Concentrations of mercury and other toxic elements in orange roughy, Hoplostethus atlanticus, from the Mid-Atlantic Ridge.

Concentrations of the elements mercury, arsenic, cadmium and lead were measured in the muscle tissue of Orange roughy (Hoplostethus atlanticus) obtained from the Mid-Atlantic Ridge during the MAR: -ECO: expedition in the North Atlantic Ocean in 2004. The age of the fish varied from 1 to 139 years. To the best of our knowledge, the concentration of the heavy metals presented here is for one of the oldest fish in the literature, in addition to the fact that very little information on arsenic in Orange roughy has been previously published. The concentration of mercury in the fillet of the fish varied between 0.06 and 1.1 µg g⁻¹ w.w. Mercury was the only element that was positively correlated to the age. The concentrations of mercury were found to be below the maximum limits for Orange roughy set by EU at 1.0 µg g⁻¹ w.w, except for a 134 year fish sample with a concentration of 1.1 µg g⁻¹ w.w.

Tissue nitrogen elimination in oxygen-breathing pigs is enhanced by fluorocarbon-derived intravascular micro-bubbles.

UNLABELLED: The present study tested the hypothesis that intravascular micro bubbles generated by i.v. infusion of a 2 % dodecafluoropentane (DDFP) emulsion will enhance tissue denitrogenation during oxygen breathing. Eleven spontaneously breathing pentobarbital anesthetized pigs were studied. Six pigs were treated with 0.08 ml/kg of DDFP-emulsion infused over 30 min and five (control) pigs received a matching dose of emulsion vehicle. Circulatory parameters were recorded. The pigs were connected via a tracheal tube to a closed circuit oxygen-primed breathing loop allowing volume measurements and nitrogen analysis by gas chromatography every 7 min. The nitrogen washout was recorded for up to four hrs in each group. The cumulative nitrogen yield during oxygen breathing was considerably larger in treated animals than in controls. Thus, the amount of nitrogen eliminated in the controls in 120 min was achieved already after 65 min in animals treated with the DDFP-emulsion. Blood pressure and cardiac output remained stable and were not different between the two groups during the four hrs of nitrogen washout. The central venous oxygen tension was significantly higher in the treated animals during oxygen breathing than in the controls. This difference was, in all probability due to enhanced oxygen transport by the micro-bubbles. CONCLUSION: Intravascular micro-bubbles generated by i.v. infusion of a small dose of 2 % DDFP-emulsion very effectively enhanced denitrogenation by oxygen breathing and deserve study as a means to improve prevention and treatment of decompression sickness.

Cardiovascular effects of verapamil and quinidine at normal and elevated ambient pressure.

Cardiovascular parameters were measured in rats before and after administration of verapamil and quinidine, a slow Ca2+ and fast Na+ channel blocker, respectively, at normal and elevated ambient pressure [5 bar (500 kPa)]. Left ventricular pressure (Pivt), maximal velocity of Plvt rise (+dP/dt) and fall (-dP/dt), and heart rate (HR), arterial systolic pressure (Pasys), and mean arterial pressure (MAP) were measured in all animals using catheters connected to pressure transducers. Cardiac output (Q), and myocardial blood flow (MBF) were detected by the microsphere technique. Total peripheral vascular resistance (TPVR), myocardial vascular resistance (MVR) and oxygen consumption of the heart (VO2) was calculated. In Groups 1a (control group; 1 bar) and 1b (test group; 1-5 bar), verapamil (1.5 mg x kg(-1)) caused a reduction in Plvt, +dP/dt, -dP/dt, Pasys, MAP, VO2, TPVR, and MVR in both groups at 1 bar (100 kPa), and these parameters remained depressed for at least 50 min in Group 1a. However, MBF increased after verapamil injection. After compression to 5 bar (500 kPa), Plvt, dP/dt, Pasys, VO2, and MBF were markedly elevated (Group 1b). No change in HR, SV, or Q was found in either of the groups. In Groups 2a (control group; 1 bar) and 2b (test group; 1-5 bar), quinidine (5 mg x kg(-1)), infused over a period of 10 min, reduced Plvt, +dP/dt, -dP/dt, MAP, Pasys, VO2, Q, stroke volume (SV), TPVR and MBF at 1 bar (100 kPa). These parameters remained depressed for almost the whole experimental period in Group 2a, while Plvt, +/-dP/dt, Pasys, MAP and VO2 were enhanced during exposure to 5 bar (500 kPa) in Group 2b. The HR was unchanged by quinidine in Group 2a, but was increased at elevated ambient pressure in Group 2b, whereas the MBF was unchanged in both groups. The present results show that verapamil and quinidine have a depressant effect on cardiac function, arterial pressure and VO2 at normal atmospheric pressure, whereas MBF was enhanced only in the verapamil group. During exposure to elevated ambient pressure, cardiac function, arterial pressure and VO2 increased despite adequate inhibition of slow Ca2+ and fast Na+ channels.

