Biomedical subjects

I Tyssebotn

Publications and source records attributed to I Tyssebotn.

At least 37 records · Page 2Linked to original sources

PubMed1992

Increased breathing gas density enhances cardiac workload.

The effect of increased breathing gas density on the left ventricular pressure (LVP), cardiac contractility (dP/dt), heart rate (HR), intrapleural pressure (P(ip)) and respiratory frequency (RF) was evaluated in pentobarbital-anaesthetized rats (n = 8) and cats (n = 6). Catheters were placed in the left cardiac ventricle via the right carotid artery to measure the LVP, in the oesophagus for indirect measurements of P(ip) and RF, and into the aorta from the right femoral artery for arterial pressure measurements. The RF fell significantly within the first 30 s and had reached a stable value 2 min after gas shift in both rats and cats. Concomitant with the RF fall, the depth of inspiration and intrapleural pressure differences in both rats and cats increased. The acid-base balance remained at control levels in both animal groups. LVP and dP/dt started to increase during the first half-minute, and reached their maximum values 2-5 min after the introduction of normoxic sulphur hexafluoride. A linear relationship between the enhanced dP/dt and the P(ip) increase was found. The HR remained unchanged in both cats and rats. These findings indicate that the breathing gas density might influence the cardiac contractility found during hyperbaric exposure, and that a gas density of five times that of air at 1 bar does not influence the diffusion of O2 and CO2 in the lung. The O2 consumption of the heart in cats and rats was calculated to rise by 25% and 30% respectively in the dense breathing gas atmosphere.

Acid-Base Equilibrium↗

PubMed1992

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.

Animals↗

PubMed1991

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.

Animals↗

PubMed1991

Respiratory frequency and distribution of cardiac output in rats breathing gas with different densities.

The effect of increased and reduced breathing-gas density on cardiac output (CO) and organ blood flow was studied with radiolabelled microspheres on pentobarbital anaesthetized rats using normoxic sulphurhexafluoride (SF6) and normoxic helium (He). The mean arterial pressure (MAP), heart rate (HR), and CO remained unchanged during exposure to any gas composition. The respiratory frequency (RF) was reduced from 98 +/- 6 (mean +/- SE) to 85 +/- 3 min-1 (p less than 0.01) in the dense breathing-gas, while the RF increased from 96 +/- 6 to 108 +/- 4 (p less than 0.01) in the He-O2 atmosphere. The arterial acid-base chemistry was mainly unaltered in any situation, indicating almost unchanged alveolar ventilation. Since the cerebral blood flow increased (30%, p less than 0.01), we suggest that SF6 gas is not a truly inert gas; blood flow to the eyes was also increased (30%, p less than 0.01). Though the pumping action of the heart (MAP X HR) remained constant, the blood flow to the left ventricular myocardium was increased (28%, p less than 0.01) by the elevated gas density. Reduced breathing-gas density increased the myocardial blood flow in the right ventricle (20%, p less than 0.02) suggesting a constrictive effect of He on the pulmonary arteries. Except for reduced renal blood flow, no blood flow changes were observed in any organ in this situation.

Animals↗

PubMed1990

Cardiovascular changes in anesthetized rats during exposure to 30 bar.

The effect of exposure to 30 bar (PHe = 29.0 bar, PN2 = 0.8 bar, PO2 = 0.2 bar) on left ventricular pressure, cardiac contractility, heart rate (HR), and arterial pressure was studied in anesthetized rats. During compression there was a progressive increase in maximal left ventricular pressure (LVPmax), maximal velocity of LVP rise (+ dP/dtmax) and fall (- dP/dtmax), systolic pressure (APsys), and pulse pressure (delta AP). The greatest increase in contractility per bar was found between 1 and 5 bar. Immediately after 30 bar was reached, LVPmax (19%), + dP/dtmax (60%), and - dP/dtmax (22%). APsys (19%), and delta AP (43%) were significantly increased from predive values, with an additional increase detected for all these variables after 60 min at 30 bar. An increase in estimated oxygen consumption (work load) of the heart was also found during compression to and at 30 bar. No changes in HR, mean arterial pressure, and end-diastolic pressure were observed during the high-pressure exposure, indicating that the inotropic changes were not due to changes in peripheral hemodynamics.

