Elevations in Intra-cranial blood flow velocities following a SCUBA Dive and the Influence of Post-dive Exercise.

The effect that a SCUBA dive has on cerebral blood flow (CBF) at rest and during exercise is poorly understood. We examined the hypothesis that the altered hemodynamic parameters following a SCUBA dive will lead to differential changes in CBF at rest and during exercise. 16 divers completed a field-based study with a single dive at a depth of 18 m sea water with a 47-min bottom time. A follow-up laboratory based study was conducted - 1 week later. Intra-cranial velocities were measured with transcranial Doppler ultrasound (TCD) pre-dive, post-dive at rest and throughout incremental exercise until exhaustion. Following the dive at rest, middle cerebral artery velocity (MCAv) was elevated 15 and 30 min after surfacing (by 3.3±5.8 and 4.0±6.9 cm/s, respectively; p<0.05); posterior cerebral artery velocity (PCAv) was increased at 30 min after surfacing (by 3.0±4.5 cm/s; p<0.05). During exercise following the dive, both MCAv and PCAv increased up to 150W followed by a decrease towards baseline at 180W (p<0.05). We found no difference in CBV during exercise between field and laboratory studies (p<0.05). The novel finding of this study is the transient elevation in resting intra-cranial velocities within 30 min following a SCUBA dive.

Influence of repeated daily diving on decompression stress.

Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.

Trimetazidine does not alter metabolic substrate oxidation in cardiac mitochondria of target patient population.

BACKGROUND AND PURPOSE: Trimetazidine, known as a metabolic modulator, is an anti-anginal drug used for treatment of stable coronary artery disease (CAD). It is proposed to act via modulation of cardiac metabolism, shifting the mitochondrial substrate utilization towards carbohydrates, thus increasing the efficiency of ATP production. This mechanism was recently challenged; however, these studies used indirect approaches and animal models, which made their conclusions questionable. The goal of the current study was to assess the effect of trimetazidine on mitochondrial substrate oxidation directly in left ventricular myocardium from CAD patients. EXPERIMENTAL APPROACH: Mitochondrial fatty acid (palmitoylcarnitine) and carbohydrate (pyruvate) oxidation were measured in permeabilized left ventricular fibres obtained during coronary artery bypass grafting surgery from CAD patients, which either had trimetazidine included in their therapy (TMZ group) or not (Control). KEY RESULTS: There was no difference between the two groups in the oxidation of either palmitoylcarnitine or pyruvate, and in the ratio of carbohydrate to fatty acid oxidation. Activity and expression of pyruvate dehydrogenase, the key regulator of carbohydrate metabolism, were also not different. Lastly, acute in vitro exposure of myocardial tissue to different concentrations of trimetazidine did not affect myocardial oxidation of fatty acid. CONCLUSION AND IMPLICATIONS: Using myocardial tissue from CAD patients, we found that trimetazidine (applied chronically in vivo or acutely in vitro) had no effect on cardiac fatty acid and carbohydrate oxidation, suggesting that the clinical effects of trimetazidine are unlikely to be due to its metabolic effects, but rather to an as yet unidentified intracardiac mechanism.

Acute effects of a single open sea air dive and post-dive posture on cardiac output and pulmonary gas exchange in recreational divers.

OBJECTIVE: To evaluate the cardiopulmonary effects of open sea scuba air diving to 39 m (30 minutes bottom time) with standard decompression. To account for possible gravity dependent effects of venous gas bubbles, the variables were measured in different post-dive body postures and compared with the baseline values before the dive in the same posture. METHODS: Eight male divers conducted two similar dives on successive days. Their posture before and after the dive was either sitting or supine, in random order. The divers were evaluated before and 30, 60, and 90 minutes after the dive. Venous bubbles were detected by precordial Doppler after the dive in four divers in the supine posture and two divers in the sitting posture. RESULTS: Arterialised oxygen tension had decreased at all times after the dive (-11.3 mm Hg, p = 0.00006), due to decreased alveolar oxygen tension, irrespective of posture. Apart from an increase in the sitting posture 30 minutes after the dive, pulmonary capacity for carbon monoxide diffusion and cardiac index decreased, mostly 60 minutes after the dive (-9%, p = 0.0003 and -20%, p = 0.0002 respectively). The decrease in cardiac index was greater in the supine posture (p = 0.0004), and the physiological dead space/tidal volume ratio increased more in the sitting position (p = 0.006). CONCLUSIONS: Field dives are associated with moderate impairments in cardiac output and gas exchange. Some of these impairments appear to depend on the posture of the diver after the dive.

Effect of a single air dive on pulmonary diffusing capacity in professional divers.

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

Theoretical considerations on the validity of the Stewart-Hamilton principle in measuring cycle-averaged flows via histogram of indicator in the pulsating compartment.