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide.

It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O2 content in the breathing gas, the elevated carrying capacity of O2 in the arterial blood results in augmented O2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O2 to poorly perfused tissues if the vasoconstriction induced by elevated O2 could be abolished or attenuated by adding CO2 to the breathing gas. Organ blood flow (QOBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (fb) fell (4 breaths x min(-1) x 100 kPa O2(-1)), with no changes in arterial CO2 tension (PaCO2), but when CO2 was added, fb and PaCO2 increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r2 = 0.72 and 0.75 respectively). Similarly, the cardiac output (Qc) and heart rate (fc) fell, while the stroke volume (SV) was unaltered, independent of PaCO2. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO2 was added. In group 2, the blood flow to the CNS rose linearly with increased PaCO2 and decreased pH. After decompression fc and SBP stayed high, while Qc returned to control values by reducing the SV; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in fc, Qc, LVP, dP/dt, SBP and most QOBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevated PaCO2 augmented O2 delivery to the CNS and eyes, but increased the susceptibility to O2 poisoning. A prolonged suppression of O2 supply to the CNS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 to the breathing gas.

Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats.

Based on a model of acute carbon monoxide (CO) poisoning in rats with an occluded left carotid artery, we have evaluated the effects of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2) on mortality and morbidity. After exposure to 2,700 ppm CO in air for 1 h, the rats were grouped and treated with air (group 1, untreated controls, in a previous study), 100 kPa O2 for 4 h (group 2), 300 kPa normoxia (group 3, pressure controls), and 300 kPa O2 (group 4) for 1 h, respectively. NBO2 started immediately, whereas HBO2 began 35 min after the end of the CO exposure. At the termination of the exposure, the four groups suffered identical levels of poisoning as indicated by the degrees of hypothermia, hypocapnia, drop in mean arterial pressure, and acidosis. Up to 48 h after the end of the CO exposure, mortalities were 76, 58, 75, and 17 in groups 1-4, respectively. The neurologic morbidities, indicated by abnormal motor behaviors and edema in the left cerebral hemispheres, were 84, 67, 83, and 42% in groups 1-4, respectively. Compared to the normoxic treatments, the HBO2, but not the NBO2, significantly reduced the mortality and the neurologic morbidity. HBO2 was also significantly better than NBO2 in increasing surviving time and survival rate. The results support the value of HBO2 in improving short-term outcome of acute CO poisoning in this rat model.

Measurement of cerebrospinal fluid pressure in conscious rats.

