Measurement TechniquesNon-invasive quantification of diaphragm kinetics using m-mode sonography Purpose: The standard conditions of spirometry (i.e., wearing a noseclip and breathing through a mouthpiece and a pneumotachograph) are likely to alter the ventilatory pattern. We used "time-motion" mode (M-mode) sonography to assess the changes in diaphragm kinetics induced by spirometry during quiet breathing.Methods: An M-mode sonographic study of the right diaphragm was performed before and during standard spirometry in eight pa~ents without respiratory disease (age 34 to 68 yr).Results: During spirometry, the diaphragm inspiratory amplitude (DIA) increased from 1.34 + 0.18 cm to 1.80 + 0, 18 cm (P = 0,007), whereas the diaphragmatic inspiratory time (T, diaph) increased from 1.27 -+_ 0.15 to 1.53 + 0.23 sec, (P = 0.015), without change in diaphragmatic total time interval (-I-tot diaph). Therefore, the diaphragm duty cycle (T, diaph /Ttot diaph) increased from 38% +--I% to 44% _ 496 (P = 0.023). The diaphragm inspiratory (DIV) and expiratory (DEV) motion velocity increased (P = 0.007).Conclusion: M-mode sonography enabled us to demonstrate that the wearing of a nose clip and breathing through a mouthpiece and a pneumotachograph induce measurable changes in diaphragm kinetics.Object-if : Les conditions de la spirom&ne standard (c.-,~-d. le port du pince-nez et la respiration ~ travers un embout buccal et un pneumotacographe) sont susceptibles d'altErer la morphologie de la ventilation. Nous avons utilisE le mode ~temps-amplitude,, (mode M) de la sonographie pour 6valuer les changements de la cinEtique diaphragmatique provoquEs par la spiromEtne pendant la respiration de repos.R~sultats : Pendant la spiromEtrie, I'amplitude inspiratoire diaphragmataque augmentait de 1,34 + 0, 18 ~ 1,80 +-0, 18 cm (P = 0,007), alors que le temps diaphragmatique inspiratoire (T, diaph) augmentmt de 1,27 _+ 0, I 5 ,~ 1,53 z 0,23 sec (P = 0,015), sans changement du temps diaphragmatique total (Trot diaph). Par consequent, le temps de I'activitE diaphragmatique (T, diaph/Ttot diaph) augmentait de 38 +_ I 96 ,~ 44 + 496 (P=0,023). La v41ocit4 de I'amplitude inspiratolre et expiratoire augmentait (P = 0,007).Conclusion : La sonographie en mode M nous a permis de dEmontrer que le port du pince-nez et la respiration h travers un embout buccal et un pneumotacographe provoquent des changements tangibles de la cin4tique diaphragmatique.From the

Thirty-nine consecutive patients with consolidated lung confirmed radiologically underwent sonography, and their sonograms were compared with results for 100 healthy subjects. The hyperechoic line of normal aerated lung and its air artifacts showed respiratory motions ("gliding sign," n = 100). Patients with pneumonia demonstrated distinct sonographic patterns. Strong linear echoes with characteristic air artifacts (air bronchogram) and anechoic tubular structures (fluid bronchogram) were visualized in 36 of 39 patients (92.30%). The superficial lung showed a homogeneous hypoechoic band termed "superficial fluid alveolograms" (n = 39) with respiratory motions in 35 of 39 patients. We conclude that sonography can evaluate pulmonary consolidation and may provide additional roentgenographic information, especially when fluid bronchograms are visualized.

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Ultrasonography is considered to have limited application in respiratory diseases because air reflects sound waves. Twenty-four patients with radiologically confirmed pneumothorax and 100 healthy subjects underwent sonography. In all normal subjects, the hyperechoic pulmonary interface showed respiratory motions termed the "gliding sign" with some comet-tail artifacts. Sonographic signs were shown in all pneumothoraces: disappearance of the gliding sign and no comet tails. The extent of collapse cannot be evaluated, but it is possible to determine its area in partial pneumothorax (N = 5). The follow-up (N = 8) showed the reappearance of the gliding sign. Ultrasonography may be helpful in diagnosing pneumothorax in certain cases.