Anesthesia↗

PubMed1990

Distribution of cardiac output in awake rats during exposure to 5 bar.

Previous studies have reported increased total myocardial blood flow (TMBF) after 15 min stable pressure in a normoxic O2-N2 and O2-He at 5 bar, although cardiac output (CO), heart rate (HR), and mean arterial pressure (MAP) remained unchanged. In the present study, 2 groups of awake rats were exposed to normoxic 5 bar atmospheres; group 1 breathing a He-O2-N2 mixture and group 2 a O2-N2 mixture. Organ blood flow was determined by the microsphere method in control (C) (group 1) and after 15 (T1) and 75 min (T2) hyperbaric exposures (groups 1 and 2). MAP and HR remained at control levels in group 2 animals and increased slightly (6-10%, P less than 0.05) in group 1 rats. CO remained unchanged during the experimental period in both groups. In group 1, TMBF had increased by 13% (P less than 0.05) at T1 and continued to increase at T2 for both groups. Blood flow to the liver and spleen increased during the exposure in both groups. Renal blood flow fell by 25% from C to T2 (P less than 0.05). The arterial blood gases and pH remained at the predive control level in group 2 rats, whereas serum corticosterone concentration fell to 60% during compression (P less than 0.01), possibly due to N2 narcosis, but increased gradually toward 80% of C value during the pressure exposure. We conclude that the increase in TMBF, which is initiated by compression to a 5-bar normoxic atmosphere, persists when stable pressure is maintained.

Animals↗

PubMed1989

Increased cardiac contractility in rats exposed to 5 bar.

The left ventricular pressure, arterial blood pressure and heart rate were studied in three series of pentobarbital-anaesthetized rats exposed to 5-bar normoxic (PO2 = 0.2 bar) environments: nitrogen-oxygen (15 and 60 min) and helium-oxygen (15 min). The maximal left ventricular pressure (LVP max) and the maximal velocities of LVP rise (+ dP/dt max) and fall (- dP/dt) were significantly (P less than 0.01) increased immediately after reaching normoxic 5 bar (He, 13-28%; N2, 13-23%) and during the exposure at 5 bar (He, 22-44%; N2, 13-18%). The pulse pressure increased significantly (He, 50-62%; N2, 30-34%; P less than 0.01) during the hyperbaric exposure. No changes in heart rate or end-diastolic and mean arterial pressure were detected. The present findings indicate an enhanced cardiac contractility (+ dP/dt max) at 5 bar, with the greatest increase found when He was used as inert gas. The increased contractility was of significant duration (at least 60 min), and was not completely reversed until 5-10 min after decompression.

Animals↗

PubMed1989

Respiratory depression by analgesics at 41 bar.

The effects of morphine and fentanyl on respiration and tissue CO2 measured transcutaneously were studied at surface and at 41 bar ambient pressure in conscious, trained rats. Morphine and fentanyl were given in equianalgesic doses i.v., 7 and 0.025 mg/kg, respectively. Fentanyl caused a rapid but brief respiratory depression which was the same at 1 and 41 bar, and essentially the same results were found in the morphine groups, although there was a longer latency and duration of action. No statistical differences in the degree of respiratory depression were found at 41 bar compared to 1 bar for either analgesic.

Animals↗

PubMed1988

Positive inotropic effect on the rat atrial myocardium compressed to 5, 10 and 30 bar.

