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Biomedical subjects

L Kaiser

Publications and source records attributed to L Kaiser.

At least 127 records · Page 7Linked to original sources
PubMed1990

Computer analysis of the exploratory behavior of insects and mites in an olfactometer.

A method of quantification of the exploratory behavior of small animals stimulated by an odorant in a four-choice olfactometer, taking into account the interindividual variability of responses, was developed: individual tracks were time sampled according to the animal's walking speed and its positions were recorded according to the X-Y coordinates of the grid set underneath the device, the mesh of the grid suiting the animal's body size. A software, written in BASIC APPLESOFT on an APPLE IIe computer, allowed us to analyze the coordinates either of a single individual or of an experimental sample, leading to: a) the quantification of the insect distribution all over the experimental chamber, expressed in a table numbered according to the grid, where the percentage of position per square either for a given time fraction or the total observation period were reported, b) a graphic representation of the data according to several levels of greys, expressing the frequentation for each square for a given duration of observation. An analysis per time fraction allowed the chronological setup of events to appreciate. c) The collection of the positions among each flow field of the olfactometer for each individual of the experimental sample, for a given duration, was translated as the percentage of time spent in each flow field. Data files gathered these percentages for further statistical treatments. This computer method, which requires little equipment and appears to be easily adaptable to the study of biological models of various size and speed such as honeybees, trichogrammas and varroas mites, is a powerful tool for behavioral studies of small organisms tested in restricted areas.

Animals↗
PubMed1990

Depression of endothelium-dependent relaxation by filarial parasite products.

Endothelium-dependent relaxation is depressed in the femoral artery of dogs with heartworm, Dirofilaria immitis, infection. Moreover, in infected dogs, the mechanism of relaxation is different. Because D. immitis is located primarily in the pulmonary circulation, these findings suggested that D. immitis releases biologically active mediators that alter distal endothelium-dependent relaxation. We tested this hypothesis in vitro. Rings of rat aorta were exposed to D. immitis (alone, in 1,000 mol wt or 100 mol wt cutoff dialysis tubing, and bioassay with conditioned medium). D. immitis alone depressed relaxation to acetylcholine, carbachol, and A23187. Nitroglycerin relaxation was not affected. Depression of acetylcholine relaxation was seen with D. immitis alone, in 1,000 mol wt dialysis tubing, and bioassay with conditioned medium. However, acetylcholine relaxation with D. immitis in 100 mol wt dialysis tubing was not different from control. It appears that D. immitis releases a small, stable, biologically active factor that alters endothelium-dependent relaxation. Its exact nature is unknown. The study of endothelial cell behavior in filariasis and modulation of endothelial cell function by filarial factors may provide important clues in understanding the pathogenesis of parasitic diseases.

Acetylcholine↗
PubMed1989

Adjusting for baseline: change or percentage change?

Clinical trials data often include baseline and response measurements on each patient. Comparisons of treatments commonly employ either change from baseline or percentage change from baseline as the analysis variable. This paper provides guidance on the choice between these two by means of plots of these variables versus baseline. I provide two examples that illustrate the problem and I discuss the impact of use of the wrong adjusted response.

Clinical Trials as Topic↗
PubMed1989

Dirofilaria immitis: alteration of endothelium-dependent relaxation in the in vivo canine femoral artery.

Pathogenic mechanisms in filarial diseases are complex and poorly understood. While examining endothelium-dependent vasodilatory responses in the in vivo canine femoral artery, we noticed that dogs with Dirofilaria immitis infection had altered vascular responsiveness. The results reported here extend our original observations on vascular reactivity in dogs with D. immitis infection (L. Kaiser, J. F. Williams, E. A. Meade, and H. V. Sparks, 1987, American Journal of Physiology 253, H1325-H1329). In noninfected dogs, acetylcholine binds to the luminal endothelial cell muscarinic receptor. This results in release of a nonprostaglandin endothelium-derived relaxing factor. The relaxing factor causes an increase in vascular smooth muscle guanylate cyclase and relaxation. However, in dogs with D. immitis infection the mechanism of relaxation to acetylcholine is different. At least two endothelium derived relaxing factors are involved: the major factor is a prostaglandin; the second factor works through vascular smooth muscle cGMP. These data suggest that adult D. immitis release pharmacologically active factors that can alter distal endothelial cell function. The notion that filarial products may alter the physiological function of endothelial cells should be considered in the pursuit of improved understanding of pathogenic mechanisms of filariasis.

