Biomedical subjects

B Friesenecker

Publications and source records attributed to B Friesenecker.

16 recordsLinked to original sources

PubMed2003

[Near drowning: epidemiology--pathophysiology--therapy].

Near-drowning is a frequent preventable accident with a significant morbidity and mortality in a previous healthy population. In most patients the primary injury is pulmonary failure due to fluid aspiration, resulting in severe arterial hypoxemia and secondary damage to other organs. Immediate interruption of hypoxia is of utmost importance in the emergency situation. Accurate neurologic prognosis cannot be predicted from initial clinical presentation, laboratory, radiological or electrophysiological examinations. Prompt resuscitation and aggressive respiratory and cardiovascular treatment are crucial for optimal survival. This review provides the reader with detailed information on epidemiology, pathophysiology, emergency decision making and general treatment in near drowning accidents.

Cardiovascular Physiological Phenomena↗

PubMed2002

Cardiac failure and multiple organ dysfunction syndrome in a patient with endocrine adenomatosis.

In this case report, we present the successful therapy of severe cardiac failure in pituitary adrenal insufficiency. A previously healthy 56-year-old-man in pituitary coma due to an atypical variant of multiple endocrine adenomatosis (pituitary adenoma and pheochromocytoma) suffered from cardiac failure resistant to catecholamine and standard hydrocortisone therapy. After two bolus injections of dexamethasone (2 x 24 mg) mean arterial pressure and cardiac function dramatically improved, probably due to restoration of permissive effects on catecholamine action and reversal of pathophysiological mechanisms of cardiac failure. We conclude that in patients with severe cardiovascular failure in pituitary coma the administration of potent glucocorticoids may be more effective in reversing cardiovascular failure than standard dosages of hydrocortisone.

Adenoma↗

PubMed2000

[Non-opioid analgesics--irreplaceable in cancer pain therapy?

Sufficient therapy of pain is essential for the treatment of tumor patients. World Health Organisation (WHO)-guidelines recommend a combination of opioids with non-opioid-analgesics (NOA) for patients with medium to strong pain. Cancer pain is often a combination of pain caused by the tumor itself, tumor associated and pain caused by therapy. Various substances act by different mechanisms and therefore combinations may demonstrate superior effects. Opioids ("central analgesics") inhibit neuronal transduction within the spinal cord, enhance inhibiting function of midbrain nuclei on ascending pain transduction and influence pain perception via modulation of the limbic system. NOAs ("peripheral analgesics") inhibit cyclooxygenase hindering activation of the peripheral nociceptor-system. There are 2 different classes of NOAs: 1) non-acidic, antipyretic analgesics like pyrazolones (metamizol) and anilin-derivates (paracetamol) and 2) non-steroidal antirheumatics (NSAR) like salicylates (acetylsalicylic acid), derivates of propionic acid (ibuprofen, naproxen), acetate acid (indomethacin, diclofenac), enolic acid (piroxicam, meloxicam) and anthranil acid (mefenamin). Adjuvant therapy is necessary to control common NSAR-side-effects like dyspepsia, ulcer and gastrointestinal bleeding. Due to its exceptional analgesic, antipyretic and spasmolytic properties, metamizol is an essential substance in tumor therapy. As agranulocytosis-incidence of 1:1,000,000 is low, good gastrointestinal and renal tolerance makes metamizol an excellent alternative to NSAR. There is scientific evidence that adequate combinations of non-opioids, opioids and adjuvant drugs, considering adverse side effects, were effective and safe in the treatment of cancer pain.

Analgesia↗

PubMed1998

Microvascular and tissue oxygen gradients in the rat mesentery.

