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D M Albrecht

Publications and source records attributed to D M Albrecht.

49 records · Page 3Linked to original sources
PubMed1996

Regional heterogeneity of cerebral blood flow response to graded volume-controlled hemorrhage.

OBJECTIVE: Of the animal models of human hemorrhagic shock, the volume-controlled hemorrhage model appears to come closer to the clinical situation than the commonly used pressure-controlled model, since the volume-controlled model allows regulatory adjustment of blood pressure. The effects of volume-controlled hemorrhage on local cerebral blood flow (LCBF) of conscious animals are not known. The present study investigates specific reaction patterns of LCBF in comparison to mean cerebral blood flow (CBF) during graded volume-controlled hemorrhagic shock in conscious rats. METHODS: Conscious, spontaneously breathing, and minimally restrained rats were subjected to different degrees of volume-controlled hemorrhage (taking either 25, 30, 35, or 40 ml arterial blood/kg body weight (b.w.). Thirty minutes after the completion of blood taking, LCBF was determined during hemorrhagic hypovolemia using the autoradiographic iodo (14C) antipyrine method. A group of untreated rats (no hemorrhage) served as controls. LCBF was determined in 34 defined brain structures and mean CBF was calculated. RESULTS: During less severe hemorrhage (25 and 30 ml/kg b.w.) mean CBF was significantly higher than in the control group (+19% and +25%). During severe hemorrhage (35 and 40 ml/kg b.w.) mean CBF remained unchanged compared to the control values, although significant increases in LCBF could be detected in many of the brain structures analyzed (maximum +44%). The mean coefficient of variation of CBF was increased, indicating a larger heterogeneity of LCBF values at shed blood volumes of 35 and 40 ml/kg b.w. CONCLUSIONS: A comprehensive and novel description of the local distribution of CBF during graded volume-controlled hemorrhage in conscious rats shows unexpected increases in LCBF and mean CBF. This "hypovolemic cerebral hyperemia" might be caused by endogenous hemodilution, thus maintaining the blood supply to the brain during hypovolemic shock.

Animals↗
PubMed1996

Coupling between local cerebral blood flow and metabolism after hypertonic/hyperoncotic fluid resuscitation from hemorrhage in conscious rats.

The effects of small volume hypertonic/hyperoncotic fluid resuscitation from hemorrhage on brain metabolism and blood flow were evaluated by autoradiographic techniques with high spatial resolution. The data were compared to fluid resuscitation with a volume equal to shed blood of isotonic 6% hydroxyethyl starch solution (HES) and a control group without hemorrhage and fluid resuscitation (n = 6 in each group). In conscious rats, volume-controlled hemorrhage for 30 min (30 mL/kg body weight, resulting in a blood loss of approximately 50% of the circulating blood volume) was followed by intravenous infusion of a hypertonic/hyperoncotic saline hydroxyethyl starch solution (HTHO; 7.5% saline/10% hydroxyethyl starch, 4.0 mL/kg body weight). Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures 2 h after fluid resuscitation by means of the quantitative autoradiographic iodo [14C]antipyrine and 2-[14C]-deoxy-D-glucose methods. Compared to the untreated control group, LCBF increased significantly in all brain regions analyzed after fluid resuscitation with HTHO (mean, +63%) or HES (mean, +56%). The increases in LCBF after fluid resuscitation were sufficient to restore cerebral oxygen delivery to the level calculated for the untreated control group. LCGU was unchanged after fluid resuscitation. The close relationship between LCGU and LCBF observed in the control group (r = 0.95) was preserved after hemorrhage and fluid resuscitation with HTHO (r = 0.97) and HES (r = 0.96), although the LCBF-to-LCGU ratio was reset to a higher level (1.5 mL/mumol in the control group and 2.7 mL/mumol after fluid resuscitation with HTHO and HES, P < 0.05). We conclude that the increase in LCBF compensates for the reduction of arterial oxygen content to maintain cerebral oxygen delivery. Therefore, "small volume resuscitation" appears to be as effective as resuscitation with large volumes of isotonic HES in meeting the circulatory and metabolic demands of the brain tissue within the first 2 h after fluid resuscitation from hemorrhage.

Animals↗
PubMed1995

Effect of cyclooxygenase inhibition in a canine model of unilateral pulmonary occlusion and reperfusion.