We describe a method of using a micro-tip transducer to measure cerebrospinal fluid pressure (CSFp) through a lateral ventricular cannula in unanesthetized, restrained, non-stressed rats. The mean value of CSFp under the anesthesia was 4.2 +/- 0.9 (mean +/- SEM, n = 6), ranging from 1.3 to 7.5 mmHg. Measurements were made daily in conscious state for 7 consecutive days after the operation. Mean value of CSFp was 9.1 +/- 0.5 mmHg (n = 42), ranging between 8.0 +/- 1.4 and 10.4 +/- 1.3 mmHg (n = 6) from day to day (P > 0.05). The permanent intraventricular cannula did not cause any detectable changes in behavior, arterial pressure, arterial blood gas, arterial blood acid-base chemistry, and water content of the punctured hemisphere. The results indicated that the method is a reliable alternative for CSFp measurement in a conscious, restrained, non-stressed rat which can be used under a variety of experimental conditions.

Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats.

This study on conscious rats with occluded left carotid artery investigates the influence of cerebral edema after acute carbon monoxide (CO) poisoning on cerebrospinal fluid pressure (CSFp) and evaluates the therapeutic effectiveness of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2). The CSFp was continuously recorded via a cannula placed in the left cerebral ventricle before, during, and for up to 6 h after exposure to 0.27% CO for 1 h. A non-sustained small increase in the CSFp and identical degrees of hypoxemia, hypocapnia, arterial hypotension, and acidosis were found during the exposure in all rats. After the CO exposure, all non-edema control rats without carotid artery ligation (n = 7) recovered completely with normal CSFp, behavior, and brain water content. All untreated (n = 7) and NBO2-treated rats (n = 7) developed a severely increased CSFp (> 50 mmHg) with neurologic motor dysfunction, and died of a severely increased CSFp (> 100 mmHg) with considerable cerebellar herniation. Except in one rat, the CSFp did not reach a dangerous level (> 25 mmHg) after the HBO2 session (300 kPa O2 for 1 h, beginning at 20 min post CO). All HBO-treated rats (n = 7) survived with less neurologic motor dysfunction and less left hemispheric edema than those in untreated and NBO2-treated rats. The results demonstrated that the increase in the CSFp was related to the left hemispheric edema, and that the cerebellar herniation was the predominant cause of death after the CO exposure. HBO2, but not NBO2, prevented the severe increase in the CSFp and thus saved the life after the CO exposure.

Effect of sodium nitroprusside-induced hypotension on the blood flow in subcutaneous and intramuscular BT4AN tumors and normal tissues in rats.

PURPOSE: To examine the effect of infusion of the vasodilator sodium nitroprusside (SNP) on the blood flow in normal tissues and BT4An tumors growing subcutaneously or intramuscularly in BD IX rats. METHODS AND MATERIALS: Sodium nitroprusside was given as a continuous intravenous infusion to keep the mean arterial pressure stable at 60 mmHg. The cardiac output, organ blood flow, and perfusion of the BT4An tumors were measured by injection of radiolabelled microspheres at control conditions and after 20 min SNP infusion in each animal. Two series of experiments were performed with two anesthetics with different mechanisms of action, Inactin and the midazolam-fentanyl-fluanisone combination (MFF), to secure reliable conclusions. RESULTS: Cardiac output, heart rate, and blood flow to the skeletal muscles, heart, and liver increased during SNP infusion in either anesthetic group. In the kidneys and particularly the skin, decreased blood flow by SNP was observed. When located subcutaneously on the foot, the blood flow in the tumor fell to 23.4% and 21.4% of the control values in the MFF- and Inactin-anesthetized animals, respectively. This was accompanied by a similar fall in the blood flow in the foot (tumor bed) itself. In the intramuscular tumor, the blood flow fell to 24.8% of the control value in the MFF group, whereas the corresponding figure was 36.2% in the Inactin group. In the surrounding muscle (tumor bed) the blood flow increased significantly, most pronounced in the MFF experiment, where it was tripled. CONCLUSION: The fall in the tumor perfusion by SNP may be exploited therapeutically to increase the tumor temperature during hyperthermia. Predominant heating of the tumor compared to the tumor bed can be expected if the tumor is growing in or near skeletal muscles.

A model for acute carbon monoxide poisoning in conscious rats.