Acetylcholine↗
PubMed1989

Heart failure depresses endothelium-dependent responses in canine femoral artery.

Vascular responses to many physiological stresses are abnormal in heart failure. Increased peripheral resistance and a reduction in the vasodilator response to exercise and ischemia are examples of this abnormal vascular control. Such abnormal vascular control in heart failure is a result of interplay between neural, hormonal, and local vascular factors. This study was designed to test the hypothesis that a specific local mechanism, endothelium-dependent relaxation to acetylcholine (ACh), is depressed in experimental heart failure. Experiments were performed on 11 purebred beagles. Experimental heart failure was induced by rapid ventricular pacing for approximately 30 days. Femoral artery diameter was measured by sonomicrometry, and dose-response relationships to ACh, norepinephrine (NE), and nitroglycerin (NTG) were done before and after inhibition of cyclooxygenase by indomethacin. Heart failure resulted in a significant depression of ACh relaxation at all concentrations. In dogs with heart failure, indomethacin enhanced the dilation response to low concentrations of ACh. Constriction to NE and dilation to NTG were unchanged by heart failure. These data demonstrate that in the canine femoral artery endothelium-dependent dilation to ACh is depressed in experimental heart failure. Depression of endothelium-dependent vasodilation represents one local mechanism for abnormal control of the vasculature in congestive heart failure.

Acetylcholine↗
PubMed1988

[Sonomorphological characterization of arteriosclerotic plaques--potentials and limitations of high-resolution B-scan sonography].

One hundred and five carotid stenoses were examined by B-scan sonography (10 MHz) and the results compared with the macroscopic and histological appearances. The most important sonographic findings depended on surface structure, echo amplitude and the presence of acoustic shadows. From the therapeutic point of view, B-scan sonography is complementary to angiography by evaluating the morphology of the plaques, particularly if the indications for surgery are ill-defined.

Adult↗
PubMed1987

Endothelial cells. Not just a cellophane wrapper.

This summary provides an overview of some of the new information about the metabolic and regulatory functions of vascular endothelial cells and discusses possible important consequences of endothelial abnormalities in disease.

Acetylcholine↗
PubMed1987

Altered endothelial cell-mediated arterial dilation in dogs with D. immitis infection.

Vascular endothelial cells regulate arterial diameter in vivo and in vitro. Stimulation of endothelial cell muscarinic receptors by acetylcholine results in the production and release of a nonprostaglandin metabolite of arachidonic acid that causes vascular smooth muscle relaxation. We examined femoral artery endothelium-dependent vasodilator responses in normal dogs and dogs with heartworm (Dirofilaria immitis) infection. Endothelium-dependent vascular reactivity was attenuated in dogs with D. immitis infection studied in the spring but not in the fall. The dilator response was inversely related to the number of female worms but not related to the presence of circulating microfilariae. Indomethacin markedly depressed responses to acetylcholine in dogs with D. immitis but did not alter acetylcholine-induced dilation in normal dogs. These data suggest that D. immitis releases substances that alter distal arterial endothelial cell arachidonic acid metabolism. The seasonal pattern may reflect the onset of maximal reproductive activity in the spring and its decline as the vector season ends in the fall.

Acetylcholine↗
PubMed1987

Effect of hemodilution on endothelium-dependent vasodilation in the in vivo canine femoral artery.

