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Biomedical subjects

W Brendel

Publications and source records attributed to W Brendel.

At least 19 recordsLinked to original sources
PubMed1994

Effect of shock waves and cisplatin on cisplatin-sensitive and -resistant rodent tumors in vivo.

The effect of a combination of shock waves with cisplatin was examined in vivo with subcutaneously implanted amelanotic melanomas (A-Mel 3) in Syrian golden hamsters and cisplatin-sensitive or cisplatin-resistant fibrosarcoma (SSK2/0 and SSK2/R2) in C3H mice. In all 3 tumor models, 4 treatment modalities were compared: control, cisplatin treatment, shock waves and the combination of shock waves and cisplatin. Shock waves significantly delayed tumor growth in all 3 tumor models when compared to the respective control group. Cisplatin alone delayed the growth of A-Mel 3 and SSK2/0, whereas SSK2/R2 remained uninfluenced by the drug. In all 3 tumor models the combined treatment with shock waves and cisplatin additively and significantly delayed tumor growth. In A-Mel-3-bearing animals the combined treatment significantly increased survival time. The growth of SSK2/0 and SSK2/R2 tumors was delayed to a similar extent by the combined treatment modality as compared to shock-wave treatment alone. This indicates that the cisplatin resistance of SSK2/R2 tumors has been overcome by the simultaneous shock wave treatment. An increased intracellular cisplatin accumulation in the tumors due to shock wave exposure is suggested as the mechanism of interaction between shock waves and cisplatin.

Animals↗
PubMed1993

[Enzyme liberation and activation of the kallikrein-kinin system in experimental pancreatitis. Studies of portal vein blood, pancreatic lymph and peritoneal effusion].

The clinical course of acute pancreatitis is strongly influenced by secondary cardiac, pulmonary and renal damage. The aim of the present study was to gather information about the compartment promoting the systemic damage. Therefore the activity of lipase, phospholipase A and plasma pro-kallikrein and the concentration of tissue kallikrein and kininogen were measured in portal venous blood, pancreatic lymph and peritoneal exudate. Anaesthetized pigs were subjected to fluid resuscitation to keep systemic haemodynamic parameters constant. The pancreas was isolated in situ. The pigs were randomly assigned to a control group (n = 9) or one of the two pancreatitis groups (n = 10 each). Pancreatitis was induced by i.a. infusion of free fatty acid (FFS) or retrograde infusion of 5% sodium taurocholate intraductally (NaT). In both pancreatitis groups the activity of lipase and phospholipase A increased. The most pronounced changes were seen in the peritoneal exudate (phospholipase A activity 40 min after induction: control 10.0 U/l, NaT 72.2 U/l). In both pancreatitis groups there was evidence for activation of the tissue kallikrein kinin system in the form of an increase in the kallikrein concentration and a decrease in the kininogen concentration. Again the changes were most pronounced in the peritoneal exudate (tissue kallikrein 40 min after induction: control 14.7 ng/ml, NaT 452 ng/ml).

Acute Disease↗
PubMed1992

Dilation of coronary microvessels by adenosine induced hypotension in dogs.

An experimental model was established for fluorescence video microscopy of coronary microvessels. Nineteen dogs were anesthetized with a narcotic. Catheters were placed for hemodynamic monitoring and sampling of arterial and coronary venous blood. Myocardial perfusion was measured with radioactive microspheres. Following thoracotomy, movements of the myocardial surface area under investigation were restricted by a specially designed heart holder. Plasma was stained with FITC labelled dextran. Diameters were determined in arteriolar and venular microvessels greater than or equal to 20 microns. Measurements were performed during baseline conditions, i.e. only the basic anesthetic drug was applied, and during coronary vasodilation by continuous infusion of adenosine in a randomized sequence. Mean arterial pressure was reduced from 85 +/- 2 mmHg during baseline to 59 +/- 1 mmHg by infusion of 16.9 +/- 2.2 mg.kg-1.h-1 adenosine. Adenosine increased left ventricular blood flow by 253%, left ventricular oxygen demand remained unchanged. A total of 495 arteriolar and 170 venular diameters were measured during baseline condition and during adenosine infusion. Arteriolar diameters increased in all vessel segments between 20 and 600 microns, however, arterioles below a critical size of 100 microns had a greater dilating capacity than larger arterioles. Maximal decrease of segmental resistance occurred in 20-40 microns arterioles and amounted to 74%, which is less than the 82% decrease of total coronary resistance. Venular diameter changes, too, were more pronounced in smaller vessels.

Adenosine↗
PubMed1991

Oleic acid induced pancreatitis in pigs.

