Biomedical subjects

G W Bergö

Publications and source records attributed to G W Bergö.

4 recordsLinked to original sources

PubMed1994

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)

Animals↗

PubMed1994

Cerebral pressure-flow and metabolic responses to sustained hypoxia: effect of CO2.

This study was designed to determine the role of CO2 in the cerebral hemodynamic, metabolic, and fluid shift responses in a conscious sheep model of acute mountain sickness (AMS). Ewes were instrumented chronically with left ventricular, aortic, inferior vena cava, sagittal sinus, and epidural catheters and exposed to 96 h of hypoxia in an environmental chamber in two groups: 1) hypocapnic [HH; n = 12; arterial PO2 (PaO2) = 40 Torr, arterial PCO2 (PaCO2) = 27 Torr] and 2) eucapnic (EH; n = 9; PaCO2 = 40 Torr, PaCO2 = 37 Torr). AMS, estimated from food and water intakes and behavior, occurred in 9 of 12 HH and 9 of 9 EH sheep. Intracranial pressure (Picp) and the pressure gradient between Picp and sagittal sinus (Psag) increased in AMS sheep only. Total and regional cerebral blood flows, except in the choroid plexus (Qcp), were elevated significantly (P < 0.05) throughout hypoxia in all sheep; cerebral blood flow was greater in EH sheep (P < 0.05). Qcp decreased in HH (P < 0.05) but remained unchanged in EH sheep. Cerebral O2 and glucose uptakes were not altered in either group. Brain edema, reflected by elevated wet-to-dry tissue weight ratios (P < 0.0001), occurred only in AMS sheep. We conclude 1) AMS is associated with cerebral edema and normal brain aerobic metabolism, 2) decreased Qcp and increased Picp-Psag gradients during HH likely compensate the increased intracranial volume in AMS, and 3) CO2 supplementation at constant PaO2 did not reduce AMS, Picp, or brain tissue edema.

Altitude Sickness↗

PubMed1993

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)

Animals↗

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↗