One of the most important functions of the blood circulation is O2 delivery to the tissue. This process occurs primarily in microvessels that also regulate blood flow and are the site of many metabolic processes that require O2. We measured the intraluminal and perivascular pO2 in rat mesenteric arterioles in vivo by using noninvasive phosphorescence quenching microscopy. From these measurements, we calculated the rate at which O2 diffuses out of microvessels from the blood. The rate of O2 efflux and the O2 gradients found in the immediate vicinity of arterioles indicate the presence of a large O2 sink at the interface between blood and tissue, a region that includes smooth muscle and endothelium. Mass balance analyses show that the loss of O2 from the arterioles in this vascular bed primarily is caused by O2 consumption in the microvascular wall. The high metabolic rate of the vessel wall relative to parenchymal tissue in the rat mesentery suggests that in addition to serving as a conduit for the delivery of O2 the microvasculature has other functions that require a significant amount of O2.

Animals↗

PubMed1998

Plasma viscosity regulates capillary perfusion during extreme hemodilution in hamster skinfold model.

Effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation was investigated in the awake hamster skinfold model. Two isovolemic hemodilution steps were performed with 6% Dextran 70 [molecular weight (MW) = 70,000] until systemic hematocrit (Hct) was reduced by 65%. A third step reduced Hct by 75% and was performed with the same solution [low viscosity (LV)] or a high-molecular-weight 6% Dextran 500 solution [MW = 500, 000, high viscosity (HV)]. Final plasma viscosities were 1.4 and 2.2 cP (baseline of 1.2 cP). Hct was reduced to 11.2 +/- 1.1% from 46.2 +/- 1.5% for LV and to 11.9 +/- 0.7% from 47.3 +/- 2.1% for HV. HV produced a greater mean arterial blood pressure than LV. Functional capillary density (FCD) was substantially higher after HV (85 +/- 12%) vs. LV (38 +/- 30%) vs. baseline (100%). PO2 levels measured with Pd-porphyrin phosphorescence microscopy were not statistically changed from baseline until after the third hemodilution step. Wall shear rate (WSR) decreased in arterioles and venules after LV and only in arterioles after HV. Wall shear stress (WSR x plasma viscosity) was substantially higher after HV vs. LV. Increased mean arterial pressure and shear stress-dependent release of endothelium-derived relaxing factor are possible mechanisms that improved arteriolar and venular blood flow and FCD after HV vs. LV exchange protocols.

Animals↗

PubMed1997

The effects of progressive anemia on jejunal mucosal and serosal tissue oxygenation in pigs.

Anemia may promote intestinal hypoxia. We studied the effects of progressive isovolemic hemodilution on jejunal mucosal (Po2muc), and serosal tissue oxygen tension (Po2ser, Clark-type surface electrodes), mucosal microvascular hemoglobin oxygen saturation (Hbo2muc), and hematocrit (Hctmuc; tissue reflectance spectophotometry) in a jejunal segment. Twelve domestic pigs were anesthetized, paralyzed, and mechanically ventilated. Laparatomy was performed, arterial supply of a jejunal segment isolated, and constant pressure pump perfused. Seven animals were progressively hemodiluted to systemic hematocrits (Hctsys) of 20%, 15%, 10%, and 6%. Baseline for Po2muc, Po2ser and Hbo2muc was 23.5 +/- 2.1 mm Hg, 57.5 +/- 4 mm Hg, and 47.0% +/- 6.4% which were not different from the five controls. Despite a significant increase in jejunal blood flow, jejunal oxygen delivery decreased and oxygen extraction ratio increased significantly at Hctsys 10% and 6%. Po2ser decreased significantly below or at Hctsys of 15%, whereas Po2muc and Hbo2muc were maintained to Hctsys of 10%, but less than 10% Hbo2muc and mesenteric venous pH decreased significantly, implying that physiological limits of jejunal microvascular adaptation to severe anemia were reached. Decrease of Hctmuc was less pronounced than Hctsys. In conclusion, redistribution of jejunal blood flow and an increase in the ratio of mucosal to systemic hematocrit are the main mechanisms maintaining mucosal oxygen supply during progressive anemia.

Anemia↗

PubMed1996

Effects of short-term endotoxemia and dopamine on mucosal oxygenation in porcine jejunum.