The contractile activity of spontaneously beating auricular preparations from the rat was studied during and after pressure exposure to 5, 10 and 30 bar in three series of experiments (compression and decompression rate: 1 bar min-1). The preparations were mounted in an organ bath within a pressure chamber and perfused with oxygenated preheated Krebs-Henseleit solution (37 degrees C, pH = 7.45) containing alpha-, beta- and muscarinic-receptor blockers and blockers of the neuronal and extraneuronal uptake mechanisms. No change in chronotropy of the cardiac preparations were observed during or after exposures to the pressures tested. Significant increase in cardiac contractility (20-40%, P less than 0.01) described by the peak tension (Tmax), the maximal velocity of tension rise (T'max) and fall (T'min) were apparent at 5 and 10 bar. Further significant elevations (60-80%, P less than 0.05) in Tmax, T'max and T'min were detected during exposure to 30 bar. The cardiac contractility increased rapidly with pressure, was approximately unchanged during stable elevated pressures at 5, 10 and 30 bar, but was maintained above control values 15 min after completed decompression. Since no change in chronotropy and loading of the preparations occurred, it is concluded that the increased contractility is due to a positive inotropy generated by the hydrostatic pressure. Furthermore, it is indicated that this positive inotropy is not related to adrenoceptor activation since the effect was achieved in the presence of alpha-, and beta-adrenoceptor blockade.

Animals↗

PubMed1988

Effect of 5 bar oxygen on cardiac output and organ blood flow in conscious rats.

The distribution of cardiac output (CO) was studied in conscious rats during hyperbaric oxygen (HBO) exposure to 5 bar for 60 min. Heart rate (HR) and arterial blood pressure (ABP) were continuously recorded. Organ blood flow and CO were measured during control, after 5 and 60 min HBO by the microsphere method. Arterial acid-base balance was measured both during control and HBO. During HBO the animals remained calm and seemed unstressed with no sign of convulsions. The arterial pH remained at control level, whereas PCO2 and HCO3 fell (P less than 0.05). The systolic ABP increased gradually during HBO, while the mean ABP was unchanged. HR started to fall at 1 bar O2 (P less than 0.05), fell markedly during compression (P less than 0.02), and remained below control level during the HBO. After atropine was given, HR increased to predive control in all animals. CO fell by 25% due to increased total peripheral vascular resistance of 27%. Blood flow to most organs fell correspondingly to CO, indicating an equally distributed vasoconstriction. Unchanged blood flow was found in the kidneys, the adrenals, and the liver. Blood flow to the right and left heart ventricles fell significantly more than the average reduction of CO. Calculation of a pump work index of the heart by the product of systolic ABP and HR showed unchanged performance, while the blood flow to the left ventricle fell by 50%, which suggests insufficient O2 supply.

Acid-Base Equilibrium↗

PubMed1988

Transcutaneous measurement of PCO2 at high ambient pressure (41 bar).

The accuracy of transcutaneous CO2 monitoring with the Kontron CO2 sensor was studied during compression to 41 bar and subsequent decompression. The PCO2 was stable and accurate during the test of the sensor in the pressure chamber, although an increase of 0.1-0.2 kPa during compression was found. The function of the transcutaneous sensor was tested in rats at 1 bar for the correlation between transcutaneous PCO2 (PtcCO2) and arterial PCO2 (PaCO2). The correlation coefficient between PtcCO2 and PaCO2 in the rat was found to be 0.93. The time difference between the 90% transcutaneous and 90% arterial response time was 4.6 +/- 0.6 min (mean +/- SEM). Finally, the use of the sensor in rats ventilated at constant minute volume during compression to 41 bar was examined. An increase in PtcCO2 of 0.2-0.4 kPa was found. The present results of transcutaneous PCO2 measurements indicate that this method may be useful in hyperbaric research and treatment.

Animals↗

PubMed1987

The effect of beta 1-adrenoceptor blockade on cardiac output and organ blood flow in conscious rats.

