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Biomedical subjects

C Risöe

Publications and source records attributed to C Risöe.

At least 19 recordsLinked to original sources
PubMed2000

Cerebral nitric oxide concentration and microcirculation during hypercapnia, hypoxia, and high intracranial pressure in pigs.

Intracerebral nitric oxide (NO) concentration was measured to establish the technique and to investigate the response of the NO concentration to CO(2)variations, hypoxia, and reduced cerebral perfusion pressure. An intracerebral nitric oxide sensor was used in 10 pigs. Cerebral microcirculation was measured by laser Doppler flowmetry. Five pigs received 40 mg/kg nitro-1-arginine methyl ester (L-NAME). Baseline NO concentration was 246 +/- 42 nM. Hypercapnia increased cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05). Hypoxia decreased NO concentration (P< 0.05). During high intracranial pressure, cerebral microcirculation decreased (P< 0.05) before the NO concentration decreased (P< 0.05), and after normalisation of the intracranial pressure the NO concentration increased, but more slowly than the cerebral microcirculation. L-NAME caused a decrease in cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05) to a new steady state, and L-NAME attenuated the changes in NO concentration after hypoxia (P< 0.05) and high intracranial pressure (P< 0.05). In conclusion, the electrochemical sensor appears to reliably detect changes in localised intracerebral NO concentration and seems to be a promising tool for direct measurement of this chemically unstable substance.

Animals↗
PubMed1998

Effect of hemorrhage on cerebral microcirculation during normal and high cerebrospinal fluid pressure in pigs.

Studies on cerebral blood flow during hypotension and high intracranial pressure are scarce. Accordingly, this study examines the effects of increased cerebrospinal fluid (CSF) pressure on the cerebral circulatory response to hemorrhage. Measurements of cerebral microcirculation with laser Doppler flowmetry was performed in 12 pentobarbital-anesthetized pigs during hemorrhage, with and without high CSF pressure. Arterial and CSF pressures were monitored. Laser Doppler microprobes were positioned on the brain surface and in the gray and white matter. High CSF pressure (80% of mean arterial pressure) was induced by infusion of artificial CSF into the cisterna magna in eight pigs, whereas four animals served as controls. The response to rapid arterial bleeding at normal and high CSF pressure was recorded. When CSF pressure was normal, bleeding of 15% and 25% of the total blood volume caused a drop of cerebral perfusion pressure to 73 and 71 mmHg, respectively, causing a decrease in the laser Doppler signal to 90+/-8% of the baseline value. During high CSF pressure, the cerebral perfusion pressure was 23 mmHg and the laser Doppler signal was 52+/-29% of baseline. Bleeding of 15% of blood volume reduced the laser Doppler signal to 0 (equal to postmortem values) in three pigs, and bleeding of 25% of the blood volume reduced the laser Doppler signal to 0 in seven of eight pigs. Consequently, a blood loss that is of minor importance for the cerebral microcirculation in the normal state may be deleterious to the circulation when combined with high CSF pressure.

Animals↗
PubMed1998

Cerebrovascular effects of high intracranial pressure after moderate hemorrhage.

Patients with head injuries often develop increased intracranial pressure after hemorrhage. The authors studied the effect of moderate hemorrhage followed by elevated intracranial pressure on cerebrovascular variables. Cerebral blood flow in 13 pigs was measured with laser Doppler flowmetry, and cerebral venous blood gases were taken from the sagittal sinus. High intracranial pressure (80% of mean arterial pressure) was induced by infusion of artificial cerebrospinal fluid into the cisterna magna, and blood pressure was reduced by bleeding to a mean of 78% of the prebleeding values in eight pigs. Five pigs served as secondary controls. High intracranial pressure before hemorrhage caused a decrease in cerebral blood flow to 34% of the baseline values, a decrease in sagittal sinus oxygen saturation to 46%, and a decrease in cerebral perfusion pressure to 36%, but did not change cerebrovascular resistance. High intracranial pressure after hemorrhage decreased cerebral blood flow to 14% of baseline values. Sagittal sinus oxygen saturation decreased to 22%, cerebral perfusion pressure decreased to 30%, and the cerebrovascular resistance increased by 355%. The moderate hypotension after hemorrhage caused a considerable enhancement of the effects of high intracranial pressure on cerebral hemodynamics.