Background: Behavioral addiction is an emerging concept based on the resemblance between symptoms or feelings provided by drugs and those obtained with various behaviors such as gambling, etc. Following an observational study of a tango dancer exhibiting criteria of dependence on this dance, we performed a survey to assess whether this case was unique or frequently encountered in the tango dancing community. Methods: We designed an online survey based on both the DSM-IV and Goodman's criteria of dependence; we added questions relative to the positive and negative effects of tango dancing and a self-evaluation of the degree of addiction to tango. The questionnaire was sent via Internet to all the tango dancers subscribing to “ToutTango”, an electronic monthly journal. The prevalence of dependence was analyzed using DSM-IV, Goodman's criteria and self-rating scores separately. Results: 1,129 tango dancers answered the questionnaire. Dependence rates were 45.1, 6.9 and 35.9%, respectively, according to the DSM-IV, Goodman's criteria and self-rating scores. Physical symptoms of withdrawal were reported by 20% of the entire sample and one-third described a strong craving for dancing. Positive effects were high both in dependent and non-dependent groups and were markedly greater than negative effects. Long practice of tango dancing did not modify the dependence rate or reduce the level of positive effects. Conclusions: Tango dancing could lead to dependence as currently defined. However, this dependence is associated with marked and sustained positive effects whilst the negative are few. Identifying the precise substratum of this dependence needs further investigation.

The value of sonography in lung diseases such as sarcoidosis is not established. Twelve patients with pulmonary sarcoidosis and eight control subjects underwent a sonographic examination using a high frequency probe (7.5 MHz). The normal lung surface showed smooth and regular hyperechoic patterns, respiratory motions, and occasionally minute interruptions with comet tails. All patients with sarcoidosis showed various surface abnormalities, which appeared irregular and rough with coarse interruptions, producing an increase of artifacts. Nodular patterns were found in nine of 12 patients (75%). Sonography also revealed abnormalities not diagnosed by chest radiographs (n = 2). These findings could offer an complementary approach for evaluating sarcoidosis.

SUMMARY The acute effect of the orally-active converting enzyme inhibitor, captopril, was compared to that of saralasin in 13 patients with rations forms of hypertension on ad libitum sodium intake. A significant difference between the effects of the two drugs on mean arterial pressure (MAP) was found ( -11 ± 3 mm Hg with saralasin, -2 4 ± 4.5 mm Hg after captopril). This difference was not correlated with control plasma renin activity (PRA). To determine the influence of the endogenous kallikrein-kinin system in the antibypertensive action of captopril, the effect of aprotinln (Apro), an inhibitor of kinin generation, on the MAP level achieved by captopril was assessed in five normal subjects and 15 patients with hypertension on ad libitum sodium intake. In normal subjects, captopril did not alter MAP, nor did Apro have any effect. In six patients with essential hypertension and normal PRA, MAP decreased by 5.5 ± 2 mm Hg following captopril, and Apro did not modify this level. In nine patients with renorascular hypertension (RVH), MAP fell by 22 ± 3 mm Hg after captopril administration, and Apro infusion induced a rise in MAP of 13 ± 1.7 mm Hg. A positive correlation between log control PRA and the effect of aprotinin was obtained (r = 0.63, p < 0.005). Apro had no effect in two patients with RVH who experienced a large drop in MAP during salasin.These results suggest that endogenous kinins as well as other substances, the generation of which is inhibited by aprotinin, may participate to the antihypertensire effect of captopril in patients with angiotensin-dependent hypertension. The lack of an aprotinin effect on the MAP level achieved during saralasin infusion suggests that the influence of the kallikrein-kinin system is related to the effect of captopril rather than the fall in arterial pressure resulting from angiotensin blockade. have permitted a rational approach of the role of the system in cardiovascular homeostasis; however, they do not share a single action (i.e., inhibition of angiotensin II). Saralasin, the widely used angiotensin II analog acting at the receptor level, displays partial agonistic activity in some circumstances, l -* while converting enzyme blockers also inhibit kininase II, the major degradation enzyme of circulating kinins, 1 and potentiate the vasodilating effect of kinins. Received December 19, 1979; revision accepted April 21, 1980. pressure induced by SQ 20,881 was associated with a rise in plasma bradykinin level in patients with normoreninemic essential hypertension, thus suggesting an influence of kinins on the antihypertensive effect of SQ 20,881. Nevertheless, no evidence for a vasodilatating effect of this increase in circulating bradykinin has been provided to date. The present studies aimed at showing that captopril, the orally active inhibitor of angiotensin-converting enzyme (SQ 14,225, D-3-mercapto-2-methylpropanoyl-L-proline),* 1 • has a more pronounced antihypertensive effect than saralasin. Moreover, to investigate the potential contribution of the kallikrein-k...