Effects of Escherichia coli lipopolysaccharide (2 micrograms.kg-1.20 min-1; LPS), given systemically (S) or via superior mesenteric artery (M), and consecutive dopamine infusion (16 micrograms.kg-1.20 min-1) on jejunal mucosal tissue O2 tension (PO2muc) and serosal tissue O2 tension (PO2ser; Clark-type surface electrodes) and jejunal mucosal microvascular hemoglobin O2 saturation (HbO2muc; tissue reflectance spectrophotometry) were investigated in a hemodynamically stable pig model. Twenty-one pigs were anesthetized, paralyzed, and mechanically ventilated. After laparotomy, a mesenteric venous catheter was inserted and a jejunal antimesenteric enterotomy performed. LPS-infused animals developed similar degrees of pulmonary hypertension. No differences in cardiac output and mean arterial blood pressure between groups were found. PO2muc and HbO2muc were significantly lower in M animals compared with control (C) [210 min; PO2muc: 7.12 +/- 1.81 (M), 19.01 +/- 3.12 mmHg (C); HbO2muc: 28.78 +/- 3.36 (M), 49.09 +/- 3.84% (C)], whereas S animals ranged in between (PO2muc: 13.36 +/- 2.2 mmHg; HbO2muc: 40.68 +/- 4.43%). Of measured PO2muc values, 12.6 (C), 20.6 (S), and 46.3% (M) ranged from 0 to 5 mmHg. PO2ser was lower in LPS animals compared with control [59.43 +/- 5.4 (C), 45.00 +/- 6.12 (S), 47.33 +/- 4.34 (M) mmHg]. Dopamine increased PO2muc and HbO2muc to similar absolute values and significantly decreased frequency of PO2muc (0-5 mmHg) in M animals. We conclude that LPS impairs mucosal tissue oxygenation independently of systemic hemodynamics. Mucosal microvascular dysfunction depends on regional LPS concentrations. Under conditions of compromised tissue oxygenation, dopamine significantly improves PO2muc and HbO2muc.

Animals↗

PubMed1995

Dopamine-1-receptor stimulation and mucosal tissue oxygenation in the porcine jejunum.

OBJECTIVE: To evaluate the effects of dopamine-1-receptor stimulation on intestinal mucosal tissue oxygenation. DESIGN: Prospective, experimental, controlled trial. SETTING: Animal research laboratory. SUBJECTS: Anesthetized domestic pigs (30 to 45 kg). INTERVENTIONS: A small segment of the jejunal mucosa and serosa was exposed by midline laparotomy and antimesenteric incision. Fenoldopam, a selective dopamine-1-receptor agonist, was infused in steps, exponentially increasing from 0.6 to 9.6 micrograms/kg/min via a central venous catheter (n = 8, fenoldopam group), whereas a second group (n = 6, saline group) was only given the solvent. MEASUREMENTS AND MAIN RESULTS: Systemic hemodynamics as well as systemic and jejunal acid base and blood gas variables were measured using an arterial catheter, a thermodilution pulmonary artery catheter, and a jejunal venous catheter. Jejunal mucosal and serosal tissue PO2 were measured by means of Clark-type surface oxygen electrodes. Oxygen saturation and relative concentration of mucosal microvascular hemoglobin were measured by means of tissue reflectance spectrophotometry. In the fenoldopam group, systemic oxygen delivery (12.5 +/- 0.8 mL/kg/min at baseline) increased by 56% (p < .001) above baseline values. Mean arterial pressure remained unchanged. Fenoldopam produced a 51% increase in mucosal PO2 (23.8 +/- 2.8 torr [3.2 +/- 0.4 kPa] at baseline; p < .001) and a 31% increase in mucosal hemoglobin oxygen saturation (55.4 +/- 8.3% at baseline; p < .001), but not change in serosal PO2 (58 +/- 4.8 torr [7.7 +/- 0.6 kPa] at baseline). CONCLUSIONS: Fenoldopam improves tissue oxygenation of the porcine jejunum in a dose-related manner. This effect is limited to the inner mucosal layer. Dopamine-1-receptor agonists should be evaluated in patients presenting with signs of intestinal mucosal ischemia.

