Evaluation of placental oxygenation by near-infrared spectroscopy in relation to ultrasound maturation grade in physiological term pregnancies.

A prospective observational study (ClinicalTrial ID: NCT05771415) was conducted to compare placental oxygenation in low-risk, uncomplicated term pregnancies measured by near-infrared spectroscopy (NIRS) in relation to the placental maturity grade determined by ultrasound assessment according to the Grannum scale. We included 34 pregnancies divided into two groups according to placental maturation. For each pregnancy, measurements were taken at the site above the central part of the placenta (test) and at the site outside of the placenta on the lower abdomen (control). Student's t-test was used to compare tissue oxygenation index (TOI) values among the study groups. The normality of distribution was proven by the Kolmogorov‒Smirnov test. In women with low placental maturity grade, the mean TOI value above the placenta was 70.38 ± 3.72, which was lower than the respective value in women with high placental maturity grade (77.99 ± 3.71; p < 0.001). The TOI values above the placenta and the control site were significantly different in both groups (70.38 ± 3.72 vs 67.83 ± 3.21 and 77.99 ± 3.71 vs 69.41 ± 3.93; p < 0.001). The results offer a new perspective on placental function based on specific non-invasive real-time oxygenation measurements. Unfortunately, and because of technical limitations, NIRS cannot yet be implemented as a routine clinical tool.

Immunohistochemical Expression of Placental Vitamin D Receptors in Pregnancies Complicated by Early and Late-Onset Preeclampsia.

The aim of our study was to determine whether the immunohistochemical expression of placental vitamin D receptors is altered in pregnancies complicated by preeclampsia. Vitamin D receptor expression was immunohistochemically analysed in the placentas of three groups: a control group, and early- and late-onset preeclampsia groups. Total immunohistochemical intensity staining of placentas showed that the control group had a median vitamin D receptor (VDR) expression significantly higher than the placentas of mothers with early- and late-onset preeclampsia. There was no difference among the three groups in a semiquantitative analysis of VDR staining of the stroma only. Vitamin D receptors showed lower median expression in preeclampsia-affected pregnancies, especially early-onset preeclampsia. Therefore, Vitamin D receptor expression may be an important marker for normal placentation and preeclampsia onset.

Assessment of ovarian reserve after unilateral diathermy with thermal doses adjusted to ovarian volume.

Women with polycystic ovary syndrome seem to have a larger ovarian reserve. However, regardless of a greater reserve, diminished ovarian reserve has been reported after laparoscopic diathermy. The aim of this article was to determine whether the doses adjusted unilateral laparoscopic ovarian drilling with diathermy (ULOD) diminishes ovarian reserve to compare with bilateral laparoscopic ovarian drilling with diathermy (BLOD). Ninety-six women were assigned in two groups. One group underwent ULOD receiving thermal doses (0-840 J per ovary) adjusted to volume one ovary. The other group underwent BLOD receiving fixed doses (600 J per ovary). Ovarian reserve markers [anti-Müllerian hormone (AMH); antral follicle count (AFC) and ovarian volume] were measured before and after surgery (1 and 6 months). Both groups showed a decrease in AMH after surgery, but it was significantly more distinct in the BLOD versus ULOD group (2.0 ng/mL versus 1.3 ng/mL; p = 0.018) in the first follow-up month and remained significantly different through the sixth follow-up month (1.9 ng/mL versus 1.15 ng/mL; p = 0.023). In contrast, in the sixth month, the ULOD versus BLOD showed a significantly greater increase AFC (p < 0.001) and volume (p = 0.013). Our findings evidenced that the dose-adjusted unilateral diathermy (60 J/cm(3)) does not have significant and long-term effects on ovarian reserve.

Ovarian torsion in adolescent with chronic immune thrombocytopenia.

Ovarian torsions in adolescence are rarity, particularly bilateral, with mostly unknown etiology. Enlargement of the ovary contributes to torsion. Young girl presenting with abdominal pains, nausea and vomiting was for two days suspected and observed as gastroenteritis. By exclusion of gastroenteritis she was admitted for gynecological work-up. Ultrasound showed significantly enlarged right ovary, with tumor-like appearance. At the laparotomy, gynecologist found torsioned, necrotic ovary and ovariectomy was performed. Histology showed massive stromal bleeding (haemorrhage). Asymptomatic enlargement of remaining ovary occurred nine months after the ovariectomy. This enlargement was accompanied with platelets' fall and the possibility of repeated torsion impended. Thrombocytopenia was suspected from the first moment, but diagnosed after the surgery. Thrombocytopenia in adolescence requires additional attention as possible cause of intra-ovarian bleeding with consecutive enlargement and may lead to torsion. Oral contraceptives regulate dysfunctional bleeding, decrease ovarian volume and by so, may minimize risk of torsion. This strategy proved effective in the case we present.

