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PubMed1978

Plasma renin activity in the intervillous space of the human placenta, in umbilical vessels and in maternal peripheral venous blood.

Plasma renin activity (PRA) was measured by bioassay in the maternal and fetal compartments: intervellous space of the placenta (IVS), maternal peripheral venous blood (MPVB), umbilical artery (A) and vein (V), in a group of normal parturients and their respective fetuses, also normal. The material was collected simultaneously from mother and fetus in the third phase of delivery. PRA valuses in the IVS of the placenta were higher than those observed in the umbilical vein, and similar to those found in the MPVB. PRA values in the umbilical cord vessels behaved as if being part of only one compartment. The mechanisms of regulation of plasma renin activity on the maternal side seem to be independent from those on the fetal side, at least under physiological condition.

Aldosterone↗
PubMed1977

[The effects of the vasodilator nitroprusside on haemodynamics and myocardial oxygen consumption during drug induced myocardial depression (author's transl)].

The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.

Animals↗
PubMed1995

Secretion and accumulation of Alzheimer's beta-protein by cultured vascular smooth muscle cells from old and young dogs.

Cultured smooth muscle cells isolated from beta-amyloid-affected blood vessels from old dogs accumulate beta-protein at early passages [5,24]. Now, we show that smooth muscle cells derived from amyloid-free brain blood vessels and peripheral arteries from old and young animals are induced by culture conditions to deposit intracellularly fibrillar and non-fibrillar beta-protein. Accumulation of beta-protein is associated with a higher secretion of beta-protein, but not with a higher secretion of beta-amyloid precursor protein (beta APP) or higher cellular content of beta APP. Gradual cessation of proliferative activity was observed in cultures that accumulate beta-protein.

Age Factors↗
PubMed1995

Selective binding of peripheral blood lymphocytes to the walls of cerebral vessels in frozen sections of human brain.

In order to identify the factors that control the binding of blood leucocytes to cerebral blood vessels we have modified and applied the frozen section assay of Stamper and Woodruff to the study of human brain. Cryostat sections of brain tissue obtained at post mortem were overlaid with blood lymphocytes and experimental conditions were defined which permitted optimum binding of the cells to transected blood vessel walls. The maximal binding of lymphocytes to cerebral vessels occurred when 6 x 10(6) lymphocytes were overlaid onto brain sections for 30 min at 7 degrees C with gentle agitation. Only a small proportion (0.01%) of the added lymphocytes bound to exposed cerebral vessels. However, lymphocytes were far more adherent than monocytes and polymorphonuclear cells (7-fold and 11-fold respectively: p < 0.001) and activation of lymphocytes with IL-2 enhanced their binding to blood vessel walls (mean 130% increase; p < 0.03). Further analysis revealed that CD4-positive T lymphocytes were the predominant cell population binding to the blood vessels. Antibody blocking studies showed that lymphocyte binding to cerebral blood vessels was inhibited by pretreating the lymphocytes with anti-CD11a, anti-CD18 or anti-CD49d (p < or = 0.02) and immunohistochemical studies revealed the presence of the counter-receptors ICAM-1 (CD54) and VCAM-1 (CD106) for these adhesion molecules in addition to the presence of E-selectin (CD62E) and P-selectin (CD62P) on the cerebral blood vessels. The establishment of a technique in situ which measures selective binding of CD4-positive peripheral lymphocytes to sections of cerebral blood vessels will assist in the molecular characterization of factors that control the interaction of leucocytes with the blood-brain barrier in health and disease.

Adult↗
PubMed1987

Peripheral and cerebrovascular actions of ethanol, acetaldehyde, and acetate: relationship to divalent cations.

Inasmuch as ethanol is thought to exert its major effects in the autonomic and central nervous systems, it is important to determine whether acute versus chronic ingestion of this abused substance exerts any direct actions on peripheral and cerebral blood vessels. Since the chronic effects of ethanol on the cardiovascular system appear to be pivotal in the etiology of hypertension, coronary heart disease, and strokelike events, it is important to elucidate and understand the effects of chronic ethanol abuse and its mechanism(s) of action on the peripheral and cerebral blood vessels. Data are reviewed which suggest that the peripheral vasodilation and hypotension which result from acute ingestion (or administration) of ethanol may, in large part, be a consequence of its direct actions on vascular smooth muscle cells, both at the macro- and microcirculatory levels. At least two mechanisms appear to contribute to this vasodilator effect: inhibition of the normal rhythm or vasomotion (spontaneous mechanical activity) of vascular smooth muscle, and depression of the contractile responses to endogenous neurohumoral substances that play a role in maintaining vascular tone and regulation of blood flow. The data acquired so far suggest that the dilator actions are related causally to interference with movement and/or translocation of Ca2+ across the vascular membranes. In addition, these actions appear to resemble the peripheral vascular effects of general anesthetics. Evidence is also reviewed which indicate that ethanol, in contrast to acting as a vasodilator in the splanchnic vasculature, is often a potent and concentration-dependent constrictor of arterioles and venules in the skeletal muscle vasculature. Direct in situ observations on the rat brain, using high resolution, quantitative TV image-intensification microscopy, indicates that administration of ethanol, irrespective of the route of administration (e.g., perivascularly, intraarterially, or systemically), produces graded concentration-dependent spasms of arterioles and venules. Concentrations of ethanol approximately equal to greater than 250 mg/dl produce intense spasms resulting in rupture of these vessels. Recent in situ studies in conscious dogs, using radiolabeled microspheres, also indicate that ethanol can produce deficits in regional brain blood flow. Studies with isolated canine middle cerebral and basilar arteries clearly demonstrate that low concentrations of ethanol (e.g., less than 10 mM) can produce concentration-dependent spasms by a direct vascular action.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetaldehyde↗
PubMed1999

