gadolinium-sensitive channels are activated during physiological changes in length and influence tension development. Moreover, cyclic adenosine monophosphate content modulates the effects of gadolinium on stretch-activated channels.

Myocardial effects of early therapy with perindopril during experimental cardiomyopathy

The effects of chronic angiotensin-converting enzyme (ACE) inhibition on intrinsic myocardial contractility of the failing myocardium have been poorly documented. In the present study, inotropy, lusitropy, and economy of force generation were studied in vitro in papillary muscles from cardiomyopathic Syrian hamster (CSH) under early perindopril therapy, i.e., therapy begun at a stage when experimental heart failure was not yet observed. One-month-old CSH from the dilated strain Bio 53.58 were randomly treated over a 5-month period with either the ACE inhibitor perindopril 1 mg/kg/day (n = 11) or placebo (n = 11), and 7 age-matched controls were given placebo. Compared with control, placebo had a lower maximum shortening velocity (Vmax) (p < 0.01) and normalized total force (p < 0.05), and a lower curvature of the force-velocity relationship (p < 0.01). It has been shown that the higher the value of the curvature, the better the myothermal economy of force generation. Compared with placebo, perindopril had a 68% inhibition of plasma ACE activity and a greater Vmax (p < 0.05), whereas total force/mm2 was similar. This resulted in a lesser decrease of the curvature compared to control (p < 0.05). Placebo had a decreased peak lengthening velocity and rate of force decline. However, compared to control, no intrinsic abnormalities of the relaxation phase were observed in either placebo or perindopril when relaxation parameters were corrected for the lower systolic performance.(ABSTRACT TRUNCATED AT 250 WORDS)