An experimental model of edematous pancreatitis in pigs was established and measurement of pancreatic macro- and microcirculatory parameters and determinations of pancreatic enzymes (lipase, phospholipase A) and vasoactive mediators (prostanoids, kallikrein, kininogen) were performed. During general anesthesia the pancreas was isolated in situ. Pancreatic microcirculatory parameters were measured using videofluorescence microscopy after iv administration of FITC-Dextran. In hourly collected samples lipase and phospholipase A activities were determined enzymatically, concentrations of kallikrein, kininogen, and selected prostanoids were measured by radioimmunoassay. Two experimental groups were studied: (1) control (n = 9); (2) edematous pancreatitis induced by injection of oleic acid into the pancreatic artery (free fatty acid, ffa; n = 10). The animals were followed up for 6 hr. Systemic hemodynamic parameters remained constant in both groups. In the pancreatitis group pancreatic blood flow and O2-consumption decreased significantly (-55 and -49%), while pancreatic vascular resistance increased significantly (+50%). During baseline conditions 41% of all capillaries were perfused. In the pancreatitis group there were both areas with persistent stasis as well as areas with continuous perfusion. However, in the latter areas the portion of perfused capillaries decreased significantly to 27%. In the control group the portion of perfused capillaries remained constant. Liberation of lipase and phospholipase A especially into lymph and ascites fluid was measured during pancreatitis. Furthermore, considerable releases of kallikrein into lymph (+50%) and ascites (+800%) and a marked consumption of kininogen in lymph (+90%) and in ascites fluid (+80%) were measured. Activation of the arachidonic acid cascade and a significant release of prostacyclin and thromboxane A2 into pancreatic venous blood and lymph was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1990

Epicardial oxygen tensions during changes in arterial PO2 in pigs.

Arterial hypoxemia decreased epicardial tissue PO2, measured by means of a multiwire surface electrode, as well as coronary venous PO2 and myocardial lactate extraction. Left ventricular blood flow increased, O2 delivery, O2 demand and O2 consumption of the left ventricle remained unchanged. Thus, epicardial and coronary venous PO2 indicated decreased capillary and interstitial PO2 rather than cellular hypoxia. A linear relation between mean epicardial PO2 and coronary venous PO2 proves both parameters equally effective in reflecting changes in myocardial tissue oxygenation. However, PO2 distribution curves provide additional information and epicardial PO2 is superior in models with regional changes of myocardial oxygenation.

Animals↗
PubMed1990

[Pancreatic circulation in experimental biliary pancreatitis].

Measurements of pancreatic micro- and macrocirculation were performed to evaluate the pancreatitis-induced changes. Pigs were anesthetized and ventilated mechanically. Hypotension induced side-effects were avoided by adequate volume replacement. After laparatomy, splenectomy and gastroectomy the animals were enterotomized. Systemic hemodynamic parameters were monitored as well as pancreatic blood flow (Q), which was measured electromagnetically, and arterial and portal-venous blood gases. Pancreatic microcirculatory parameters were observed using fluorescence-videomicroscopy after i.v. administration of FITC dextran 150 and FITC labeled autologous erythrocytes. The pigs were randomly assigned to a control (n = 9) and a pancreatitis group (n = 10), the later being induced by the retrograde infusion of sodium-taurocholate. Systemic and pancreatic macrohemodynamic parameters remained constant in both groups, except for avdO2 and O2-consumption (O2-c) decreasing significantly in the pancreatitis group. At baseline 42% of all capillaries were perfused in both groups. In pancreatitis we detected focal areas with persistent stasis and areas which were continuously perfused. In these areas the portion of capillaries perfused by erythrocytes increased significantly to 67%. This was accompanied by an extravasation of FITC dextran. The finding of an unchanged Q beside reduced O2-c and avdO2 during pancreatitis is explained by the changes in pancreatic microcirculation. Focal stasis was observed beside areas showing typical signs of an acute inflammation: increased macromolecular permeability and capillary recruitment, e.g. oedema and hyperaemia.

Acute Disease↗
PubMed1990

Early gallstone recurrence rate after successful shock-wave therapy.

Extracorporeal shock-wave lithotripsy combined with adjuvant bile-acid dissolution therapy results in complete clearance of stone fragments in a high percentage of selected patients with radiolucent gallbladder calculi. With the gallbladder in situ, these patients are at risk of stone recurrence. Therefore, the early rate of stone recurrence after successful lithotripsy was evaluated. Fifty-eight of the first 60 consecutive patients who became stone free underwent follow-up examinations at least 1 yr (range, 12-37 mo; mean +/- SD, 18 +/- 6) after discontinuation of adjuvant bile-acid therapy. Five patients reported recurrent biliary pain within 1 yr after lithotripsy, and recurrent gallstones were detected. Fifty-three patients were asymptomatic during the first yr, and no recurrence was detected. Thus, the rate of gallstone recurrence was 9% within 1 yr. The rate of gallstone recurrence up to 3 yr was estimated by actuarial analysis. The probability of stone recurrence was 11% (+/- 4%) at 1.5 yr, and no further increase was observed up to 3 yr. Gallstone recurrence within 1 yr after successful shock-wave therapy has to be expected in approximately the same percentage of patients as has been reported in earlier postdissolution trials. It causes recurrent biliary pain in most cases.