These experiments were designed to establish an animal model of acute carbon monoxide (CO) poisoning in awake habituated rats. On the day before exposure, under a brief anesthesia, a Levine preparation (unilateral common carotid artery occlusion) was performed on group 1 (n = 8) and 2 (n = 28), but not on group 3 rats (n = 8). Group 1 rats were exposed to air as control. Groups 2 and 3 rats were exposed to 0.27% CO in air for 60 min [carboxyhemoglobin (HbCO) = 70%] followed by a 2-day recovery in air. The Levine preparation per se did not induce any detectable physiologic effects on group 1 rats. Identical cardiovascular and metabolic responses to CO occurred in groups 2 and 3. After the CO exposure, all group 3 rats lived for 2 days with normal neurologic index (NI). In group 2 (n = 25 post-CO), 84% of the rats showed increased NI and edema of the ipsilateral cerebral hemisphere, and 76% of the rats died 8.7 +/- 1.7 h after the CO exposure. NI correlated with the brain edema (rs = 0.748, P < 0.001) and inversely correlated with the survival time after the CO exposure (rs = -0.777, P < 0.001). We therefore may conclude that exposure of the Levine-prepared rats to 0.27% CO in air for 60 min will provide a valuable model for testing of different treatments for CO poisoning.

Effects of gas density and ambient pressure on myocardial contractility in the rat.

BACKGROUND: Cardiac contractility and myocardial blood flow have been shown to increase when anesthetized and awake rats were exposed to normoxic 0.5 MPa ambient pressure, independent of inert gas composition. Similar changes have been demonstrated in anesthetized rats breathing a dense (relative density (RD) 5) SF6-O2 gas mixture at normobaric pressure. HYPOTHESIS: The purpose of the present study was to further explore whether cardiac contractility increases during hyperbaric exposure as a response to the elevated atmospheric pressure per se or rather as a response to increased breathing gas density. METHODS: Arterial pressure, left ventricular pressure (LVP), central venous pressure and intra-esophageal pressure were monitored in anesthetized rats during simulated dives. The rats were exposed to various gas mixtures (air, SF6-N2-O2, He-N2-O2), partial pressures of O2 (PIO2 0.02 and 0.03 MPa) ambient pressure (PTot 0.1-0.3 MPa) and gas density (RD 1-10.1). RESULTS: Cardiac contractility increased briefly by 5-10% (p < 0.05) during mild hyperoxia (PIO2 0.03 MPa). A concomitant stepwise increase in RD (1-10.1) and PTot (0.1-0.3 MPa) by adding SF6 to air, increased maximal rate of LVP rise (+dP/dt) and fall (-dP/dt) by 30% (p < 0.01). Two groups of rats exposed to either a high density SF6-N2-O2 (RD 5.5) or a normal density He-N2-O2 (RD 1.2) breathing gas of identical PTot 0.2 MPa demonstrated similar rise in dP/dt (peak 72%, p < 0.05). CONCLUSION: At moderately increased ambient pressure, pressure per se increases cardiac contractility independently of the breathing gas density.

Cerebral blood flow and systemic hemodynamics during exposure to 2 kPa CO2-300 kPa O2 in rats.

Cerebral blood flow (CBF), systemic hemodynamics, and arterial blood gases were measured during control conditions and during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2) in awake rats. The respiratory frequency fell with no change of arterial PCO2 (PaCO2) in group 1, but in group 2, respiratory frequency and PaCO2 increased linearly. The cardiac output (CO) and heart rate (HR) fell and systolic arterial pressure (SAP) rose independent of PACO2. O2 breathing caused CBF to fall by 30% in group 1, whereas CBF rose linearly with the PaCO2 increase and pH decline in group 2. Regional CBF (rCBF) fell in group 1, whereas rCBF rose gradually in all regions in group 2, but the responses varied similarly in both groups. Regional brain O2 supply was unaltered in most areas. However, the O2 supply was possibly reduced in the brain stem in group 1 but markedly increased in group 2. After decompression, HR and SAP were high, whereas CO returned to its control value. CBF and all rCBF levels remained markedly elevated in group 2. In group 1, CBF returned to control levels. By contrast, rCBF and O2 delivery to brain stem regions remained subnormal. In conclusion, the O2-induced changes in HR, CO, and SAP were not influenced by hypercapnia. CBF and rCBF fell despite unaltered PaCO2, whereas hypercapnia prevented these declines. An uneven effect of O2 was observed on rCBF, most pronounced in brain stem regions, independent of the PaCO2. There was a prolonged suppression of O2 supply to brain stem regions both during and after the exposure to O2 in the absence of CO2.