Observation of increased venous gas emboli after wet dives compared to dry dives.

INTRODUCTION: Testing of decompression procedures has been performed both in the dry and during immersion, assuming that the results can be directly compared. To test this, the aim of the present paper was to compare the number of venous gas bubbles observed following a short, deep and a shallow, long air dive performed dry in a hyperbaric chamber and following actual dives in open water. METHODS: Fourteen experienced male divers participated in the study; seven performed dry and wet dives to 24 metres' sea water (msw) for 70 minutes; seven divers performed dry and wet dives to 54 msw for 20 minutes. Decompression followed a Bühlmann decompression procedure. Immediately following the dive, pulmonary artery bubble formation was monitored for two hours. The results were graded according to the method of Eftedal and Brubakk. RESULTS: All divers completed the dive protocol, none of them showed any signs of decompression sickness. During the observation period, following the shallow dives, the bubbles increased from 0.1 bubbles per cm ² after the dry dive to 1.4 bubbles per cm ² after the wet dive. Following the deep dives, the bubbles increased from 0.1 bubbles per cm ² in the dry dive to 2.4 bubbles per cm ² in the wet dive. Both results are highly significant (P = 0.0001 or less). CONCLUSIONS: The study has shown that diving in water produces significantly more gas bubble formation than dry diving. The number of venous gas bubbles observed after decompression in water according to a rather conservative procedure, indicates that accepted standard decompression procedures nevertheless induce considerable decompression stress. We suggest that decompression procedures should aim at keeping venous bubble formation as low as possible.

Glossopharyngeal insufflation induces cardioinhibitory syncope in apnea divers.

Apnea divers increase intrathoracic pressure voluntarily by taking a deep breath followed by glossopharyngeal insufflation. Because apnea divers sometimes experience hypotension and syncope during the maneuver, they may serve as a model to study the mechanisms of syncope. We recorded changes in hemodynamics and sympathetic vasomotor tone with microneurography during breath holding with glossopharyngeal insufflation. Five men became hypotensive and fainted during breath holding with glossopharyngeal insufflation within the first minute. In four divers, heart rate dropped suddenly to a minimum of 38 ± 4 beats/min. Therefore, cardioinhibitory syncope was more common than low cardiac output syncope.

Involuntary breathing movements improve cerebral oxygenation during apnea struggle phase in elite divers.

We investigated whether the involuntary breathing movements (IBM) during the struggle phase of breath holding, together with peripheral vasoconstriction and progressive hypercapnia, have a positive effect in maintaining cerebral blood volume. The central hemodynamics, arterial oxygen saturation, brain regional oxyhemoglobin (bHbO(2)), deoxyhemoglobin, and total hemoglobin changes and IBM were monitored during maximal dry breath holds in eight elite divers. The frequency of IBM increased (by approximately 100%), and their duration decreased ( approximately 30%), toward the end of the struggle phase, whereas the amplitude was unchanged (compared with the beginning of the struggle phase). In all subjects, a consistent increase in brain regional deoxyhemoglobin and total hemoglobin was also found during struggle phase, whereas bHbO(2) changed biphasically: it initially increased until the middle of the struggle phase, with the subsequent relative decline at the end of the breath hold. Mean arterial pressure was elevated during the struggle phase, although there was no further rise in the peripheral resistance, suggesting unchanged peripheral vasoconstriction and implying the beneficial influence of the IBM on the cardiac output recovery (primarily by restoration of the stroke volume). The IBM-induced short-lasting, sudden increases in mean arterial pressure were followed by similar oscillations in bHbO(2). These results suggest that an increase in the cerebral blood volume observed during the struggle phase of dry apnea is most likely caused by the IBM at the time of the hypercapnia-induced cerebral vasodilatation and peripheral vasoconstriction.

Changes in platelet size and spleen volume in response to selective and non-selective beta-adrenoceptor blockade in hypertensive patients.