The vasodilation responses to increased blood flow and acetylcholine require endothelial cells. We noticed that dogs with low hematocrit had reduced endothelial cell dependent responses; infusion of whole blood often restored the responses. Therefore, experiments were designed to test the hypothesis that hemodilution attenuates endothelial cell-dependent dilation. An extracorporeal shunt was created from the femoral artery to the jugular vein in pentobarbital-anesthetized dogs. Femoral artery diameter was measured by sonomicrometry. Blood flow was controlled by a screw clamp placed distally on the shunt tubing, and flow was increased from control (10% maximum) to maximum by opening the clamp for 3 mins. Hemodilution was achieved by withdrawal of whole blood and infusion of either 1) saline, 2) physiologic salt solution (PSS, containing 2.7 mM CaCl2), 3) saline with CaCl2 (2.7 mM), or 4) PSS without CaCl2. Endothelial cell-dependent dilations were evaluated after a 50% decrease in hematocrit. Hemodilution with either PSS or saline with CaCl2 did not decrease dilation responses to increased flow or acetylcholine. However, hemodilution with saline or PSS without CaCl2 markedly attenuated endothelium-dependent dilations. Ionized plasma calcium concentration decreased with saline and PSS without CaCl2 hemodilution, but it was maintained with PSS and saline with CaCl2 hemodilution. These data suggest that a 50% decrease in hematocrit does not influence endothelium-dependent dilation if plasma calcium is maintained. Our data support in vitro results that suggest that extracellular calcium is necessary for the release of endothelium-derived relaxing factor. Furthermore, relatively small changes in ionized calcium, within the physiologic range, have large effects on endothelial cell-mediated dilator responses to flow and acetylcholine. However, relatively large changes in hematocrit have no effect on the endothelium-dependent responses.

Acetylcholine↗
PubMed1986

Methylene blue and ETYA block flow-dependent dilation in canine femoral artery.

Flow-dependent dilation of the canine femoral artery is endothelial cell dependent and is not mediated by prostaglandins, adrenergic or cholinergic receptors, an ascending message from the microcirculation, or by myogenic mechanisms. We investigated the mechanism of flow dilation in 38 pentobarbital anesthetized dogs. A femoral artery-jugular vein shunt was constructed, and femoral artery diameter was continuously measured (sonomicrometer crystals) during control and maximum flow (1 l/min). Inhibition of prostaglandin formation by indomethacin did not alter the dilation response to increased flow, but the lipoxygenase-cyclooxygenase inhibitor 5, 8, 11, 14 eicosatetraynoic acid (ETYA) irreversibly inhibited the dilation response to increased flow. The guanylate cyclase inhibitor, methylene blue, caused a dose-dependent decrease in the dilation response to increased flow. Pretreatment with the H1 receptor antagonist tripelennamine sensitized the vessel to the inhibitory effects of methylene blue. Both methylene blue and ETYA shifted the ED50 for acetylcholine relaxation two orders of magnitude to the right, but did not alter the ability of the vessel to dilate or constrict to other stimuli. These data suggest that both cyclic GMP and a non-prostaglandin metabolite of arachidonic acid are involved in flow dilation. We propose that endothelial cells release a metabolite of arachidonic acid that stimulates vascular smooth muscle guanylate cyclase leading to relaxation. The role of histamine in this system is unknown.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1986

Endothelium-dependent flow-induced dilation of canine femoral and saphenous arteries.

We have characterized the dilation response to increased blood flow in the canine femoral and saphenous arteries. An arterio-venous shunt was created and changes in arterial diameter measured by sonomicrometer crystals. Increasing shunt flow approximately 10-fold caused a 9% increase in femoral and 15% increase in saphenous artery diameter. The dilation response consisted of a transient decrease in diameter, followed by a rapid dilation and a slow return to control when flow was decreased. The increased diameter was not a result of decreased transmural pressure or alterations in pulse pressure. After removing the endothelial cells, the vessels did not dilate to increased flow or topical acetylcholine (10(-5) M), but responses to norepinephrine (10(-5) M) and sodium nitroprusside (10(-4) M) were unaltered. Indomethacin, theophylline or propranolol did not affect the flow-induced dilation. Quinacrine, an inhibitor of phospholipase A2, attenuated the dilation response in a dose-dependent manner. We conclude that increased blood flow affects endothelial cells, causing an active dilation of arterial smooth muscle.

Acetylcholine↗
PubMed1986

Mediation of flow-dependent arterial dilation by endothelial cells.

