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Biomedical subjects

Ivan Palada

Publications and source records attributed to Ivan Palada.

11 recordsLinked to original sources

The effects of acute oral antioxidants on diving-induced alterations in human cardiovascular function.

Diving-induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non-randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow-mediated dilatation (FMD) and heart function with increased mean PAP. Twenty-four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P = 0.005), while right ventricle ejection fraction (RV-EF), left ventricle EF and endocardial fractional shortening were reduced much less (approximately 2-3%). At the same time RV end-systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post-dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24-48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.

Administration, Oral↗

Increased pulmonary vascular resistance and reduced stroke volume in association with CO2 retention and inferior vena cava dilatation.

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO(2) and O(2) were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO(2) increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (approximately 4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO(2) retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.

Adaptation, Physiological↗

A single open sea air dive increases pulmonary artery pressure and reduces right ventricular function in professional divers.

After decompression from dives, bubbles are frequently observed in the right ventricular outflow tract and may lead to vascular damage, pulmonary arterial hypertension and right ventricular overload. No data exist on the effect of open sea diving on the pulmonary artery pressure (PAP). Eight professional divers performed an open sea air dive to 30 msw. Before and postdive a Doppler echocardiographic study was undertaken. Systolic pulmonary artery pressure (SPAP) was estimated from measurement of peak flow velocity of the tricuspid regurgitant jet; the ratio between pulmonary artery acceleration times (AccT) and right ventricular ejection time (RVET) was used as an estimate of the mean PAP. No evidence of either patent foramen ovale or intra-pulmonary shunt was found in any subject postdive after performing a Valsalva maneuver. SPAP increased from 25 +/- 3 to 33 +/- 2 mmHg and AccT/RVET ratio decreased from 0.44 +/- 0.04 to 0.3 +/- 0.02 20 min after the dive, respectively. Pulmonary vascular resistance increased from 1.2 +/- 0.1 to 1.4 +/- 0.1 Woods Units. Postdive right ventricle end-diastolic and end-systolic volumes were increased for about 19% (P = 0.001) and 33% (P = 0.001) and right ejection fraction decreased about for 6% (P = 0.001). Cardiac output decreased from 4.8 +/- 0.9 (l min(-1)) to 4.0 +/- 0.6 at 40 min postdive due to decreases in heart rate and stroke volume. This study shows that a single open sea dive may be associated with right heart overload due to increased pressure in the pulmonary artery.

Adult↗

Red wine induced modulation of vascular function: separating the role of polyphenols, ethanol, and urates.

By using red wine (RW), dealcoholized red wine (DARW), polyphenols-stripped red wine (PSRW), ethanol-water solution (ET), and water (W), the role of wine polyphenols, ethanol, and urate on vascular function was examined in humans (n = 9 per beverage) and on isolated rat aortic rings (n = 9). Healthy males randomly consumed each beverage in a cross-over design. Plasma ethanol, catechin, and urate concentrations were measured before and 30, 60 and 120 minutes after beverage intake. Endothelial function was assessed before and 60 minutes after beverage consumption by normalized flow-mediated dilation (FMD). RW and DARW induced similar vasodilatation in the isolated vessels whereas PSRW, ET, and W did not. All ethanol-containing beverages induced similar basal vasodilatation of brachial artery. Only intake of RW resulted in enhancement of endothelial response, despite similar plasma catechin concentration after DARW. The borderline effect of RW on FMD (P = 0.0531) became significant after FMD normalization (P = 0.0043) that neutralized blunting effect of ethanol-induced basal vasodilatation. Effects of PSRW and ET did not differ although plasma urate increased after PSRW and not after ET, indicating lack of urate influence on endothelial response. Acute vascular effects of RW, mediated by polyphenols, cannot be predicted by plasma catechin concentration only.

Adult↗

Exogenous nitric oxide and bubble formation in divers.