OBJECTIVE: To assess the effects of the cyclooxygenase inhibitor diclofenac in a canine model of pulmonary occlusion and reperfusion of the left lower lobe (LLL). DESIGN: Twelve adult beagle dogs (13-17 kg) were randomly assigned to a control group (n = 6) and a diclofenac-treated group (n = 6). Animals in the treatment group received 20 mg diclofenac sodium/kg as a single dose both before the experiment and at the end of surgical preparation; six animals served as controls. INTERVENTIONS: In the anesthetized animals, the left upper and middle lobes were resected. Circulation and ventilation of the LLL were selectively blocked by clamping. Complete occlusion of the LLL (30 min) was followed by periods of selective reperfusion (10 min, RP) and combined reperfusion and reventilation (120 min, RP/RV). MEASUREMENTS AND RESULTS: Reperfusion of the LLL resulted in a significant increase in pulmonary arterial pressure (Ppa) in the early RP/RV period as compared to baseline values (25.3 +/- 4.7 vs 15.8 +/- 1.9 mmHg, p < 0.05, paired t-test). This increase was significantly inhibited in the diclofenac-treated animals (17.0 +/- 2.0 mmHg, p < 0.01 vs controls, ANOVA). Gravimetrically determined extravascular lung water (EVLW) showed no significant difference in the continuously ventilated lobes of the right lung between diclofenac-treated animals (3.8 ml/g dry weight) and controls (3.9 +/- 0.9 ml/g dry weight) at the end of the experiment. EVLW, however, increased significantly in the LLL of control animals after 2 h of combined reperfusion and reventilation, whereas this increase was significantly inhibited in the diclofenac-treated animals (4.5 +/- 0.7 ml/g dry weight in the diclofenac group vs 6.5 +/- 1.3 ml/g dry weight in the control group, p < 0.05). CONCLUSIONS: Diclofenac inhibits the increase in both pulmonary arterial pressure and EVLW during reperfusion and reventilation of LLL. Thus, these changes appear to be mediated by cyclooxygenase metabolites.

Analysis of Variance↗
PubMed1995

Optimal preoperative titrated dosage of hypertonic-hyperoncotic solutions in cardiac risk patients.

Hypertonic-iso/hyperoncotic solutions have been the subject of numerous studies, mostly used in a fixed dosage (4 mL/kg bw or 250 mL). Nearly no study exists to prove whether this is the appropriate dosage especially in cardiac risk patients with accompanying diseases. We have compared preoperative volume loading with either 10% hydroxyethyl-starch/7.5% NaCl (HHT-HES) or 10% hydroxyethyl-starch/.9% NaCl (HES) in 50 mL bolus infusions. Volume loading was done with either HES or HHT-HES in 2 x 20 patients before aortic aneurysmectomy. The endpoint of stepwise infusion represented the highest cardiac index (CI) at the lowest possible wedge pressure (PCWP) (turning point of each individual Frank Starling relation). 167.5 mL (+/- 45.5 mL = 2.41 mL/kg bw) of HHT-HES and 440 mL (+/- 26.15 mL = 6.33 mL/kg bw) of HES were necessary. We observed a significant higher increase of the CI in the HHT-HES group. Significant increases of PCWP, pulmonary artery pressure, and central venous pressure occurred within the groups without any significant differences between the groups (p < .05). Results of the study showed: 1) The commonly used fixed dosage of 4 mL/kg bw of HHT-HES is too high in cardiac risk patients with slight hypovolemia. 2) HHT-HES should be given in an individual titration. 3) In the HHT-HES group we observed a positive inotropic effect (higher CI). 4) With the individual titration of HHT-HES no negative side effects occurred (especially no hypotension).

Aged↗
PubMed1994

Lack of dependence of cerebral blood flow on blood viscosity after blood exchange with a Newtonian O2 carrier.