The acute effects of the beta 1-adrenoceptor inhibition by atenolol were investigated on conscious rats. Cardiac output and organ blood flow were measured by 15-microns radiolabelled microspheres during control and 20 min after administration of atenolol (1 mg/kg body wt). Arterial blood pressure and heart rate were measured continuously. Arterial blood gases and pH were determined immediately after the two microsphere injections and arterial blood samplings. The mean arterial blood pressure fell significantly shortly after the injection of atenolol and was reduced by 9% (p less than 0.02) after 20 min. Heart rate fell by 17% (p less than 0.05). The total peripheral vascular resistance increased by 25% (p less than 0.05). At the same time the arterial acid-base chemistry remained unaltered from the control. The cardiac output fell by 24% (p less than 0.05). Blood flow fell to all organs and tissues (0-67%) except to the brain, adrenals, liver, ears and diaphragm. The greatest decrease was seen in perfusion of the adipose tissue (67%) and of the spleen (60%), indicating that the blood flow to these organs are normally highly influenced by beta 1-adrenoceptor stimulation. The estimated work load of the heart was reduced by 20% which correlated well to a reduction of myocardial blood flow to the same degree.

Animals↗

PubMed1986

Hyperbaric exposure to a 5 ATA He-N2-O2 atmosphere affects the cardiac function and organ blood flow distribution in awake trained rats.

Previous studies on rats have demonstrated an increased myocardial blood flow (MBF) in spite of an unchanged cardiac output (CO), mean arterial pressure (MAP), and heart rate (HR) when rats were exposed to a 5 ATA ambient pressure (PN2 = 4.8 ATA, PO2 = 0.2 ATA). We have investigated the changes in CO and organ blood flow by the microsphere method on 9 awake, trained rats exposed to a 5 ATA ambient pressure with surface pressure of N2 (= 0.8 ATA) and O2 (= 0.2 ATA), increasing the ambient pressure with He. The chamber temperature was 30-31 degrees C. CO and organ blood flow were measured in control and after 15 min under pressure. No changes were observed in CO, HR, or MAP during the hyperbaric exposure, indicating unchanged external work of the heart when calculated as MAP X HR. The pulse pressure however increased significantly (P less than 0.05). MBF increased at the same time by 36% (P less than 0.01), equally distributed in the right and left ventricles (P less than 0.01). The fact that myocardial perfusion increases when ambient pressure is elevated, independent of atmospheric inert gas composition, invites the conclusion that this change is due to the ambient pressure itself and not to a specific effect of N2 or He as inert gas at 5 ATA. The blood flow to the adrenals increased by 77% (P less than 0.01), the liver by 105% (P less than 0.05), while the blood flow to the skeletal muscles decreased by 30% (P less than 0.05). The blood flow to the lungs, the paws, and the outer ear increased, most likely due to the high ambient temperature in the chamber. We may conclude that HR does not change in a normoxic hyperbaric atmosphere. High ambient pressure increases the pulse pressure, but the MAP and CO remain unchanged. These changes and the changes in organ blood flow need well-balanced neuronal or hormonal reflexes to distribute an unchanged CO under pressure. The exact explanation is not known.

Animals↗

PubMed1985

Blood flow heterogeneity in the renal cortex during burn shock in dogs.

Blood flow distribution and occurrence of intermittent, patchy ischaemia in the renal cortex were investigated in anaesthetized dogs before and during burn shock. Severe or moderate thermal injury was induced by scalding 30% of body surface by 90 degrees C or 70 degrees C hot water. Local blood flow in outer and inner cortex was measured by microspheres and by electrodes recording hydrogen gas washout rates. The haematocrit rose much more in the moderately than in the severely scalded dogs, due to marked haemolysis in the latter group. Cortical blood flow was reduced more after severe than after moderate thermal injury. A significant redistribution of blood flow from outer to inner cortex was not demonstrated. Abrupt shifts in local washout rates were observed in most dogs during shock, but was consistently more frequent in the moderately scalded dogs. Such episodes of patchy intermittent ischaemia were not seen after inhibition of prostaglandin synthesis by indomethacin. Thus, prostaglandins may mediate focal vasoconstriction in the renal cortex during burn shock in dogs.

Animals↗

PubMed1985

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).

Animals↗

PubMed1985

Effect of high ambient pressure and oxygen tension on organ blood flow in conscious trained rats.