Animals↗

PubMed1995

Cellular basis of inflammation, edema and the activity of Daflon 500 mg.

Inflammation activates leukocytes causing the release of agents that disrupt the endothelial barrier to such an extent that retention of plasma protein is impaired. This phenomenon can be observed using microvascular methods in which ischemia-reperfusion-induced inflammation-like condition are analyzed in terms of the increased adherence of leukocytes to the venular endothelium. Pretreatment with Daflon 500 mg, a purified, micronized, flavonoid fraction consisting of 90% diosmin and 10% hesperidin, prior to the induction of 4 h of tourniquet ischemia significantly lowers the number of adherent leukocytes. This observation is linked to the protective effect of flavonoids in the treatment of edema, as decreased activation is also associated with a decreased platelet and complement system activation, leading to a lowered release of histamine and decreased leukocyte-dependent endothelial damage. It is proposed that attenuation of leukocyte adherence during ischemia-reperfusion is evidence of the protective endothelial effect of Daflon 500 mg and its ability to control edema in clinical situation.

Animals↗

PubMed1994

Sodium-taurocholate-induced acute necrotizing pancreatitis does not affect jejunal oxygenation in pigs.

OBJECTIVE: To study the influence of experimentally induced acute necrotizing pancreatitis on jejunal oxygen transport, jejunal oxygen consumption, and mucosal PO2. DESIGN: Prospective, randomized trial. SETTING: Animal laboratory. SUBJECTS: Domestic pigs aged 7 to 8 wks. INTERVENTIONS: Two groups of pigs were anesthetized with midazolam and sufentanyl, mechanically ventilated, and hemodynamically monitored. In controls (n = 9) and in animals with acute necrotizing pancreatitis (n = 9), a segment of the jejunum was isolated and autoperfused in situ. Through an antimesenteric enterotomy, an area of jejunal mucosa was exposed for mucosal PO2 measurements. Acute necrotizing pancreatitis was induced by the injection of 10 mL of 10% sodium-taurocholate into the main pancreatic duct. Both groups received normal saline solution to keep pulmonary artery occlusion pressure constant. MEASUREMENTS: Mucosal PO2 was assessed with a modified Clark-type multiwire surface electrode. After two baseline measurements, systemic and regional oxygen transport variables and mucosal PO2 were determined at designated intervals (20, 40, 60, 100, 120, 160, 200, 240, 280 mins). MAIN RESULTS: Systemic hemodynamics and oxygen transport were maintained in both groups. In contrast to controls, all animals with pancreatitis showed gross macroscopic and histologic evidence of severe acute necrotizing pancreatitis at autopsy. There were no significant differences between groups in jejunal blood flow, oxygen transport, oxygen consumption, oxygen extraction ratio, or mucosal PO2. CONCLUSIONS: Our results demonstrate that, under conditions of sustained systemic hemodynamics, jejunal oxygen transport and mucosal oxygenation are well maintained during the early course of sodium-taurocholate-induced acute necrotizing pancreatitis.

Acute Disease↗

PubMed1994

Vasomotion induces regular major oscillations in jejunal mucosal tissue oxygenation.