Adult↗
PubMed1990

Biological effects of shock waves: cell disruption, viability, and proliferation of L1210 cells exposed to shock waves in vitro.

L1210 cells were exposed in suspension to shock waves generated with a Dornier XL1 lithotripter. After 1000 discharges at 25 kV, the number of nondisrupted cells was 15% and the number of trypan blue excluding cells was 7% as compared to 100% in sham treated controls; the shock-wave effect was more prominent at higher voltages and less prominent at higher discharge numbers when compared at similar electrical input energies. Overall proliferation of cells which were trypan blue negative after exposure exceeded 70% of the proliferation of sham treated controls, except after 1000 shocks at 25 kV, where proliferation was reduced to 42%. The latter reduction in proliferation was found to be due to a reduced growth for 24 h after exposure, with a return to normal proliferation during the following days. Limiting dilution analysis revealed that the reduced growth was mainly due to a transitory increase of the doubling time and not to a reduction of the number of proliferating cells. Cell disruption by shock waves was completely inhibited by exposing the cells at an elevated pressure of 101 atmospheres, pointing to the possible involvement of cavitation in the shock wave effect.

Animals↗
PubMed1990

Influence of the shock wave application mode on the growth of A-Mel 3 and SSK2 tumors in vivo.

We examined the influence of different shock wave application modes with a Dornier XL1 electrohydraulic lithotripter on the growth of A-Mel 3 and SSK2 tumors implanted under the dorsal skin of hamsters or mice. In a basic protocol, 500 shock waves a day on 4 consecutive days were administered at a discharge rate of 100 waves per minute and focused to the tumor center. This did not affect A-Mel 3 growth. A similar result was obtained with the basic protocol modified to 1000 shock waves a day and a wave application rate of 100 shock waves per second. Growth of A-Mel 3 and SSK2 tumors was significantly delayed, when the basic protocol was used, but the 500 shock waves a day were distributed over four points at the tumor edges and the tumor center. With the same shock wave protocol, lowering the water level over the tumor from 10 cm to 1 cm induced temporary regressions of SSK2 tumors. This was not due to the higher energy applied to the tumor, since twice the number of shock waves (1000 a day instead of 500 a day) was applied at a high water level and did not induce regressions. Four consecutive treatments with intervals between treatments shortened to 3 h and an additional treatment 12 h later at a low water level completely controlled tumor growth in 8 out of 12 SSK2 tumors for more than 150 days. The result showed that addition of a reflected wave from the water surface was most important for the shock wave effect, and suggested that shock wave devices generating similar wave forms should be applied for tumor therapy.

Animals↗
PubMed1990

Biological effects of shock waves: effect of shock waves on the liver and gallbladder wall of dogs--administration rate dependence.

The effect of extracoporeal shock waves on the liver and the gallbladder wall was compared in two groups of dogs exposed to 1500 shock waves generated in an electrohydraulic lithotripter with 15 kV and 80 nF. The waves were focused on the gallbladder wall. In the experimental group, a shock wave burst of 10 consecutive waves with an interval of 10 ms between the waves was administered each second; in the control group, single shocks were released each second. The day following shock wave exposure, the dogs were anaesthetized, killed and then dissected. In the liver, subcapsular and intraparenchymal focal haemorrhages occurred in the high pressure field and venous thrombi in portal veins. There was a nonsignificant trend towards an increased number of venous thrombi after burst application. The gallbladder wall was haemorrhagic and oedematous, the mucosa was ulcerated in the focal area; blood clots were found in nearly all gallbladders. No differences were detected between the groups. The free plasma haemoglobin was only increased after fast shock wave administration. Increased haemolysis and the trend towards an increased number of thrombi favour cavitation as a mechanism of shock wave damage. The similar extent of tissue damage suggests that shock wave bursts can be applied for gallstone destruction in humans if the major liver vessels are kept out of the high pressure field.

Animals↗
PubMed1990

Biological effects of shock waves: cavitation by shock waves in piglet liver.

