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.

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.

Effect of 71 ATA He-O2 on organ blood flow in the rat.

Cardiac output and organ blood flow to major organs were investigated in awake rats at 1 atmosphere absolute (ATA) air and at 71 ATA He-O2. Radioactively labeled microspheres [15 +/- 1 (SD) micron] were injected into the left ventricle during constant-rate arterial blood sampling at 1 ATA air and subsequently at 71 ATA He-O2. Intra-arterial blood pressure was continuously recorded. The partial pressure of O2 was kept between 0.4 and 0.6 ATA. The results indicate that the mean blood pressure, heart rate, cardiac output, and organ blood flow are essentially unaltered in the rat at 71 ATA except for increased blood flow to the liver (122%, P less than 0.05), whereas the blood flow to the adrenals, the diaphragm, and the leg muscle fell (P less than 0.05).

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)

Antipyrine and acetaminophen kinetics in the rat: comparison of data based on blood samples from the cut tail and a cannulated femoral artery.

Antipyrine and acetaminophen kinetics were determined from concentration data obtained by simultaneous blood sampling from the cut end of the tail and a cannulated femoral artery in the rat. Significant differences in concentrations and kinetics for both drugs were found by comparison of the two sampling sites. The hypothesis that the differences were due to a low tail blood flow was tested. The tail blood flow was measured with a microsphere technique, and tail antipyrine concentrations were calculated from the relationship between arterial antipyrine concentration, tail flow, and time for comparison with the observed antipyrine concentrations. Mean blood flow of the rat tail was 0.02 ml/min/ml tail tissue at 22 degrees, which was 8.8 and 0.9% of the liver and kidney flow, respectively. Tail flow increased more than twofold by elevation of the tail temperature to 37 degrees. The calculated tail antipyrine concentration versus time curve showed a very close correspondence to the observed antipyrine tail concentration versus time curves. The results show that tail flow is a major determinant of antipyrine tail concentration in the rat. Kinetic data based on blood samples from the cut end of the tail, therefore, should be interpreted with caution.

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.

Inotropic and chronotropic effects of isoprenaline in rats exposed to 30 bar.

Inotropic and chronotropic responses to the beta-agonist, isoprenaline (ISO) were studied with a transducer located in the left ventricle and a catheter placed in the left femoral artery in anesthetized rats at 1 and 30 bar. The hemodynamic control values were equal in both series. During ISO infusion the chronotropy increased equally (34%) at 1 and 30 bar. The inotropy increased by 38% during ISO infusion at 1 bar (Series 1). Increased inotropy (44%), and unchanged chronotropy were found during compression to 30 bar (Series 2). The ISO evoked inotropic responses in absolute values were greater at 30 bar than at 1 bar. Nevertheless, an equal relative (%) increase in inotropy was found during ISO infusion at 30 bar compared to 1 bar. The cardiac oxygen consumption was estimated to be 65% higher at 30 bar during ISO infusion compared to that at 1 bar.

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.

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)

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.

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.

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.

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.

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.

Renal cortical blood flow distribution measured by hydrogen clearance during dopamine and acetylcholine infusion. Effect of electrode thickness and position in cortex.

Blood flow distribution in the renal cortex was investigated in control and during i.a. infusion of dopamine (DA) and acetylcholine (Ach) in dogs. Local blood flow in outer cortex (OCF) and in inner cortex (ICF) was measured by platinum electrodes detecting hydrogen washout rate in tissue. Mean cortical blood flow measured by hydrogen washout rate in the renal vein (CFV) was compared with renal arterial blood flow (RAF) measured by electromagnetic flowmeter. With electrodes of 0.05-0.2 mm diameter control blood flow rates in outer and inner cortex were 4.57 +/- (S.D.) 1.73 ml/min.g, and 4.35 +/- 0.57 ml/min.g, which is higher than found using 0.2-0.5 mm electrodes in this and previous studies. OCF and ICF increased proportionally during intraarterial infusion of DA or Ach. The increase in local blood flow per unit volume was about 20% less than the increase in RAF, most likely due to an increase in renal volume and a reduced vasodilatory response in the surrounding of some electrodes. CFV rose almost to the same degree as RAF, showing a diffusion equilibrium for hydrogen gas even at maximal flow rate. During vasoconstriction induced by high doses of DA, OCF and ICF fell proportionately. Thus, equal vascular responses in outer and inner cortex were observed during both vasodilator and vasoconstrictor infusion. This indicates that changes in sodium excretion with renal blood flow may not be associated with a redistribution of cortical peritubular blood flow.

Effect of high ambient pressure and oxygen tension on organ blood flow in the anesthetized rat.

Cardiac output (CO) and blood flow to major organs were investigated in pentobarbital-anesthetized rats using 85Sr- and 141Ce-labeled microspheres (MS) (15 +/- 1 microns (SD)) injected into the left ventricle. Since MS dissolved in dextran cannot be used in albino rats, the method was evaluated using MS dissolved in Ficoll-70. Two subsequent MS injections were administered to each rat at normal gas atmospheric pressure (Group 1). The results demonstrated homogeneous mixing of MS dissolved in Ficoll-70 and good reproducibility of hemodynamic measurements using ventricular injection. In three other series, control measurements were performed in each rat at a normal gas atmosphere and at atmospheric pressure, and in one of the following experimental situations: at 5.0 atmospheres absolute (ATA) of ambient pressure and normal O2 tension (PO2 - 0.2 ATA) (Group 2); at an ambient pressure of 5 ATA and high O2 tension (PO2 = 1.0 ATA) (Group 3); and at normal ambient pressure and high O2 tension (PO2 = 1.0 ATA) (Group 4). The inert gas was nitrogen. Cardiac output, heart rate, and mean arterial pressure did not change in any group. Renal blood flow fell by 15% (P less than 0.05) in all groups except in Group 1. Myocardial and cerebral blood flow increased by 30% (P less than 0.05) in groups 2 and 3. Blood flow in the diaphragm fell by 40% (P less than 0.001) in Group 4.