Repeated exposure to 5 bar normoxic He-N2 changes cerebral blood flow distribution in rats.

The regional cerebral blood flow (rCBF), arterial pressure (AP), heart rate, respiratory frequency, and arterial acid-base chemistry were measured during control periods at 1 bar air and after 15 and 60 min at 5 bar normoxic He (4.0 bar)-N2 (0.8 bar) in two groups of awake habituated rats. Group 1 (10 control rats) were exposed 40 times while restrained for 1 h in the pressure chamber at 1 bar air. Group 2 (10 rats) were restrained and exposed 40 times to normoxic 5 bar He-N2 atmosphere in the pressure chamber for 45 min. During the control period, the systolic and mean AP levels were higher (P < 0.05), whereas the average CBF and nine rCBF values were lower in the preexposed group. During 5-bar exposure, the systolic AP rose significantly in both groups, whereas the mean AP remained at the control level or was reduced. The arterial O2, CO2, and HCO3 changed identically in both groups relative to hyperventilation. Generally, the total and local CBF values increased during the first 15 min in both groups and for 60 min in the preexposed rats. After 60 min of exposure, the flow returned toward the control level in most regions in both groups, whereas the flow was still elevated in the cerebellum and mesencephalon in the control rats and in the bulbus olfactorius, mesencephalon, medulla oblongata, spinal cord, and posterior part of cortex cerebri in preexposed animals. Hypothalamic rCBF in control rats was reduced after 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of exposure to oxygen at 101 and 150 kPa on the cerebral circulation and oxygen supply in conscious rats.

Hyperbaric oxygen at pressures of 300 to 500 kPa has been shown to induce changed distribution of cerebral blood flow (QCBF) in rats, in places reducing the supply of the supplementary O2. Thus, in the present study, the effect of hyperoxia at 101 (group 1, n = 9) and 150 (group 2, n = 9) kPa O2 on cerebral blood flow distribution and central haemodynamics was tested in conscious, habituated rats. During the control period the systolic arterial pressure (BPs), heart rate (fc), breathing frequency (fb), cardiac output (Qc), arterial acid-base chemistry and glucose, as well as QCBF distribution (rQCBF) were similar in the two groups of animals. During O2 exposure, the acid-base chemistry remained unchanged. The haemoglobin decreased in group 2, but remained unchanged in group 1. The fc decreased rapidly in both groups during the change in gas composition, after which fc remained constant both in group 1 and in group 2, for whom pressure was increased. The Qc and fb decreased and BPs increased similarly in the two groups. Total QCBF and rQCBF decreased to the same extent in both groups, and the rQCBF changes were equally scattered. In group 1, breathing of pure O2 did not increase the O2 supply to any cerebral region except to the thalamus and colliculi after 60 min, whereas the O2 supply to the hypothalamus decreased and remained low. In group 2, the O2 supply was unchanged compared to the control period in all regions. These findings agree with previous observations during exposures to higher O2 pressures. In air after O2 exposure the acid-base chemistry remained normal. The fc and fb increased to higher levels than during the control period. The BPs remained high. The brain blood flows were increased, inducing elevated O2 supply to several brain regions compared to the control period. In conclusion, O2 supply to the central nervous system was found to be in the main unchanged during breathing of O2 at 101 kPa and 150 kPa.