Whether the increase in cerebral blood flow measured after hemodilution is mediated by a decrease in blood viscosity or in oxygen delivery to the brain is debated. In the present study, blood was replaced by an oxygen-carrying blood substitute, ultrapurified, polymerized, bovine hemoglobin (UPBHB). In contrast to normal blood, UPBHB yields a constant and defined viscosity in the brain circulation, since its viscosity is not dependent on the shear rate. CBF was determined after blood exchange with UPBHB in one group of conscious rats (UPBHB group) and in another group of blood-exchanged conscious rats in which viscosity was increased fourfold by the addition of 2% polyvinylpyrrolidone (PVP), mw 750,000 (UPBHB-PVP group). Local CBF (LCBF) was measured in 34 brain structures by means of the quantitative iodo(14C)antipyrine method. After blood replacement, systemic parameters such as cardiac index, arterial blood pressure, blood gases, and acid-base status were not different between the UPBHB and the UPBHB-PVP groups. In particular, arterial oxygen content was similar in both groups. Compared with a control group without blood exchange, LCBF was increased after blood exchange in the different brain structures by 60-102% (UPBHB group) and by 33-101% (UPBHB-PVP group). Mean CBF was increased by 77% in the UPBHB group and by 69% in the UPBHB-PVP group. No significant differences were observed in the values of LCBF or mean CBF between the UPBHB group and the UPBHB-PVP group. The results show that a fourfold variation in the viscosity of a Newtonian blood substitute does not result in differences in CBF values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Autoradiographic determination of regional cerebral blood flow and metabolism in conscious rats after fluid resuscitation from haemorrhage with a haemoglobin-based oxygen carrier.

The effects of resuscitation fluids on the brain have been investigated in previous studies by global measurements of cerebral blood flow and metabolism. In this study we have examined the effects of a novel haemoglobin-based oxygen carrier on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) after resuscitation from a volume-controlled haemorrhage of 30 min (3.0 ml/100 g body weight) with ultrapurified, polymerized, bovine haemoglobin (UPBHB). LCBF and LCGU were measured in 34 brain structures of conscious rats 2 h after resuscitation using quantitative iodo(14C)antipyrine and 2-(14C)-deoxy-D-glucose methods. The data were compared with a control group without haemorrhage and fluid resuscitation. In the haemorrhage group, LCBF increased after resuscitation by 12-56% in the different brain structures (mean 36%). LCGU changed less (0 to +18%, mean +9%). In the control group there was a close relationship between LCGU and LCBF (r = 0.95). After fluid resuscitation the relationship was preserved (r = 0.95), although it was reset at a higher ratio of LCBF to LCGU (P < 0.05). We conclude that fluid resuscitation of a 30 min volume-controlled haemorrhage using the haemoglobin-based oxygen carrier, UPBHB, induced a moderate degree of heterogeneity in the resulting changes of LCGU and LCBF. Local disturbances of cerebral blood flow or metabolism were not observed.

Animals↗
PubMed1994

Effects of a perfluorocarbon emulsion on regional cerebral blood flow and metabolism after fluid resuscitation from hemorrhage in conscious rats.

Regional cerebral blood flow and metabolism were investigated after addition of a small volume of perfluorocarbon (PFC) emulsion to the resuscitation fluid after hemorrhage. Severe volume-controlled hemorrhage (40 mL/kg body weight (bw) withdrawn over 30 min followed by hypovolemia of 30 min duration) was induced in conscious rats. While breathing 100% oxygen, the intravascular volume was repleted by the infusion of either 6% hydroxyethyl starch (mean mol wt 200,000/0.5; HES) or 6% hydroxyethyl starch plus perflubron (90% wt/vol emulsion of perfluoroctylbromide, 3 mL/kg bw; HES-PFOB). Two hours after fluid resuscitation either iodo[14C]antipyrine or 2[14C]deoxy-D-glucose were infused. Local cerebral blood flow (LCBF) or local cerebral glucose utilization (LCGU) were determined in 34 brain structures using quantitative autoradiography. Local cerebral metabolism was not disturbed in the HES and the HES-PFOB groups after fluid resuscitation, although slight reductions (mean -14%) were measured (HES-PFOB vs HES; P < 0.05). The HES-PFOB group showed LCBF values that were higher in the different brain structures than those of the HES group (mean +30%). A close correlation was found between LCGU and LCBF of the 34 brain structures in both groups (HES: r = 0.96, P < 0.01; HES-PFOB: r = 0.98, P < 0.01), whereas the LCBF-to-LCGU ratio was reset from 2.2 mL/mumol in the HES group to 3.4 mL/mumol in the HES-PFOB group (P < 0.05). The higher blood flows in the HES-PFOB group were sufficient to restore cerebral oxygen delivery to normal levels at a reduced arterial oxygen content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats.