It has been heuristically shown that the Stewart-Hamilton principle, adapted to external counting observables of system indicator histogram, A(t), its cycle-averaged equilibrium count rate, A(equ), and indicator volume of distribution in the body, V(body), is F/V(body) = A(equ)/integral of o infinity A(t)dt, where F is the cycle-averaged cardiac output. Since the method lacks the theoretical plausibility, it remained unclear whether it is an approximation and what conditions warrant its usability. This paper presents an exact derivation of the above equation. To fulfill it the generalizations of the stationary theory of indicator kinetics were set up that allowed for the conditions of pulsatile flows and volumes and the dependence of the distribution of transit times of indicator on the phase of the cardiac cycle. The assumptions utilized were that the tracer enters the compartment well mixed and convectively carried by the blood in concentrations that do not vary in the single cycle to a material extent. The method yields the cardiac output, even when the flow to a compartment is only a part of it, provided that the fraction of indicator that traversed the system equals the fraction of cardiac output that perfuses the compartment. It was shown that, when applied to a regurgitant ventricle, the method obtains the forward flow and that separate application of the method to each of the ventricles provides the theoretical basis for evaluation of the central-circulatory shunts.

Increase of lung transfer factor in early sarcoidosis.

Dynamic spirometry and the lung transfer factor for CO (TLCO) were determined in 41 non-smoking patients with sarcoidosis before and after steroid treatment. Dynamic spirometry revealed usual stage-dependent restrictive and/or obstructive abnormalities; only maximal expiratory flow rate at 75% FVC (MEF75) was significantly increased after steroid treatment in stage 2 patients. The new finding is that TLCO was increased in stage 1 [on average 21% above the predicted values (p.v.)], but it was decreased in stage 2 (11% below p.v.) and stage 3 (27% below p.v.). The increase in TLCO in stage 1 was predominantly caused by an increase in TLCO membrane component (Dm) (33% above p.v.), while the pulmonary capillary blood volume (Vc') increased less (19% above p.v.). Steroid treatment significantly reduced TLCO, Dm and Vc' in stage 1 (for 14, 17 and 18% of the respective baseline values), whereas it caused TLCO and Dm increases in stage 2 (for 8 and 10% of the respective baseline values). In conclusion, a TLCO in pulmonary sarcoidosis may not only be decreased in its advanced stages, but also exhibit increased values, which appeared related to the subclinical inflammatory reaction in the stage 1 patients.

Triggers of acute myocardial infarction regarding its site.

We have studied the incidence of possible triggers of the myocardial infarction regarding its site in 750 patients with anterior and 731 patients with inferior infarction. Infarctions occurred most frequently without recalling any triggering activity, especially in patients with anterior infarction (67 vs. 44%). Physical effort as the possible precipitator was also more frequent in anterior infarctions (22 vs. 16%). However, the onset of inferior infarction was more frequent during meteorological stress (9 vs. 2%), emotional stress (10 vs. 3%), after overeating (13 vs. 3%) and nicotine abuse (6 vs. 1.5%). These triggers were independent and highly significant (P < 0.02 in each case) discriminators of the site of myocardial infarction. Bimodal circadian rhythm, with primary peak between 6 and 9 h a.m. and the secondary peak between 3 and 6 p.m. was observed in patients which did not recall any triggering activity, and this was more pronounced in patients with inferior infarction. These results support the hypothesis that the influence of the vegetative tone is most pronounced in the onset of myocardial infarction of inferior wall.

Association between asbestos-related pleural plaques and resting hyperventilation.

This study reports an association between pleural plaques and resting hyperventilation in a group of workers exposed to asbestos. Information on exposure level, pack-years of cigarette smoking, chest radiographs, ventilation parameters, single-breath diffusing lung capacity, and arterial gases were obtained for 344 workers. After the exclusion of 37 workers for isolated parenchymal fibrosis, combined pleuroparenchymal fibrosis, or diffuse pleural thickening, 55 subjects with isolated pleural plaques were evaluated against 252 no-plaque workers. A quantitative pleural score revealed mild pleural disease. Forty-four workers with plaques (80%) had hypocapnia induced by resting hyperventilation. The quantitative pleural score correlated significantly with the partial pressure of carbon dioxide in arterial blood (correlation coefficient = 0.7). A decrement in forced vital capacity was associated with plaques, whether controlled for age, smoking, and exposure or not. It was concluded that the resting hyperventilation observed in some asbestos-exposed subjects is related to the presence of mild pleural plaques and a restrictive disorder.

Non-stationary theory of blood-borne tracers.

