Biomedical subjects

G W Bergø

Publications and source records attributed to G W Bergø.

10 recordsLinked to original sources

PubMed2001

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.

Air Pressure↗

PubMed1995

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.

Acid-Base Equilibrium↗

PubMed1995

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.

Animals↗

PubMed1995

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)

Animals↗

PubMed1994

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.

Anesthesia↗

PubMed1993

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)

Adaptation, Physiological↗

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↗

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

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↗

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↗