The mucosa of the small intestine has some unique microcirculatory features that may result in significant tissue oxygenation changes even under physiological conditions. To prove this hypothesis we investigated mucosal and serosal oxygenation in an autoperfused, innervated jejunal segment in pigs. Eight animals (30-40 kg) were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa and serosa was exposed by a midline laparotomy and an antimesenteric incision. Mucosal and serosal oxygen tensions were measured using Clark-type surface oxygen electrodes. Mucosal hemoglobin saturation and concentration were determined by tissue reflectance spectrophotometry. Systemic hemodynamics, mesenteric-venous acid base, and blood gas variables, as well as systemic acid-base and blood gas variables and jejunal electromyogenic potentials, were recorded. Measurements were performed after a rest period at 0, 30, 60, and 90 min. All animals remained hemodynamically stable. At time 0 the jejunal oxygen extraction ratio was 0.33 +/- 0.05, the mean serosal PO2 was 60.25 +/- 7.69, the mean mucosal PO2 was 25.47 +/- 4.41 mmHg, and the mean mucosal hemoglobin saturation was 46.36 +/- 6.22%. Mean values did not change with time. In contrast to serosal PO2, mucosal PO2, mucosal hemoglobin oxygen saturation, and hemoglobin concentration showed rhythmic oscillations with a frequency of 3.4-5 cycles/min that were unrelated to systemic hemodynamic parameters, respiratory frequency, and intestinal peristalsis. From this we concluded that the jejunal mucosa demonstrates significant, regular changes in oxygenation parameters that are locally mediated. We speculate that the physiological basis for this phenomenon is the countercurrent arrangement of microvessels in conjunction with vasomotion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Capillary perfusion during ischemia-reperfusion in subcutaneous connective tissue and skin muscle.

Ischemia-reperfusion injury was investigated in terms of functional capillary density (FCD), capillary red blood cell velocity (cRBCv), and arteriolar and venular diameter after 4-h ischemia in the unanesthetized hamster skin-fold preparation. Animals in group 1 were studied by transillumination. Group 2 received a bolus injection of fluorescein isothiocyanate (FITC)-dextran (mol wt 150,000) and was studied by transillumination (zone 1) and epi-illumination (zone 2). In group 1, FCD decreased after ischemia (92% of baseline, 30 min), returning to control up to 24 h. cRBCv increased after reperfusion, being 175% of baseline at 24 h. Arterioles and venules dilated for 24 h after reperfusion. In group 2/zone 2, FCD progressively decreased to 11% of control, arteriolar dilation was inhibited, and cRBCv increased 30 min and 2 h after reperfusion. Tissue perfusion index (FCD x cRBCv) increased 158% in group 1 at 24 h, did not change in group 2/zone 1, and was 9% of control at 24 h in group 2/zone 2 (P < or = 0.05). We conclude that increased perfusion is a normal reaction to ischemia-reperfusion injury in this model, and previously observed capillary no reflow is due to FITC-dextran phototoxicity.

Animals↗

PubMed1994

Dopamine and mucosal oxygenation in the porcine jejunum.

The effect of intravenously delivered dopamine on jejunal tissue oxygenation was studied in 12 pigs anesthetized with midazolam and sufentanil and mechanically ventilated. A small segment of the jejunal mucosa and serosa was exposed by midline laparotomy and antimesenteric incision. Mucosal and serosal tissue PO2, mucosal microvascular hemoglobin oxygen saturation, and mucosal hemoglobin concentration were measured by means of Clark-type oxygen electrodes and tissue reflectance spectrophotometry, respectively. In five animals electromyogenic potentials of the jejunal wall were recorded. Measurements were performed under baseline conditions and after intravenous infusion of 2, 4, 8, 16, 32, and again 2 micrograms.kg-1.min-1 of dopamine. The drug produced a dose-related increase in mucosal PO2 (from 26.5 Torr at baseline to 49 Torr at 32 micrograms of dopamine; P < 0.001) and mucosal hemoglobin oxygen saturation (from 55.1 to 70.1%; P < 0.03) but no change in serosal PO2 (from 70.6 to 65.5 Torr). In nine animals baseline mucosal PO2 and mucosal hemoglobin oxygen saturation showed rhythmic oscillations with a frequency of 2.5-5 cycles/min that could not be related to electromyogenic potentials. Dopamine decreased the oscillation amplitude of these two parameters (P < 0.001), and at doses > 16 micrograms.kg-1.min-1 they were no longer present. Dopamine therefore improves mucosal oxygenation of the porcine jejunum in a selective and dose-related manner. At higher doses the preexisting oscillatory pattern of mucosal oxygenation, which is most likely due to vasomotion, is impeded.