When blood flow in a large artery is increased the vessel dilates. This flow-dependent dilation requires endothelial cells, and is not mediated by an ascending message from the microcirculation or a myogenic mechanism. Adrenergic, cholinergic, or ganglionic blockade does not alter the dilation response. Inhibition of cyclo-oxygenase by indomethacin has no effect, but inhibition of both lipoxygenase and cyclo-oxygenase by 5,8,11,14-eicosatetraynoic acid (ETYA) inhibits the dilation and shifts the acetylcholine dose response curve to the right. Inhibition of guanylate cyclase by methylene blue blocks the dilation response and shifts the acetylcholine dose response curve to the right. This suggests that both cyclic GMP and a nonprostaglandin metabolite of arachidonic acid are involved in the dilation response to increased flow. We propose that increased blood flow initiates an initial response, which results in endothelial cell production and release of a nonprostaglandin metabolite of arachidonic acid. This metabolite stimulates vascular smooth muscle guanylate cyclase, leading to increased cyclic GMP and vasodilation.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1985

Paternity testing. 2: Likelihood ratio tests.

It is known that the so-called paternity index is also a likelihood ratio statistic for testing that an alleged father is the true father. Unfortunately the likelihood ratio test can sometimes lead to unsatisfactory results because of its dependence on the phenotype combinations of the mother and child. A new, conditional likelihood ratio test, which we call the ancillary test, is proposed in which statistical testing is carried out conditionally on the phenotypes of the mother and alleged father. An exact procedure is available which can be executed with reasonable facility on a microcomputer.

Blood Group Antigens↗
PubMed1985

Aluminum-induced anemia.

Although many questions still remain unanswered, it is clear that aluminum causes a microcytic hypoproliferative anemia and is one factor responsible for worsening anemia in patients with end-stage renal disease. Time course studies in a rat model have shown that the anemia is preceded by microcytosis; this has not yet been examined in man. The exact mechanism of aluminum-induced anemia is unknown, however it appears to involve inhibition of heme synthesis, either by inhibition of enzyme activity or interference with iron incorporation or utilization. The interrelationship between aluminum and iron, zinc, lead, or other metals in this anemia is also unknown, as are the effects of aluminum on erythroid colony forming units. The role of parathyroid hormone on aluminum-induced anemia has not been examined. Presently treatment of aluminum-induced anemia involves removal of the source of the aluminum, although recent studies with desferrioxamine show promise. It is unclear, however, exactly how desferrioxamine improves this anemia. It is clear, however, that aluminum in the dialysate can cause clinical problems including anemia, and that these problems can be substantially reduced if not eliminated by water treatment.

Aluminum↗
PubMed1984

Microcytic anemia secondary to intraperitoneal aluminum in normal and uremic rats.

Dialysis patients exposed to high aluminum (Al) dialysate develop a microcytic anemia which is reversed by deionization (DI) of the dialysate. Because DI removes substances in addition to Al which are known to cause anemia, these experiments were undertaken to determine if Al causes anemia and if the anemia of uremia can be enhanced by Al. Four groups of rats were studied: sham control (A) N = 6; uremic control (B) N = 6; Al-loaded non-uremic (C) N = 7; and Al-loaded uremic (D) N = 5. Aluminum treatment was 1 mg Al intraperitoneally daily for 6 weeks. Uremic rats (B+D) were 1 5/6 nephrectomized; non-uremic (A+C) were sham-operated. Blood samples (200 microliter) were obtained prior to (C1) and weekly during treatment (T1 to T6) and analyzed by Coulter Counter. No significant difference in hemoglobin (Hb), hematocrit (Hct), or mean cell volume (MCV) was noted at C1 X At T3, MCV of Al-treated rats (C+D) was significantly less than sham control (A) (55.1 +/- 0.5 and 53.0 +/- 0.8 vs. 60.8 +/- 1.5 mu3, P less than 0.05). At T6, MCV, Hb, and Hct of Al-loaded uremic rats (D) (49 +/- 0.5 mu3; 11.8 +/- 0.5 g/dl; 25.1 +/- 2%) were significantly less than both A (58.6 +/- 1.3 mu3; 16.1 +/- 0.4 g/dl; 44.8 +/- 0.3%) and B (58.7 +/- 1.4 mu3; 13.8 +/- 0.4 g/dl; 33.6 +/- 0.5%) (P less than 0.05) and MCV, Hb, and Hct of Al-loaded non-uremic rats (C) (51.7 +/- 1.7 mu3; 12.6 +/- 0.3 g/dl; 29.4 +/- 1.5%) was significantly less than A (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