PURPOSE: Prevention of bubble formation is a central goal in standard decompression procedures. Previously we have shown that exercise 20-24 h prior to a dive reduces bubble formation and increases survival in rats exposed to a simulated dive. Furthermore, we have demonstrated that nitric oxide (NO) may be involved in this protection; blocking the production of NO increases bubble formation while giving rats a long-lasting NO donor 20 h and immediately prior to a dive reduces bubble formation. This study determined whether a short-lasting NO donor, nitroglycerine, reduced bubble formation after standard dives and decompression in man. METHODS: A total of 16 experienced divers were randomly assigned into two groups. One group performed two dives to 30 m of seawater (msw) for 30 min breathing air, and performed exercise at an intensity corresponding to 30% of maximal oxygen uptake during the bottom time. The second group performed two simulated dives to 18 msw for 80 min breathing air in a hyperbaric chamber, and remained sedentary during the bottom period. The first dive for each diver served as the control dive, whereas the divers received 0.4 mg of nitroglycerine by oral spray 30 min before the second dive. Following the dive, gas bubbles in the pulmonary artery were recorded using ultrasound. RESULTS: The open-water dive resulted in significantly more gas bubbles than the dry dive (0.87 +/- 1.3 vs 0.12 +/- 0.23 bubbles per square centimeter). Nitroglycerine reduced bubble formation significantly in both dives from 0.87 +/- 1.3 to 0.32 +/- 0.7 in the in-water dive and from 0.12 +/- 0.23 to 0.03 +/- 0.03 bubbles per square centimeter in the chamber dive. CONCLUSION: The present study demonstrates that intake of a short-lasting NO donor reduces bubble formation following decompression after different dives.

Adult↗

Venous bubble count declines during strenuous exercise after an open sea dive to 30 m.

INTRODUCTION: The effect of post-dive exercise on bubble formation remains controversial, although the current practice of divers and aviators is to avoid strenuous exercise after diving. Previously, we have shown that exercising 24 h before a dive, or during a decompression stop, significantly reduces bubble formation in man. The objective of this study was to determine whether a short period of strenuous post-dive exercise promotes venous bubble formation. METHODS: Seven male military divers performed an open-sea field dive to a maximum depth of 30 m for 30 min. At maximum depth, subjects performed mild underwater fin swimming, followed by standard decompression. Diving was followed by a post-dive exercise session consisting of short, strenuous incremental upright cycle ergometry, up to 85% of maximal oxygen uptake, for about 10 min. Subjects were monitored for venous gas bubbles in the right heart with an echo-imaging system starting 20 min post-dive while in the supine position, during cycle ergometry in the seated upright position, and immediately after exercise in a supine position. RESULTS: The average number of bubbles was 1.5 +/- 1.4 bubbles x cm(-2) 20 min after diving. Changes in posture from supine to seated upright resulted in significant reduction of bubbles to 0.6 +/- 1.3 bubbles x cm(-2) (p = 0.043), with further reduction to 0.2 +/- 0.3 bubbles x cm(-2) at the end of exercise (p = 0.02). No cases of DCS or intra-pulmonary shunt were observed during or following post-dive exercise. DISCUSSION: These results suggest that post-dive strenuous exercise after a single field dive reduces post-dive gas bubble formation in well-trained military divers. Additional findings are needed for normal sports divers.

Adult↗

Muscle oxygen supply during cold face immersion in breath-hold divers and controls.

INTRODUCTION: The human diving reflex is characterized by bradycardia, decreased cardiac output, and peripheral vasoconstriction, and has an oxygen-conserving effect both at rest and during exercise. However, the resultant time course and extent of muscle desaturation is unknown. METHODS: We used near-infrared spectroscopy to continuously measure the decrease in tissue oxygen saturation (StO2) in the calf muscle during a series of breath-holds. Subjects were seven trained divers (TD) and eight untrained controls (UC). Other measured variables included arterial blood pressure, heart rate, and arterial oxygen saturation (SaO2). Each subject performed five maximal apneas during face immersion in cold water with 2-min recovery intervals between breath-holds. RESULTS: On average, total apnea time for TD was significantly longer than for UC (772.6 +/- 40.9 s vs. 499.1 +/- 118.2 s, respectively). Further, TD had a more pronounced decrease in StO2 than UC (70.6 +/- 15.3% for TD vs. 87.9 +/- 6.1% UC for the fifth and longest apnea). When values for the two groups were compared at the mean breakpoint time for UC, there was no difference in StO2 and SaO2 remained at baseline. By contrast, at the same time point in all five apneas, UC experienced simultaneous, significantly larger reductions in SaO2 and StO2. DISCUSSION: These data indicate that TD have an attenuated diving reflex compared with UC at the same breath-hold times (the breakpoint for UC). In addition, muscle desaturation occurs earlier than arterial desaturation in both groups; the fact that this effect was less pronounced in TD suggests a training effect. This study provides further evidence for the oxygen-conserving effect of the human diving reflex in maintaining the oxygen supply of vital organs.

Adult↗

Exercise-induced intrapulmonary shunting of venous gas emboli does not occur after open-sea diving.

Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 m breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at approximately 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.

Adaptation, Physiological↗

Effect of human splenic contraction on variation in circulating blood cell counts.