Animals↗

PubMed1994

Functional capillary density changes during blood substitution with alpha alpha Hb and dextran 70: influence on oxygen delivery.

The effectiveness of a blood substitute is ultimately determined by the rate at which O2 arrives to the capillaries and the functional capillary density i.e., the number of flowing capillaries per unit volume of tissue. We use this rationale to analyze the effectiveness of isovolemic blood substitution with alpha alpha Hb (3,5-bis(dibromosalicyl)fumarate) compared to isooncotic and isovolemic hemodilution with dextran 70. Progressive hemodilution with each solution was performed in the awake hamster skinfold model by simultaneous isovolemic exchange of blood until the systemic hematocrit was reduced to 30% of control. Systemic hematocrit, blood pressure, heart rate were monitored. To determine O2 delivery at the microcirculatory level, functional capillary density, RBC velocity, RBC flux, capillary hematocrit were measured. Functional capillary density was maintained during moderate hemodilution with dextran 70, whereas alpha alpha Hb exchange caused a gradual reduction in the number of flowing capillaries. O2 delivery to tissue was calculated from total O2 content (RBC and plasma Hb or RBC only), blood flow, and functional capillary density. Our findings suggest that augmentation of the O2 content of blood with alpha alpha Hb substitution produces similar results in terms of capillary O2 delivery and capacity as isovolemic and isooncotic hemodilution with dextran 70.

Animals↗

PubMedDate not supplied

Oral administration of purified micronized flavonoid fraction suppresses leukocyte adhesion in ischemia-reperfusion injury: in vivo observations in the hamster skin fold.

The effect of a clinically used purified micronized flavonoid fraction (90% diosmin and 10% hesperidin) on leukocyte-endothelial cell interaction during ischemia-reperfusion injury was studied in the microcirculation of unanesthetized hamsters fitted with a skin fold window chamber. The drug was given orally in suspension with arabic gum (30 mg/kg) 8 h prior to induction of 4-hour tourniquet ischemia in the chamber window. Leukocyte-endothelial cell interaction was observed using fluorescence intravital microscopy in postcapillary venules (15-70 microns in diameter) at control and during reperfusion at 30 min and 2 and 24 h. Leukocytes were classified according to their flow pattern as (1) 'passers', including 'free flowing' leukocytes and those which were 'flowing with endothelial contact', and (2) 'immobilized' leukocytes. Untreated animals exhibited a significant increase of 'immobilized' leukocytes and of those 'flowing with endothelial contact' during reperfusion. Flavonoid-treated animals displayed a statistically significant lower number of 'immobilized' leukocytes at all time points during reperfusion. There was no change in the number of leukocytes 'flowing with endothelial contact' relative to the untreated animals. Since firm leukocyte attachment to the endothelial wall and subsequent emigration of leukocytes into the interstitium is a mechanism for tissue damage during inflammation, attenuation of this phenomenon during conditions of ischemia-reperfusion can in part explain previous observations that this purified micronized flavonoid fraction decreases edema formation.

Administration, Oral↗

PubMedDate not supplied

Capillary flow impairment and functional capillary density.

Functional capillary density is variable in both normal and diseased tissue. When this parameter is defined as the number of capillaries that possess red blood cell transit, changes in functional capillary density reflect mechanisms that modulate the entrance of red blood cells into the capillaries. These mechanisms have anatomical origin, whereby the capillary diameter changes, and may also be hydrodynamic, when flow conditions prevent red blood cells from entering a capillary branch. An intrinsic feature of both processes is that capillaries undergo lumenal changes. Capillary lumen is determined by a composite of mechanical and cellular factors, where intravascular pressure is one of the principal determinants affecting diameter as a consequence of the elastic properties of the capillary/tissue system. The hydration of the surrounding tissue and the cellular volume regulation of the endothelium are additional factors. There is increasing evidence that capillaries possess contractility and that this phenomenon has spontaneous components. Consequently, functional capillary density is the resultant of both passive and active processes present at the level of individual vessels.

Animals↗