Measurement of delivery and metabolism of tirapazamine to tumour tissue using the multilayered cell culture model.

PURPOSE: Efficient extravascular penetration is essential for the optimal activity of most anticancer drugs and is particularly relevant to bioreductive cytotoxins which target hypoxic cells that can be located distal to functional blood vessels within tumours. Tirapazamine (3-amino-1,2,4-benzotriazine-1,4-di-N-oxide; Triazone; SR 259075; formerly SR 4233) is a lead bioreductive cytotoxin currently undergoing clinical evaluation. It exhibits preferential cytotoxicity towards cells at reduced oxygen tension, and could complement existing anticancer therapies where hypoxic cells are believed to constitute a refractory population. We assessed the ability of tirapazamine to penetrate tumour tissue using an in vitro multilayered cell culture (MCC) model. METHODS: Diffusion of tirapazamine through oxic and hypoxic multilayered cell cultures composed of SiHa. human cervical carcinoma cells, was measured using a dual reservoir diffusion apparatus from which samples were quantified via HPLC. Drug concentration kinetics from both reservoirs were analysed using a mathematical model for diffusion and metabolism within the MCC. Results were then applied to a second mathematical model which described extravascular drug penetration within a tumour cord, the sheath of cells surrounding a blood vessel. RESULTS: The diffusion coefficient of tirapazamine within SiHa MCCs was determined as 7.0+/-0.5 x 10(-7) cm2/s and the maximal metabolic rate for hypoxic MCCs, Vmax, as 1.5+/-0.4 microM/s. The thickness of individual tissue cultures was determined by diffusion of tritiated water (HTO). A linear relationship was shown to exist between tissue thickness and the inverse of permeability to HTO. Experimental results were used to simulate drug distribution within a tumour cord. These simulations indicate that, when tirapazamine is administered via intravenous infusion, a stable tirapazamine distribution throughout the cord occurs within 15 min with cells most peripheral to the blood vessel exposed to only 10% of the blood drug concentration. Under these conditions, the simulations predict cell kill to be limited to the first 75 microm of tissue surrounding a blood vessel. CONCLUSION: This study indicates that extravascular penetration of tirapazamine to peripheral cells existing at low oxygen tension may be limited by the metabolism of tirapazamine by more proximal cells existing at moderate oxygen tension. Simulations found that tirapazamine reached only 10% of the blood concentration at cells most peripheral to blood vessels. These results indicate that tirapazamine would be significantly cytotoxic only to cells located within approximately 75 microm of blood vessels. Further MCC-based modelling of extravascular drug penetration would serve as a means of identifying new antitumour agents with location-specific activity.

Algorithms↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed1992

Basement membranes in adenoid cystic carcinoma. An immunohistochemical study.

Tissue samples from 30 patients with adenoid cystic carcinoma and 20 with adenocarcinoma of salivary gland origin were studied by immunohistochemical staining with specific antibodies to the four macromolecules that are present in normal basement membranes: type IV collagen, laminin, heparan sulfate proteoglycan, and entactin. In the adenoid cystic carcinoma samples, the four proteins were localized in different types of extracellular matrices in the tumor, namely pseudocystic spaces, hyaline stroma, and around tumor cell nests. The staining intensity was enhanced by pretreatment with hyaluronidase. The tumor cells of adenoid cystic carcinoma showed a tendency to proliferate with individual cells in contact with the basement membrane and to infiltrate through basement membrane-rich tissues, such as peripheral nerves, blood vessels, and skeletal muscles. In contrast, only circumferential staining of tumor cell nests was obtained in adenocarcinoma samples. The results suggest that adenoid cystic carcinoma is a tumor with affinity for basement membranes, and this basic feature is reflected in its histology and presumably in its biologic behavior. Immunostaining with antibodies to basement membrane proteins appears to be useful for differential diagnosis of some types of these two carcinomas.