1. The human spleen sequesters 200-250 mL densely packed red blood cells. Up to 50% of this viscous blood is actively expelled into the systemic circulation during strenuous exercise or simulated apnoea (breath-hold) diving. The contribution of splenic contraction to changes in the circulating volume of red blood cells (RBCV), as well as the venous concentration of white blood cells (WBC) and platelets (PLT), was investigated following repeated breath-hold apnoeas. 2. Eighteen trained apnoea divers and 18 intact and six splenectomized subjects without diving experience repeated five maximal apnoeas with face immersion in cold water, with 2 min intervals between successive attempts. Venous blood samples were taken before and between consecutive apnoeas, as well as at 0, 10 and 20 min after the last breath hold. Arterial pressure, heart rate and transcutaneous partial pressure of oxygen and carbon dioxide were monitored continuously. 3. Plasma protein concentration decreased by 5.8, 2.2 and 9% in apnoea divers, untrained and splenectomized subjects, respectively, indicating an expansion of plasma volume. The RBCV and venous concentration of WBC, corrected for changes in plasma volume, increased in both trained apnoea divers (4.9+/-1.0 and 14.9+/-3.1%, respectively) and intact subjects (1.7+/-0.8 and 7.2+/-1.8%, respectively), whereas in splenectomized subjects there was no change in RBCV and a delayed increase in WBC concentration. Furthermore, an initial lymphocytosis detected during repeated breath holds in divers and intact subjects was completely absent in splenectomized subjects. None of the groups showed significant changes in PLT concentrations. The well-recognized diving response to apnoea (bradycardia and increased blood pressure) was seen during all breath-hold attempts in all subjects. 4. Repeated breath-holds (apnoeas) contribute to increased RBCV and venous blood concentrations of WBC through splenic contraction.

Adult↗

Exercise during a 3-min decompression stop reduces postdive venous gas bubbles.

PURPOSE: Decompression sickness is initiated by the formation of gas bubbles in tissue and blood if the divers return to surface pressure too fast. The effect of exercise before, during, and after dive on bubble formation is still controversial. We have reported recently that strenuous aerobic exercise 24 h before simulated dive ameliorates venous bubble formation. The objective of this field study was to evaluate whether mild, continuous exercise during decompression has a similar impact. METHODS: Ten healthy, military male divers performed an open-sea field dive to 30 m of sea water breathing air, remaining at pressure for 30 min. During the bottom and decompression the subjects performed fin underwater swimming at about 30% of maximal oxygen uptake. Each diver underwent two randomly assigned dives, one with and one without exercise during the 3-min decompression period. Monitoring of venous gas emboli was performed in the right heart with ultrasonic scanner every 20 min for 60 min after reaching surface pressure in supine rest and during forced two-cough procedure. RESULTS: The study demonstrates that a mild, continuous exercise during decompression significantly reduced the average number of bubbles in the pulmonary artery from 0.9 +/- 0.8 to 0.3 +/- 0.5 bubbles per square centimeter in supine rest, as well as during two-cough procedure, which decreased from 4.6 +/- 4.5 to 0.9 +/- 0.9 bubbles per square centimeter. No symptoms of decompression sickness were observed in any subject. CONCLUSION: These results, obtained in the field conditions, indicate that a mild, underwater swimming during a 3-min decompression period reduces postdive gas bubbles formation.

Croatia↗

Anthropological and clinical characteristics in adolescent women with dysmenorrhea.

The aim of this study was to examine the prevalence of dysmenorrhea in female adolescents and the influence of anthropological characteristics and lifestyle factors on menstrual pain. Two hundred and ninety seven girls from several elementary and secondary schools were interviewed about the presence of the menstrual pain, their age, height and weight, menarcheal age, menstrual cycles quality, smoking and sexual activity. There were 164 (55%) subjects with and one hundred and thirty three (45%) without dysmenorrhea. The adolescents with dysmenorrhea answered the questions about missing activities and taking pills for pain. No difference was observed between the girls with and the girls without dysmenorrhea in their chronological age, height, weight, menarcheal age, menstrual cycles quality, cigarette smoking and sexual activity. In the group of dysmenorrheic adolescents there was infrequent missing activities and bedrest, but missing school was observed in 22 percent and taking pills for pain was observed in 96 percent of the subjects. Young girls who experienced menstrual pain are good candidates for a prophylactic therapy, such as hormonal contraception. A replication of this study is needed for public health services in the future to improve the quality of life of the dysmenorrheic young women.

Adolescent↗