Animals↗
PubMed1997

Local variations in the cerebral microcirculatory response to hypercapnia and haemorrhage.

This study evaluates local variations of the cerebral vasomotor responses to hypercapnia and haemorrhagic hypotension in a pig model. Four laser Doppler flow probes were used in each pig. There was considerable variation in laser Doppler signals between the four probes in baseline recordings. The increases in flow after CO2 administration in 7 pigs had a mean coefficient of variation of 0.43 +/- 0.31, and the flow changes after blood loss in another 7 pigs had a mean coefficient of variation of 0.45 +/- 0.34. The range of flow changes within each animal was large; the probe with the highest CO2 response showed on the average a 273% +/- 157% larger CO2 response than the probe with the lowest CO2 response. Correspondingly, the probe with the best preserved blood flow after blood loss had on the average a flow value of 93% +/- 12% of the baseline value, while the probe that changed most with haemorrhage had a flow value of 44% +/- 24% of the baseline value. Single laser Doppler recordings have been used for the monitoring of cerebral blood flow in neurosurgical critical care, but our results suggest that a single laser Doppler flow probe is not an adequate method to monitor vasoreactivity in neurosurgical patients because flow signals from one probe may be unrepresentative for other sites in the brain.

Animals↗
PubMed1995

Cerebral blood flow measured with intracerebral laser-Dopplerflow probes and radioactive microspheres.

We have measured cerebral blood flow with intracerebral laser-Doppler microprobes in pentobarbital-anesthetized pigs. We compared the results with measurements from laser-Doppler probes placed on the surface of the brain and with blood flow estimation by the radioactive microsphere method. The cerebral blood flow was varied by alterations in inspired carbon dioxide, hemorrhagic hypotension, and high cerebrospinal fluid pressure. The intracerebral probes and the surface probes showed parallel responses to variations in cerebral blood flow. The correlation was closest between surface probes and the intracerebral probes measuring from the cerebral cortex (r = 0.46; P < 0.005). The r value between laser-Doppler flowmetry and radioactive microspheres was 0.41 (P < 0.0005) for all measurements. The correlation to microspheres was best for the probes located 3 or 10 mm into the brain and poorest for the surface probe. In conclusion, intracerebral laser-Doppler flow measurements reflect changes in blood flow, and the technique appears useful for continuous estimates of cerebral blood flow.

Animals↗
PubMed1994

Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler echocardiography.

OBJECTIVES: The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade. BACKGROUND: Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle. METHODS: In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling. RESULTS: There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution. CONCLUSIONS: Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.

Animals↗
PubMed1994

Effect of carotid sinus baroreceptor reflex on hepatic and splenic vascular capacitance in vagotomized dogs.

Mechanisms of how baroreflex activation changes splanchnic vascular volumes were studied in eight vagotomized dogs, anesthetized by chloralose/urethan. Hepatic and splenic vascular volume changes were determined from organ dimensions by sonomicrometry. Pulsatile carotid sinus pressure (CSP) in isolated and separately perfused carotid sinuses was changed among 200, 120, and 40 mmHg. Lowering CSP from 120 to 40 mmHg significantly decreased both hepatic and splenic vascular volume (at similar portal pressure) by 1.9 +/- 0.5 and 1.8 +/- 0.6 ml/kg body wt, respectively. Increasing CSP from 120 to 200 mmHg tended to increase regional vascular volumes (P = NS). The combined volume change of liver and spleen between CSP 40 and 200 mmHg was 4.2 +/- 0.6 ml/kg body wt (P < 0.001). Pressure-volume (dimension) curves at high, low, and baseline CSP were determined to separate active and passive mechanisms of vascular volume changes. Changes in CSP did not change regional vascular compliance. Low CSP significantly decreased unstressed liver and unstressed splenic volume by 3.3 +/- 0.9 and 1.9 +/- 0.5 ml/kg body wt, respectively. These results indicate that liver and spleen both contribute to blood volume mobilization by vasoconstriction during low CSP and that the carotid sinus baroreceptor reflex modulates hepatic and splenic vascular capacitance by changing unstressed volume rather than by changing vascular compliance.