Adenocarcinoma↗
PubMed1990

Regional pharmacokinetics. I. Physiological and physicochemical basis.

Systemic pharmacokinetics is the study of the time-course of drug concentrations in 'systemic' blood sampled from either an arterial, central venous or peripheral venous blood vessel. It is generally not suitable for studying the pharmacokinetics of drugs in individual organs of the body, when the blood concentrations of a drug are changing rapidly, or when the physiological or pathophysiological status of a patient is unstable. Regional pharmacokinetics addresses some of these limitations and is based on the study of the factors influencing drug concentrations in specific regions (tissues, organs) of the body due to the movement of drug from blood into and out of the region (drug 'uptake' and 'elution', respectively). It provides a vital link between systemic pharmacokinetics and molecular pharmacology. The physiological basis of regional pharmacokinetics is a function of the interactions of the drug between the cells and proteins in blood, the blood flow supplying a region, the structure of the capillaries of the region and the types of specific and non-specific binding within the region. The physicochemical basis of regional pharmacokinetics is a function of the factors influencing the rate and extent of diffusion of a drug through aqueous and lipid mediums, such as molecular weight, ionization, charge, and lipophilicity.

Animals↗
PubMed1994

Initiation of satellite cell replication in bupivacaine-induced myonecrosis.

To determine how and when the satellite cells are stimulated to replicate in muscle regeneration, the rat soleus muscle was examined chronologically after bupivacaine-induced myonecrosis. Bromodeoxyuridine and desmin-positive mononuclear cells, indicating the start of satellite cell replication, were seen 25 h after bupivacaine treatment when macrophages had already invaded the sarcoplasm of necrotic fiber. These findings suggest that muscle regeneration starts as early as the time at which macrophages begin to scavenge necrotic material. Proliferating myoblasts increased in number, reaching a maximum at 49 h after myonecrosis, and decreased in number 3 days after the myoblasts fused with each other form myotubes. The satellite cell proliferation after bupivacaine-induced myonecrosis began at almost the same time as in crush injury, and earlier than after muscle transplantation using whole intact or minced muscle fragments. The earlier beginning and more rapid regenerating process probably resulted from the preservation of intact satellite cells, blood vessels and peripheral nerves in the bupivacaine-induced myonecrosis.

Animals↗
PubMed1997

[Filaria: a tropical disease as the etiology of acute scrotum].

In the diagnosis and treatment of acute scrotal pain and swelling it is important to differentiate between testicular torsion and epididymo-orchitis. A special case of a thirty-eight-year-old male asylant from Nepal was presented in the urological service with acute scrotal pain. To exclude testicular torsion, a diagnostic exploration of the scrotum was done with the findings of an acute funiculitis with abscess formation. Under surgical drainage of abscess together with medical treatment the acute inflammation disappeared. The diagnosis of filarial funiculitis was made after identifying the microfilariae in a blood vessel and in the peripheral blood smear. A filaricide medication with diethylcarbamacine citran was administered with good symptomatic relief.

Acute Disease↗
PubMed1995

Dexamethasone and activators of the protein kinase A and C signal transduction pathways regulate neuronal calcitonin gene-related peptide expression and release.

Primary cultures of adult rat dorsal root ganglia (DRG) neurons were used to determine if activation of either the protein kinase A or C signal transduction pathways or treatment with the synthetic glucocorticoid dexamethasone modulate neuronal calcitonin gene-related peptide (CGRP) synthesis and release. DRG are the sites of neuronal cell bodies known to produce abundant CGRP levels, and to send axons peripherally to blood vessels and centrally to the spinal cord. Using immunocytochemical techniques, we confirmed that synthesis of immunoreactive CGRP (iCGRP) is restricted to a subpopulation of DRG neurons. Subsequently, we determined that treatment (24 h) of the neurons with either dibutyryl cAMP (1 mM) or phorbol 12-myristate 13-acetate (2 microM) increased CGRP mRNA content 2.2 +/- 0.4 (n = 6, p < 0.03) and 3.0 +/- 0.6-fold (n = 6, P < 0.02) respectively, while secreted iCGRP levels were increased 1.8 +/- 0.2 (n = 14, P < 0.005) and 4.5 +/- 1.0 (n = 14, P < 0.001)-fold over control levels. Treatment of the neurons with dexamethasone alone had no effect on CGRP expression; however, this agent was able to significantly attenuate the stimulatory effects of NGF on both CGRP mRNA accumulation and release of iCGRP. Time course studies demonstrated that in the phorbol ester treated neurons CGRP mRNA levels continued to increase at 48 h, while maximal induction with dibutyryl cAMP occurred at approximately 12 h. These results indicate that local and/or circulating factors which act through the protein kinase A and C signal transduction pathways upregulate both CGRP expression and release, while glucocorticoids attenuate the stimulatory effects of NGF.

Animals↗