Cardiac output and blood flow to different organs and tissues were investigated in conscious trained rats using radiolabeled microspheres (MS) injected into the left ventricle. Two subsequent MS injections were administered to each rat at normal gas atmosphere and pressure (control) and in one of the following experimental situations: at normal ambient pressure and high partial pressure of O2 (PO2 = 1.0 ATA) (Group 1); an ambient pressure of 5 ATA and high partial pressure of O2 (PO2 = 1.0 ATA) (Group 2); and at ambient pressure of 5 ATA and normal partial pressure of O2 (PO2 = 0.2 ATA). The inert gas was nitrogen. Cardiac output fell in Groups 1 and 2 with high PO2 (P less than 0.05), and was unchanged in Group 3 with normal PO2. Heart rate decreased in Groups 1 (NS) and 2 (P less than 0.01), and was unchanged in Group 3. The arterial pressure remained unchanged while the renal blood flow decreased (P less than 0.05) in all groups. The myocardial blood flow fell (P less than 0.05) in both groups with decreased cardiac output, and was increased by 25% (P less than 0.05) in normoxia (Group 3) with maintained cardiac output. The blood flow to the adrenal glands fell (P less than 0.05) in both groups with high PO2, and increased in the normoxic Group 3 (NS). The blood flow to the splanchnic area fell in all groups. The cerebral blood flow and blood flow to the eyes fell in both groups with high PO2 (P less than 0.05), and were constant in normoxia.

Animals↗

PubMed1983

The effect of hemorrhagic hypotension on total and local renal blood flow in the rat.

The effect of hemorrhagic hypotension (HH) on local and total renal blood flow was studied in rats. Cortical blood flow, measured as H2 gas clearance, was determined before and during HH with a mean arterial blood pressure of 50 mm Hg. During the initial 10-15 min of bleeding renal cortical vascular resistance was unchanged, and total renal blood flow autoregulatory ability was abolished. Cortical vascular resistance thereafter increased steadily to twice the control level after 90 min of HH. At this time, retransfusion of the shed blood improved cortical blood flow due to increased arterial blood pressure, not to reduced cortical vascular resistance. In a second group, total and local renal blood flows were obtained from 125I-iodoantipyrine uptake rate after 2 h of HH with arterial blood pressure maintained at 50 mm Hg. Total renal blood flow was reduced to 20% of control with no change in blood flow distribution between outer and inner cortical or medullary zones. Both cortical blood flow and intrazonal local renal blood flow heterogeneity had increased at the end of the HH period. However, ischemic and extremely low flow sectors comprising cortex and outer medulla were observed only in 1 of the 10 kidneys studied with the 125I-iodoantipyrine technique. In only 1 of 8 animals studied with the H2 gas method were intermittent sudden changes in cortical blood flow observed during HH. Since hematocrit tended to fall during HH, these observations support the concept that local flow intermittence is predominantly associated with high hematocrit shocks.

Animals↗

PubMed1983

The effect of water deprivation on local renal blood flow and filtration in the laboratory rat.

The effects of longlasting dehydration on total and local renal blood flow and glomerular filtration rate have not been studied previously in the laboratory rat. We therefore determined zonal renal blood flow (ZRBF) in cortical and medullary zones by the 125I-iodoantipyrine and H2 gas washout techniques. After 8 days of water deprivation renal blood flow (RBF) was reduced by 65% and renal vascular resistance (RVR) had increased by 110%. Half the RVR increase could be ascribed to increased blood viscosity as reflected by increased hematocrit (42 to 60%). Fractional ZRBF decreased by 5% in the outer half and increased by 5% in the inner half of the cortex. Measurements of the relative single nephron glomerular filtration rate (sngfr) of superficial and deep nephrons, determined by the 14C-ferrocyanide technique, indicated no detectable changes in filtrate distribution. Both ZRBF and sngfr heterogeneity had increased in dehydrated as compared to control rats. In one rat studied with the H2 gas washout method, local ischemia and intermittent blood flow occurred. Similarly, cortical patches of nonfiltering nephrons were observed in another rat. These findings suggest that the increased heterogeneity of intrarenal flow and filtration may involve, and in part be due to, intermittent local changes in blood flow.

Animals↗