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

Animals↗
PubMed1993

[Modified hemoglobin as a blood substitute in a rat model].

The use of modified haemoglobin solutions as blood substitutes has been investigated extensively during the past decades. Ultrapurified, polymerised bovine haemoglobin (upbHb) is a promising new substance in this respect. It was the aim of the present investigation to study the cardiovascular and respiratory effects of massive blood replacement with upbHb in a new model of conscious rats with continuous haemodynamic monitoring. METHODS. The right femoral artery and vein of 13 male Sprague-Dawley rats were catheterised during halothane-N2O-O2 anaesthesia. A thermistor catheter was placed in the descending aorta via the left femoral artery for measuring cardiac output by the thermodilution method. After recovery from anaesthesia blood replacement was achieved by arterial blood withdrawal and simultaneous venous infusion of upbHb in equal amounts. The haematocrit was lowered to < 3% and the animals were then left undisturbed in a rat restrainer while breathing room air. RESULTS. The animals showed no signs of disturbed behaviour patterns, distress, or adverse reactions. There were no significant changes in cardiac index and oxygen delivery during the investigation period of 4 h. A marked increase in mean arterial pressure (MABP) and systemic vascular resistance (SVR) of 30% was observed while stroke volume remained unchanged. Blood gases, acid-base status, and plasma glucose showed no major changes. Plasma oncotic pressure increased during the investigation period. CONCLUSIONS. The results indicate that there is adequate oxygenation and sufficient systemic oxygen delivery in conscious and drug-free rats after isovolaemic haemodilution with upbHb to a final haematocrit of < 3%. In contrast to previous haemodilution studies, which have tested non-oxygen-carrying solutions, no changes in cardiac index were observed. The cause of the increase in MAP and SVR remains to be established.

Animals↗
PubMed1993

[Myxedema coma as a rare postoperative complication].

Myxedema coma is characterized by severe lack of thyroid hormones, unconsciousness and serious restriction of vital functions. The mortality rate still ranges between 50 and 80%. In patients with inapparent hypothyroidism myxedema coma occasionally follows surgery, anesthesia or severe infection. A case of myxedema coma following surgery is reported. CASE REPORT. A 46-year-old woman was anesthesized for hip replacement. The intraoperative cardiovascular situation was characterized by hypotension and tachycardia. On the first postoperative day, unexpectedly a cardiac arrest occurred. Resuscitation with high doses of epinephrine was successful. There was no evidence of myocardial infarction, hypoxia and pulmonary embolism as causative factors for cardiac arrest. A pulmonary artery catheter was inserted and showed low cardiac output. Catecholamines and intravascular fluids were administered without hemodynamic improvement. In the next 5 days pneumonia was followed by ARDS and acute renal failure. After successful treatment of these complications the patient remained in deep coma. An intracerebral disease could be excluded by computerized tomography. Evaluation showed low thyroid hormones (T3; T4) and elevated TSH. The diagnosis of a myxedema coma was assumed. After failure of oral therapy with L-thyroxine (0.025-0.05 mg/day) for 10 days, intravenous therapy with 0.5 mg L-thyroxine was performed. Thirty-six hours later the patient regained consciousness, without cardiac complications. The patient progressed uneventfully under oral therapy with 0.1 mg L-thyroxine and was discharged from the hospital 6 weeks later. DISCUSSION. Pathophysiology and symptomatology of a case of postoperative myxedema coma are described (Tables 1-4). In this patient, the following symptoms occurred: low thyroid hormones (T3; T4), elevated TSH, deep coma, decreased ventilatory response to CO2, diminished myocardial contractility under catecholamine stimulation, impaired renal water excretion. After failure of oral substitution of L-thyroxine, intravenous therapy had to be performed in spite of the high risk of further cardiac complications in this patient. This led to complete recovery with normal neuropsychological and cardiopulmonary parameters. CONCLUSION. Myxedema coma is a rare complication in postoperative care, but in cases of inexplicable unconsciousness thyroid failure should be excluded. If myxedema coma is evident, intravenous therapy with L-thyroxine should be performed under the conditions of extended monitoring.

Coma↗
PubMed1991

Doppler CO2-test in patients with vertebrobasilar ischemia.

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.

Aged↗