Shock waves are known to generate cavitation in vitro. In vivo, extracorporeal shock waves may cause haemorrhages in tissues. Two types of changes were detected by conventional, real-time B-scan ultrasound when shock waves were administered to 5 piglet livers in vivo: transient changes consisting of bright signals in intrahepatic branches of the portal vein and tributaries of the hepatic vein, presumed to originate from gas bubbles, and stationary changes consisting of brightening of the area along the long axis of the high pressure field, presumed to indicate an increased number of gas-filled bubbles in this area. Transient changes appeared from the start of shock wave administration; bright signals were seen in liver vessels for several hundred microseconds before they were flushed away with the blood flow. Stationary changes appeared later, increased in intensity over several hundred shock waves and persisted for minutes after cessation of shock wave administration. Both types of signals were interpreted as direct evidence that lithotripter shock waves generated cavitation in vivo. Similar signals were received in the partly degassed water of the lithotripter tub. At autopsy of the piglets, focal intralobular haemorrhages and thrombi of portal veins were detected in the shock wave path. The occurrence of cavitation and tissue damage in the same gross area suggests that cavitation might be involved in the generation of tissue damage by shock waves.

Animals↗
PubMed1990

Pulmonary hypertension after heparin-protamine: roles of left-sided infusion, histamine, and platelet-activating factor.

Severe pulmonary hypertension after protamine neutralization of heparin is an infrequent but life-threatening event following cardiopulmonary bypass. The effect of left ventricular infusion of protamine on pulmonary hypertension as well as a possible role of platelet-activating factor (PAF) or histamine in the heparin-protamine reaction was investigated in 30 pigs in four different groups during general anesthesia. Group 1 animals received 250 IU/kg heparin, followed by 100 mg protamine intravenously after 15 min. In group 2 protamine was infused into the left ventricle. Group 3 animals received the histamine H1- and H2-antagonists clemastine and ranitidine 5 min before protamine infusion. In group 4 the PAF receptor blocker WEB 2086 was given 5 min before protamine. Platelet-activating factor was measured by a bioassay in serum samples of group 1 and group 4 animals. In all four groups protamine caused severe pulmonary hypertension, thromboxane A2 release, and a transient decrease in leukocyte counts. No PAF release was detected after protamine infusion. Neither left ventricular infusion of protamine nor histamine or PAF antagonists prevented or attenuated the reactions after protamine infusion. The authors conclude that left ventricular infusion of protamine provides no protection from pulmonary hypertension, and that histamine and PAF are not involved in the acute pulmonary vasoconstriction after protamine neutralization of heparin.

Animals↗
PubMed1990

Proliferation rates of lymphocytes in subcutaneously transposed spleen and peripheral blood after heterotopic heart transplantation in rats.

In a transplantation model using Dark Agouti rats as heart donors and Lewis rats as recipients, mean graft survival time was 7.1 days in GII, receiving no immunosuppression, and 31.4 days in GIII, animals immunosuppressed by DSG. A higher percentage of Lb in the spleen than in the PB in the transplanted groups was detected on certain days. HCT sharply decreased in immunosuppressed animals, thus suggesting a reversible suppression of erythropoesis induced by DSG.

Animals↗
PubMed1989

A new method of investigating the efficacy of regional thermotherapy in subcutaneous xenografts of nude mice.

A new method of investigating the efficacy of regional thermotherapy in subcutaneous xenografts of nude mice is reported. The use of high frequency hyperthermia was well tolerated by the sensitive animals and allowed an exact continuous temperature measurement in different tumor regions. The interstitial procedure in this model could be the best approach for later clinical use in urology, e.g. for prostate treatment and is an alternative to the transrectal hyperthermia application.

Animals↗
PubMed1989

In vitro cytotoxic activity of lithotripter shock waves combined with adriamycin or with cisplatin on L1210 mouse leukemia cells.

The effect of a combined treatment with shock waves generated by a lithotripter and Adriamycin or cisplatin was examined in cells that acutely survived exposure to shock waves and proliferated afterwards. Batches of 2 x 10(6) cells were exposed to the respective drug for 50 min or for 50 min plus 72 h. During the 50-min drug exposure 500 shock waves were applied at 25 kV. The growth as a percentage of the control was determined after 72 h by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cells treated with shock waves alone showed a growth inhibition as compared to control cells. For a 50-min drug exposure with Adriamycin the dose enhancement ratio did not exceed 1.3. For a 50-min drug exposure with cisplatin at concentrations of 0.5 micrograms/ml and 5.0 micrograms/ml, growth (as a percentage of the control) after combined treatment was significantly reduced as compared to cisplatin treatment alone; the dose enhancement ratio was 3.2 at 50% growth compared to the control. This indicates that shock waves can increase the susceptibility of L1210 cells to cisplatin. For a 50-min plus 72-h drug exposure no effect of an additional treatment with shock waves, as compared to chemotherapy alone, could be observed.

Animals↗