Animals↗
PubMed1994

Effect of enalaprilat on splanchnic vascular capacitance during acute ischemic heart failure in dogs.

This study investigates the effect of angiotensin-converting-enzyme inhibition by intravenous enalaprilat (100 micrograms/kg) on splanchnic vascular capacitance during acute left ventricular failure induced by coronary microembolization in alpha-chloralose/urethan anesthetized dogs. Changes in hepatic and splenic vascular volumes were determined from organ diameters (sonomicrometry) at 15, 30, and 45 min after enalaprilat injection. Changes in vascular capacitance were assessed from organ pressure-diameter curves obtained during transient hepatic outflow occlusion. Thirty minutes after enalaprilat, hepatic volume was increased by 52 +/- 14 ml (P < 0.01), and portal and hepatic vein pressures were decreased from 10.2 +/- 0.9 to 8.7 +/- 0.8 mmHg (P < 0.01) and from 3.9 +/- 1.6 to 3.1 +/- 0.7 mmHg (P < 0.05), respectively. Splenic volume did not change. Enalaprilat shifted the hepatic pressure-diameter curve upward, resulting in a larger hepatic volume at any given pressure. Curve intercept was increased, suggesting an increase in unstressed vascular volume. Curve slope was unchanged. In conclusion, enalaprilat increased hepatic vascular volume during acute left ventricular failure in dogs. The pressure-diameter curve shift suggests a reduction in the smooth muscle tone of hepatic capacitance vessels.

Acute Disease↗
PubMed1993

Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.

BACKGROUND: Color M-mode Doppler echocardiography has been suggested as a new noninvasive technique for assessing left ventricular diastolic function. The present study investigated intraventricular filling pattern by color M-mode Doppler in patients during percutaneous transluminal coronary angioplasty (PTCA). In a dog model of myocardial ischemia, the color M-mode flow pattern was related to indices of global and regional myocardial function. METHODS AND RESULTS: From color M-mode images, the time difference (TD) between occurrence of peak velocity in the apical region and at the mitral tip was determined in 20 patients and eight anesthetized dogs during coronary occlusions. During PTCA, the timing of peak velocity was progressively delayed from mitral valve to apex. Consistent with this, the dog model showed delayed apical filling during coronary occlusion; TD increased from 18 +/- 4 to 71 +/- 9 milliseconds (P < .01). In the ischemic region, systolic shortening (sonomicrometry) decreased from 20 +/- 3% to -5 +/- 2% (p < .01). The one-third filling fraction decreased from 59 +/- 5% to 31 +/- 6% (P < .01) and correlated with TD (r = .85, P < .01). The time constant of isovolumic relaxation (tau) increased slightly and correlated with TD (r = .81, P < .01). Pacing tachycardia, caval constriction, and volume loading were performed to mimic the ischemia-induced changes in heart rate, stroke volume, and intracavitary filling pressure, respectively. There were no significant changes in TD or tau during these interventions. CONCLUSIONS: Color M-mode Doppler echocardiography showed a marked delay of apical peak filling velocity during PTCA. The experimental data suggest that this reflects retarded filling of the ischemic ventricle. Thus, color M-mode Doppler may provide a useful method for assessing diastolic dysfunction.

Adult↗
PubMed1992

Nitroprusside and regional vascular capacitance in patients with severe congestive heart failure.