Although cardiac mechanical activity causes periodic fluctuations of the regional volumes and flows through the cardiac chambers and great vessels, hitherto, the developed theory of blood-borne tracers has rested upon stationarity of flow, volume and distribution of transit time. Allowing for an arbitrary indicator injection, a more general theory is presented that accounts for periodic changes in the transport laws, flows and volumes of the system. When indicator particles are not thoroughly mixed with the entering blood, the intracycle changes violate most of the stationary equations. However, assuming complete mixing of indicator at the system inlet, in concentrations that do not change during the single cycle, this enables generalized counterparts of some of the most important stationary relations to be established. The difference between the indicator mean transit time calculated from the stationary assumptions and the one which allows for periodic kinetics is illustrated in radioangiographic assessment of the left ventricular ejection fraction.

Role of digoxin in right ventricular failure due to chronic cor pulmonale.

The effect of digoxin in the treatment of decompensated chronic cor pulmonale was investigated in a randomized double-blind, cross-over, placebo-controlled trial. A total of 34 successive patients with evident right heart failure were included in the study. The mean maintenance daily dose of digoxin was 0.30 +/- 0.03 mg with the mean serum level of 1.7 +/- 0.7 nmol/L. The severity of heart failure was assessed according to a clinicoradiographic scoring system (Heart Failure Score). The heart failure worsened during the placebo-period in eight (23.5%) patients (four with atrial fibrillation, two with a third heart sound (S3), one with a cardiothoracic ratio of more than 0.5 and one with sinus rhythm). By regression analysis, the heart failure significantly worsened only in the subgroup of patients with atrial fibrillation. Digoxin was successfully (without worsening of the heart failure) discontinued in 26 (76.5%) patients. No significant improvement was observed in the patients with S3 gallop. It was concluded that digoxin had no beneficial effect in chronic cor pulmonale patients with heart failure, except in those with atrial fibrillation.

Gated versus first-pass radioangiography in the evaluation of left-to-right shunts.

Excluding regurgitant ventricles and multiple shunting, left-to-right shunts of the central circulation can be evaluated from the difference between the right ventricular stroke counts (SCRV) and the left ventricular stroke counts (SCLV), which are obtained from gated radioangiography. The pulmonary-to-systemic flow ratio (QP/Qs) is equated to SCRV/SCLV in atrial shunts and to SCLV/SCRV in ventricular and ductal shunts. In this paper, the potentials of the stroke count method have been compared to the gamma fit first-pass technique, incorporating the recent refinements in ductal shunts and deconvolution of the pulmonary curve. In 17 patients with left-to-right shunt, the stroke count method and the gamma fit method correlated moderately with oximetry (r = .71 and .87), respectively. The gamma variate method appeared superior in the detection and estimation of small shunts, whereas when QP/Qs was two or larger, the stroke count method yielded closer agreement with oximetry data.

Carcinoembryonic antigen immunoreactivity patterns in colorectal cancer: Correlation with morphologic parameters.

The expression of carcinoembryonic antigen (CEA) was analyzed immunohistochemically in 100 colorectal cancer specimens. The tumors were divided into three groups, according to the predominant staining pattern which was either apical, cytoplasmic or stromal. CEA localization was apical in 26 cases, cytoplasmic in 48 and stromal in 26 cases. Overall, well differentiated tumors showed apical CEA, whereas the poorly differentiated tumors showed stromal staining. Significant correlation was noted between the CEA staining patterns and histological grading (P<0.001), nuclear grading (P<0.001), mucin synthesis (P<0.01), blood vessels, lymphatic vessels and peripheral nerve invasion (P<0.01), and lymph node metastasis (P<0.01). CEA staining pattern was not correlated with patients' age, sex or gross appearance of tumors and their site of origin, nor the Dukes' classificcation. It is concluded that the CEA immunoreactivity pattern may provide data that are relevant for the prognosis of the neoplastic disease.

Correlation between radiological and functional findings in workers exposed to chrysotile asbestos.

The relationship between the extent of respiratory disease from chest radiographs and the severity of functional impairment was assessed in 185 workers with long-term exposure to asbestos in an asbestos-cement factory. The workers were divided into seven subgroups according to functional abnormality findings (restrictive, obstructive, mixed restrictive-obstructive, reduced diffusion capacity, increased diffusion capacity, small airway disease and normal). Restrictive functional abnormality was present in 29% of the workers, obstructive and mixed in 3% small airway disease in 4%, reduced diffusion capacity in 4% increased diffusion capacity in 7%, while the remaining 49% were normal. The subjects with radiological diffuse pleural disease were characterized by FVC reduction, whereas in those with mixed pleural-parenchymal radiological abnormalities both FVC and DLCO were reduced. FVC and DLCO decrements correlated well with the increasing grades of profusion according to the ILO classification. In the group of workers with normal chest radiographs and normal spirometry, a decrease or increase in lung diffusion capacity for CO (DLCO) was an isolated finding. In addition, a correlation existed between the length of exposure and functional parameters (reduced FVC and DLCO, while FEV1/FVC increased with longer exposure). The study shows that reduced lung function indices can be found in subjects without radiological evidence for parenchymal asbestosis (ILO grade 1/1 profusion or greater). The results suggest that asbestos exposure, in addition to lung diffusion capacity decrease, can be accompanied by an increase in lung diffusion capacity.