Effect of beta 1-adrenoceptor blockade in rats at 5 bar ambient pressure.

Conscious rats exposed to 5 bar (500 kPa) ambient pressure show increased total myocardial blood flow (TMBF) and enhanced cardiac contractility in spite of unaltered mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO). Four groups of awake, adapted rats were given injections of atenolol at 1 bar air or 5 bar normoxic N2, or both. Atenolol injected at 1 bar caused a marked reduction of HR, MAP, peak left ventricular pressure (LVP), and rate of LVP rise (+dP/dt) and fall (-dP/dt). In spite of beta 1-adrenoceptor blockade, ambient pressure rise increased HR, LVP, +dP/dt, -dP/dt, TMBF, and calculated cardiac O2 consumption (P < 0.05). A second atenolol injection at 5 bar caused a brief reduction in HR but did not affect cardiac contractility. Rats receiving the first atenolol injection at 5 bar demonstrated unchanged TMBF. We conclude that beta 1-adrenoceptor blockade does not annual the increase in cardiac contractility associated with hyperbaria.

Systemic hemodynamics during hyperbaric oxygen exposure in rats.

The effect of 1-5 bar O2 on left ventricular pressure (LVP), maximal velocity of LVP rise (+dP/dt) and fall (-dP/dt), systolic arterial pressure (APsys), pulse pressure (delta AP), heart rate (HR), and respiratory frequency (RF) was studied in anesthetized and conscious rats. At 1 bar O2, all blood pressure parameters increased significantly (9-56%) in both groups of rats, while RF fell (11-12%). HR fell only in conscious rats, while arrhythmias occurred in both groups. Compression to 5 bar O2 induced a significant further increase in all blood pressure parameters. HR fell further in the conscious rats. Arrhythmias were observed in increasing number during compression and at 5 bar O2. Elevation in estimated oxygen-consumption of the heart was found both during compression and at 5 bar O2. We conclude that O2 exposure markedly stimulates the myocardium by elevating the LVP, +dP/dt, and -dP/dt, thus elevating APsys and delta AP. Arrhythmias developed in both groups, while bradycardia occurred only in conscious rats.

Cerebral blood flow distribution and systemic haemodynamic changes after repeated hyperbaric oxygen exposures in rats.

The effects of acute and repeated exposures to 500 kPa O2 on the distribution of cerebral blood flow (QCBF) and systemic haemodynamics were assessed in awake rats. After habituation, the control rats (group 1, n = 7) were restrained for 1 h daily for 8 days in air at 101 kPa, while the test rats (group 2, n = 8) were exposed to 500 kPa O2 for 1 h daily for 8 consecutive days. During a final exposure, both groups were exposed to 500 kPa O2. Systolic (BPs) and mean arterial blood pressure (BPa), and heart rate (fc) were measured continuously from implanted arterial catheters; while cardiac output (Qc) and regional QCBF (rQCBF) were measured by the microsphere method in air before the O2 exposure, and after both 5 min and 60 min at 500 kPa O2 in all the animals. The baseline measurements in air of BPs and BPa were higher and fc was lower in group 2, while the acid-base chemistries were similar in the two groups. Total QCBF was similar in both groups. However in group 2, blood flows and calculated O2 supplies to colliculi, hippocampus, hypothalamus, and most cerebral cortical regions were higher, but lower to pons and medulla oblongata. During O2 exposure Qc and fc decreased, and BPa, BPs, and peripheral vascular resistance increased in all the rats. Arterial partial pressure of CO2 and [HCO3-] decreased in group 1, but remained at baseline levels in group 2. Total QCBF and rQCBF decreased in both groups, and the rQCBF distribution was altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Unilateral frontal decortication changes cerebral blood flow distribution during hyperbaric oxygen exposure in rats.