1. The spleen contains approximately one-third of all the body's platelets. These platelets are relatively larger and haemostatically more active than platelets in the systemic circulation and can be released into the systemic circulation by stimulation of alpha-adrenoceptors or inhibition of beta-adrenoceptors. In the present study, we evaluated the effects of selective (bisoprol) and non-selective (carvedilol) beta-blockers agents on mean platelet volume (MPV) and spleen size in hypertensive patients at rest and after exercise. 2. Blood pressure, heart rate, platelet count, MPV and spleen volume were measured in 18 newly diagnosed hypertensive patients, as well as in nine healthy control subjects, subjected to treadmill exercise test at their first visit and, for the hypertensive group, after 15 and 30 days of treatment with the selective beta(1)-adrenoceptor antagonist bisoprolol 5 mg/day (n = 9) or the non-selective alpha(1)-, beta(1)- and beta(2)-adrenoceptor antagonist carvedilol 25 mg/day (n = 9). 3. Increases in resting MPV values with concomitant decreases in spleen volume were found after 15 and 30 days treatment with either bisoprolol or carvedilol. The pronounced decrease in splenic volume after exercise and the increased MPV and platelet counts seen at first visit were halved after 15 and 30 days of treatment with either drug. 4. We conclude that in hypertensive patients treated with either selective or non-selective beta-blockers, the spleen contracts and MPV increases, which may increase the risk of atherothrombosis.

Effects of indomethacin on cerebrovascular response to hypercapnea and hypocapnea in breath-hold diving and obstructive sleep apnea.

We tested whether breath hold divers (BHD) and obstructive sleep apnea (OSA) subjects had similar middle cerebral artery velocity (MCAV) responses to hypercapnea and hypocapnea. We analyzed changes in MCAV (cm/s) in response to hypocapnea and hyperoxic hypercapnea during placebo or after 90 min of oral indomethacin (100 mg) in BHD (N=7) and OSA (N=7). During control hypercapnea MCAV increased for 54.4% in BHD and 48.4% in OSA. Indomethacin blunted the MCAV increase in response to hypercapnea in BHD (P=0.02), but not in OSA. Indomethacin attenuated the mean arterial pressure response in BHD, but not in OSA. The blunted MCAV responses to hypercapnea with indomethacin in BHD, but not in OSA patients suggests that (a) the normal contribution of local vasodilating mechanisms to the cerebrovascular responses to hypercapnea is absent in OSA patients and (b) exposure to chronic/repeated apneas is not causal per se in limiting the contribution of vasodilating mechanisms to the cerebrovascular responses to hypercapnea in OSA.

Cardiovascular regulation during apnea in elite divers.

Involuntary apnea during sleep elicits sustained arterial hypertension through sympathetic activation; however, little is known about voluntary apnea, particularly in elite athletes. Their physiological adjustments are largely unknown. We measured blood pressure, heart rate, hemoglobin oxygen saturation, muscle sympathetic nerve activity, and vascular resistance before and during maximal end-inspiratory breath holds in 20 elite divers and in 15 matched control subjects. At baseline, arterial pressure and heart rate were similar in both groups. Maximal apnea time was longer in divers (1.7+/-0.4 versus 3.9+/-1.1 minutes; P<0.0001), and it was accompanied by marked oxygen desaturation (97.6+/-0.7% versus 77.6+/-13.9%; P<0.0001). At the end of apnea, divers showed a >5-fold greater muscle sympathetic nerve activity increase (P<0.01) with a massively increased pressor response compared with control subjects (9+/-5 versus 32+/-15 mm Hg; P<0.001). Vascular resistance increased in both groups, but more so in divers (79+/-46% versus 140+/-82%; P<0.01). Heart rate did not change in either group. The rise in muscle sympathetic nerve activity correlated with oxygen desaturation (r(2)=0.26; P<0.01) and with the increase in mean arterial pressure (r(2)=0.40; P<0.0001). In elite divers, breath holds for several minutes result in an excessive chemoreflex activation of sympathetic vasoconstrictor activity. Extensive sympathetically mediated peripheral vasoconstriction may help to maintain adequate oxygen supply to vital organs under asphyxic conditions that untrained subjects are not able to tolerate voluntarily. Our results are relevant to conditions featuring periodic apnea.

Effects of tetrahydrobiopterin on venous bubble grade and acute diving-induced changes in cardiovascular function.