BACKGROUND: This study investigates the effects of sodium nitroprusside on regional vascular capacitance in eight patients with severe congestive heart failure (New York Heart Association class IV) and pulmonary hypertension. METHODS AND RESULTS: Regional relative blood volumes in the splanchnic and pulmonary region were determined by equilibrium blood pool scintigraphy. Hepatic venous wedge pressure and the mean of pulmonary artery and pulmonary capillary wedge pressure were used to represent the distending pressures of the splanchnic and pulmonary capacitance vessels, respectively. The dose of sodium nitroprusside was increased stepwise until systolic pulmonary artery pressure decreased below 50 mm Hg. This caused reductions in mean aortic pressure from 89 +/- 5 to 66 +/- 3 mm Hg (p less than 0.005), in pulmonary capillary wedge pressure from 31 +/- 1 to 16 +/- 2 mm Hg (p less than 0.001), and in hepatic venous wedge pressure from 10.0 +/- 1.0 to 5.9 +/- 0.6 mm Hg (p less than 0.005). Intestinal blood volume increased by 26 +/- 7% (p less than 0.005), whereas hepatic blood volume decreased by 9 +/- 3% (p less than 0.02). Pulmonary blood volume was unchanged. Analysis of intestinal and pulmonary vascular pressure-volume relations showed larger or equal blood volumes contained at lower distending pressures, indicating that sodium nitroprusside reduced smooth muscle tone of the capacitance vessels in these regions. The reduction of hepatic blood volume was compatible with passive expulsion of blood subsequent to reduced venous pressure. There was no change in the count rate from the spleen. CONCLUSIONS: Nitroprusside reduced venous pressure in patients with congestive heart failure by active relaxation of intestinal and pulmonary capacitance vessels. Hepatic vascular volume was probably reduced by a passive mechanism.

Gated Blood-Pool Imaging↗
PubMed1991

Blood volume changes in liver and spleen during cardiogenic shock in dogs.

Changes in vascular capacitance of the liver and spleen were studied in seven anesthetized dogs during cardiogenic shock induced by coronary microembolization. Left ventricular end-diastolic pressure increased from 2 +/- 2 to 28 +/- 4 mmHg (P less than 0.001), and mean aortic pressure decreased from 111 +/- 7 to 56 +/- 9 mmHg (P less than 0.001). Hepatic venous pressure increased from 1.8 +/- 0.6 to 5.0 +/- 1.0 mmHg (P less than 0.05). Portal venous pressure did not change. Blood volume changes were assessed from sonomicrometric measurements of organ diameters. Hepatic diameter increased after embolization, corresponding to an estimated 54 +/- 14 ml increase of hepatic blood volume (P less than 0.01). Splenic diameter gradually decreased during shock until an estimated 33 +/- 12 ml of blood had been released (P less than 0.05). Occlusion of hepatic venous outflow by a balloon catheter was used to cause ramp changes in hepatic volume and hepatic venous pressure so that a pressure-volume curve could be estimated. Analysis of the hepatic curves showed an increase in unstressed volume with no change in vascular compliance during shock. The blood volume increase could in part be attributed to increased outflow pressure, but active dilation of hepatic capacitance vessels probably contributed. Splenic curves were shifted downward, suggesting expulsion of blood by active contraction.

Animals↗
PubMed1991

Splanchnic vascular capacitance and positive end-expiratory pressure in dogs.

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

Animals↗
PubMed1985

Influence of neural pathways on the pyrexial response to surgical trauma.

Epidural analgesia inhibits several metabolic effects of trauma. Some of these effects are generated by the endogenous fever mediator interleukin-1. Postoperative fever was therefore studied in 52 patients, 25 of whom had had epidural analgesia and 27 general anaesthesia. Transvesical prostatectomy was used as standard surgical trauma. Most of the patients had postoperative temperature rise exceeding 0.5 degree C, but the rise was not influenced by epidural analgesia. These data suggest that the release of endogenous fever mediator is not under control of afferent pathways from the region of trauma. The findings are also consistent with regulation of interleukin-1 release which is independent of adrenal stimulation, cyclic AMP or beta-endorphin, as epidural analgesia prevents postoperative increase of these hormones.

Aged↗
PubMed1984

Free thyroxine in myocardial infarction.

High values for the free thyroxine fraction were found in the serum of 24 patients during the early phase of myocardial infarction. A strong correlation between the free thyroxine fraction and free fatty acids suggests that they compete for protein binding sites. The increase in free thyroxine may have undesirable effects on myocardial oxygen demand during acute myocardial infarction.

Adult↗
PubMedDate not supplied

Serum lipids during treatment with glucose-insulin-potassium in myocardial infarction.

Total cholesterol, phospholipids, and triglycerides in serum were studied during myocardial infarction in a patient group treated with glucose, insulin and potassium (GIK), and a conventionally treated group. There was no difference in the typical changes of cholesterol and phospholipids between the groups, but the GIK-treated group had a late rise in triglycerides.

Cholesterol↗