Distribution of rCBF was measured with 10.7 +/- 0.5 microns differently radiolabelled microspheres (MS) during control at 1 bar air, and after 5 and 35 min at 5 bar (0.5 MPa) 95% O2 on awake, habituated rats 10 d after right-sided frontal decortication. A decreased tolerance to hyperbaric O2 was found compared to normal rats of the same strain. The systolic arterial pressure increased during O2 exposure (11%, p < 0.05), the mean arterial pressure remained unchanged, but the cardiac output and heart rate fell by 29 and 14% (p < 0.01), respectively. The arterial acid-base balance remained normal during O2 exposure, although a small reduction of CO2 (24%) and HCO3 (11%) was observed (p < 0.01 and p < 0.05), possibly due to increased alveolar ventilation caused by an elevated respiratory rate of 24% (p < 0.05). The arterial O2 content at 5 bar increased by about 30% (p < 0.01). During control, blood flow in 16 regions of each hemisphere was found to be lower, more scattered, and differently distributed on the lesioned side. After 5 min at 5 bar, the blood flow fell in nearly all regions of the brain (up to 40%), similarly in the two brain halves. During the 35 min exposure, the blood flow increased, so that 60% of the examined areas on the lesioned side had blood flow levels of control or above, in contrast to the undisturbed side where blood flow remained below control values. The O2 supply to different regions varied similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Repeated normoxic hyperbaric exposures induce haemodynamic and myocardial changes in rats.

The effect of repeated exposure to ambient pressures of 5 bar (500 kPa), in atmospheres comprising normal partial pressures of oxygen [0.2 bar (20 kPa)] and nitrogen [0.8 bar (80 kPa)] and 4 bar (400 kPa) helium, on cardiac function and morphology was assessed in conscious rats. Ten test rats underwent chamber dives daily for 40 consecutive days, and ten control rats were exposed in the same chamber for an equal period of time, but in air at 1 bar (100 kPa). Cardiac output (Qc) and myocardial blood flow (Qmyocardial) were determined by the microsphere method. After 40 days, the body mass was 7% greater in the control than in the test rats (P < 0.05), although they were given exactly the same amount of standard food. The test rats had a significantly higher (7% absolute, 12% ventricular mass to body mass, P < 0.05) heart mass (left ventricular myocardium, including the ventricular septum) than the control rats. The percentage tissue dry mass of the right and left ventricles was equal in the two groups. Microscopic examination revealed a number of small focal necroses in the left ventricle of the test rats but none in the control rats. The left ventricular pressure (LVP) and the maximum velocity of LVP increase (contractility) and decrease were significantly increased (25%-96%, P < 0.001) in the pre-exposed compared to the control rats at 1 bar (100 kPa). The systolic arterial pressure, heart rate and respiratory frequency were similar in the two groups at 1 bar (100 kPa).(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral blood flow distribution during exposure to 5 bar oxygen in awake rats.

The regional cerebral blood flow (rCBF) and cardiac output (CO) were measured in conscious rats by the microsphere method during control, after 5 and 60 min at 5 bar O2, and 5 min after decompression to air. The arterial acid-base balance was essentially unchanged during hyperbaric O2 and after decompression, except for a slightly reduced CO2 and HCO3 during the O2 exposure. The heart rate (HR) fell at 1 bar O2, continued to fall during compression, and remained low. A marked HR rise occurred in air after decompression. The systolic arterial pressure (AP) increased, while mean AP was constant during the O2 exposure. The CO and total cerebral blood flow fell in proportion to the arterial O2 content increase. The rCBF was unevenly distributed in control, and fell to a disparate degree and remained low in some regions during O2 exposure. Due to the rCBF fall, the O2 supply was limited, the glucose supply was reduced, and CO2 and heat transport probably were limited, suggesting a labile metabolic state locally in the brain. After decompression, blood flow remained low in several regions, making hypoxia likely for a considerable time in several brain areas, whereas the rest of the brain had normalized or increased blood flow. The HR and systolic AP remained high for at least 30 min after decompression.