INTRODUCTION: Self-contained underwater breathing apparatus diving reduces cardiovascular function and increases pulmonary artery pressure (PAP) up to 3 days after a single dive. Acute antioxidants partially attenuated arterial endothelial dysfunction, whereas cardiac and PA functions were unaffected. We tested the hypothesis that acute tetrahydobiopterin (BH(4)), as a cofactor of endothelial nitric oxide (NO) synthase, reduces bubble grade (BG) and attenuates alteration in cardiovascular function after diving because of increased NO bioavailability. MATERIALS AND METHODS: Mean PAP (mPAP), PA acceleration time and right ventricle ejection time, left ventricle ejection fraction (LV-EF) and BG were measured after oral placebo (P), vitamin C (C) or a combination of vitamin C and BH(4) (BH(4)) in a randomized, placebo controlled trial before and after field dive to 30 m of sea water for 30 min bottom time. RESULTS: Eight recreational divers performed three dives with a 3-days period between them. Regarding the primary hypothesis, no difference was observed between post-dive changes in BG (2.1 +/- 2.2 bubbles cm(-2) for P, 3.4 +/- 3.9 for C and 3.6 +/- 2.1 for BH(4)), mPAP (25.6 +/- 6.5 mmHg for P, 25.9 +/- 8.6 for C and 22.6 +/- 3.5 for BH(4)) and LV-EF (62.6 +/- 4.6% for P, 61.4 +/- 3.9 for C and 61.6 +/- 3.7 for BH(4)) with all three conditions. CONCLUSION: This suggests that co-administration of BH(4) and vitamin C does not improve heart and pulmonary artery function after diving.

Expression of endothelial selectin ligands on human leukocytes following dive.

The fact that impaired endothelial-dependent vasodilatation after scuba diving often occurs without visible changes in the endothelial layer implies its biochemical origin. Since Lewisx(CD15) and sialyl-Lewisx(CD15s) are granulocyte and monocyte carbohydrate antigens recognized as ligands by endothelial selectins, we assumed that they could be sensitive markers for impaired vasodilatation following diving. Using flow cytometry, we determined the CD15 and CD15s peripheral blood mononuclear cells of eight divers, 30 mins before and 50 mins after a single dive to 54 m for 20 mins bottom time. The number of gas bubbles in the right heart was monitored by ultrasound. Gas bubbles were seen in all eight divers, with the average number of bubbles/cm2 1.9+/-1.9. The proportion of CD15+monocytes increased 2-fold after the dive as well as the subpopulation of monocytes highly expressing CD15s. The absolute number of monocytes was slightly, but not significantly, increased after the dive, whereas the absolute number of granulocytes was markedly elevated (up to 61%). There were no significant correlations between bubble formation and CD15+monocyte expression (r=-0.56; P=0.17), as well as with monocytes highly expressing CD15s (r=0.43; P=0.29). This study suggests that biochemical changes induced by scuba diving primarily activate existing monocytes rather than increase the number of monocytes at a time of acute arterial endothelial dysfunction.

High-grade bubbles in left and right heart in an asymptomatic diver at rest after surfacing.

INTRODUCTION: Most decompression procedures induce the formation of asymptomatic venous gas bubbles. They can be classified as "silent bubbles," which are asymptomatic compared to paradoxical arterialization of venous gas emboli, which can lead to serious neurologic damage. The penetration of such gas bubbles into the arterial circulation is due to pulmonary barotrauma, intrapulmonary (I-P) passage after massive bubble formation ("chokes"), or intracardiac shunting. Venous gas bubbles can be monitored and graded with echocardiographic scanning. CASE: We believe this is the first case to be reported of a recreational diver who, after surfacing from a dive, developed grade 5 ("white-out") venous gas bubbles in the right heart with evidence of I-P shunt at rest without any symptoms of decompression sickness. Grade 4 gas bubbles were found on the left side of the heart, indicating significant I-P shunting even at rest. CONCLUSION: We observed venous bubbles crossing through the I-P shunt during post-dive recovery at rest in a diver who developed "white out" of venous bubbles. Previously, the maximum bubble grade 5 had been observed in experimental animals, but not in humans. Moreover, a significant bubble grade was found on the left side of the heart, indicating a need for further studies to investigate the mechanisms of post-dive changes in peripheral and central circulation.

Restoration of hemodynamics in apnea struggle phase in association with involuntary breathing movements.

Involuntary breathing movements (IBM) that occur in the struggle phase of maximal apneas produce waves of negative intrathoracic pressure. This could augment the venous return, increasing thereby the cardiac output and gas exchange, and release the fresh blood from venous pools of spleen and liver. To test these hypotheses we used photoplethysmography and ultrasound for assessment of hemodynamics and spleen size before, during and after maximal dry apneas at large lung volume in 7 trained divers. During the easy-going phase cardiac output was reduced about 40%, due to reduction in stroke volume and in presence of reduced inferior vena cava venous return, while the spleen contracted for about 60 ml. Towards the end of the struggle phase, in presence of intense IBM, the spleen volume further decreased for about 70 ml, while cardiac output and caval flow almost renormalized. In conclusion, IBM coincide with splenic volume reduction and restoration of hemodynamics, likely facilitating the use of the last oxygen reserves before apnea cessation.