Early intracranial infections after brain missile injuries--the role of computer tomography in diagnosis and treatment.

During the war in Croatia, from August 1991 until December 1994, 138 soldiers were treated at the Split University Hospital for different brain injuries inflicted by missiles. Nine of these 138 patients developed intracranial infection. This retrospective study reports on the outcome of these 9 intracranial infections caused by penetrating missile head injuries. In case of clinically suspected infection, computerized tomography scan was obtained at two time points during the course of infection in the same patient. Scans were obtained with and without contrast media, 7 to 14 days after the injury and the 4 weeks later. The role of computerized tomography in the detection and follow-up of various intracranial infections and long-term consequences were evaluated.

Spleen volume changes during adrenergic stimulation with low doses of epinephrine.

It is generally accepted that the spleen contraction is a consequence of humoral stimulation but recent data suggest a role of neural mechanisms. This study tested the hypothesis that the reduction in spleen size in response to low dose epinephrine infusion is a consequence of neurally mediated unloading of baroreceptors. Continuous ultrasonic measurements of spleen volume in response to intravenous infusion of low doses of epinephrine (0.06 µg/kg/min for 6 minutes, followed 0.12 µg/kg/min for 3 minutes) were performed with simultaneous continuous noninvasive measurements of cardiovascular parameters in thirteen subjects. In subgroup of six subjects we also continuously measured muscle sympathetic nerve activity (MSNA) as an index of peripheral sympathetic activation. Significant spleen contraction (≈30%, p=0.008) was observed early after the onset of epinephrine infusion and was preceded by a decrease in total peripheral resistance (41%, p=0.001) and mean arterial pressure (6.2%, p=0.02) and an increase in heart rate (27%, p=0.001) and total MSNA (120%, p=0.02). Our results demonstrate rapid spleen contraction induced by low-dose epinephrine infusion in conditions of decreased blood pressure and increased MSNA suggesting that the spleen may represent a constitutive part of the sympathetic nervous system under stressful situations.

Venous gas bubble formation and decompression risk after scuba diving in persons with chronic spinal cord injury and able-bodied controls.

STUDY DESIGN: Prospective study. OBJECTIVE: To evaluate the formation of venous gas bubbles following open-sea scuba dives in persons with chronic spinal cord injury (SCI) and in able-bodied diving instructors (C) and to assess the risk for decompression sickness (DCS). SETTING: Field study at the Island of Krk, Croatia. METHODS: Gas bubbles were monitored with an ultrasound scanner 40 min after surfacing. The probability of DCS (P((DCS))) was estimated from the recorded depth-time profile using a decompression model. RESULTS: Divers completed six dives in 3 days using a modified Bühlmann decompression model, and none developed signs of DCS. Mean P((DCS)) was similar in both groups, SCI (0.51+/-0.2%) and C (0.64+/-0.27%), and was seen to increase with subsequent dives. Number of bubbles (bubbles per cm(2)) was low in both groups on all 3 days of diving. CONCLUSIONS: We have used the P((DCS)) as a severity index of diving exposure. Overall, the severity of exposure in SCI subjects was consistent with the range of typical recreational dives, suggesting that the diving profile used is very safe.

Diving-induced venous gas emboli do not increase pulmonary artery pressure.

Venous gas emboli are frequently observed in divers even if proper decompression procedures are followed. This study was initiated to determine if pulmonary artery pressure increases in asymptomatic divers, which could increase the risk of arterial embolization due to passage of venous gas emboli from the right to the left side of the heart. Recordings of venous gas emboli and estimation of pulmonary artery pressure by non-invasive transthoracic echocardiography were applied in 10 recreational scuba diving volunteers before and 20, 40, 60, and 80 min after simulated dives to 18 m (80 min bottom time) in a hyperbaric chamber. The ratio between pulmonary artery acceleration time and right ventricular ejection time was used as an estimate of pulmonary artery pressure. None of investigated divers had signs of decompression sickness. Despite the post-dive presence of the venous gas emboli, measured in the region of the pulmonary valve annulus (mean=1.71 bubbles.cm-2, 40 min after dive), the ratio between pulmonary artery acceleration time and right ventricular ejection time did not decrease, but actually increased (from 0.43+/-0.06 to 0.49+/-0.06, 40 min after dive; p<0.05), suggesting a decrease in pulmonary artery pressure after the dive. We conclude that diving-induced venous gas bubbles do not cause significant changes in the central circulation which could increase the risk of arterial embolization.