Central chemoreflex sensitivity and sympathetic neural outflow in elite breath-hold divers.

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 +/- 1.2 diving fish-catching competitions and 76.4 +/- 14.6 apnea training sessions with the last apnea 3-5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO(2), and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO(2) to 60 Torr. Baseline MSNA frequency was 31 +/- 11 bursts/min in divers and 33 +/- 13 bursts/min in control subjects. Total MSNA activity was 1.8 +/- 1.5 AU/min in divers and 1.8 +/- 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO(2) increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

The increase in human plasma antioxidant capacity after red wine consumption is due to both plasma urate and wine polyphenols.

By using red wine, dealcoholized red wine, polyphenols-stripped red wine, ethanol-water solution and water, the role of wine polyphenols and induction of plasma urate elevation on plasma antioxidant capacity was examined in humans (n=9 per beverage). Healthy males randomly consumed each beverage in a cross-over design. Plasma antioxidant capacity (measured by ferric reducing antioxidant power, FRAP), ethanol, catechin and urate concentrations were determined before and 30, 60, 90, 120 and 180 min after beverage intake. Dealcoholized red wine and polyphenols-stripped red wine induced similar increase in FRAP values which represented nearly half the effect of the original red wine. This indicates that consumption of red wine involves two separate mechanisms in elevation of plasma FRAP values and both wine phenols and plasma urate contribute to that effect.

Antioxidant pretreatment and reduced arterial endothelial dysfunction after diving.

INTRODUCTION: We have recently shown that a single air dive leads to acute arterial vasodilation and impairment of endothelium-dependent vasodilatation in humans. Additionally we have found that predive antioxidants at the upper recommended daily allowance partially prevented some of the negative effects of the dive. In this study we prospectively evaluated the effect of long-term antioxidants at a lower RDA dose on arterial endothelial function. METHODS: Eight professional male divers performed an open sea air dive to 30 msw. Brachial artery flow-mediated dilation (FMD) was assessed before and after diving. RESULTS: The first dive, without antioxidants, caused significant brachial arterial diameter increase from 3.85 +/- 0.55 to 4.04 +/- 0.5 mm and a significant reduction of FMD from 7.6 +/- 2.7 to 2.8 +/- 2.1%. The second dive, with antioxidants, showed unchanged arterial diameter and significant reduction of FMD from 8.11 +/- 2.4 to 6.8 +/- 1.4%. The FMD reduction was significantly less with antioxidants. Vascular smooth muscle function, assessed by nitroglycerine (endothelium-independent dilation), was unaffected by diving. DISCUSSION: This study shows that long-term antioxidant treatment at a lower RDA dose ending 3-4 h before a dive reduces the endothelial dysfunction in divers. Since the scuba dive was of a similar depth and duration to those practiced by numerous recreational divers, this study raises the possibility of routine predive supplementation with antioxidants.

Spleen and cardiovascular function during short apneas in divers.

We investigated the spleen volume changes as related to the cardiovascular responses during short-duration apneas at rest. We used dynamic ultrasound splenic imaging and noninvasive photoplethysmographic cardiovascular measurements before, during, and after 15-20 s apneas in seven trained divers. The role of baroreflex was studied by intravenous bolus of vasodilating drug trinitrosan during tidal breathing. The role of lung volume was studied by comparing the apneas at near-maximal lung volume with apneas after inhaling tidal volume, with and without cold forehead stimulation. In apneas at near maximal lung volume, a 20% reduction in splenic volume (P = 0.03) was observed as early as 3 s after the onset of breath holding. Around that time the heart rate increased, the mean arterial pressure abruptly decreased from 89.6 to 66.7 mmHg (P = 0.02), and cardiac output decreased, on account of reduction in stroke volume. Intravenous application of trinitrosan resulted in approximately 6-mmHg decrement in mean arterial pressure, while the splenic volume decreased for approximately 13%. In apneas at low lung volume, the early splenic contraction was also observed, 10% without and 12% with cold forehead stimulation, although the mean arterial pressure did not change or even increased, respectively. In conclusion, the spleen contraction is present at the beginning of apnea, accentuated by cold forehead stimulation. At large, but not small, lung volume, this initial contraction is probably facilitated by downloaded baroreflex in conditions of decreased blood pressure and cardiac output.