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PubMed2004

Influence of pentoxifylline on perforin expression in human PBMC.

Pentoxifylline (PTX) is a methylxanthine derivative that unspecifically inhibits phosphodiesterase activity and thus, it increases intracellular concentration of cyclic nucleotides. Currently, PTX is commonly and chronically used in peripheral blood vessel diseases. Besides its well-known influence on rheologic properties of blood, PTX has also been found to decrease secretion of some cytokines such as IL-12, TNF and IFN-gamma and thus it could exert immunomodulatory activity. Furthermore, PTX inhibits lymphocyte cytotoxicity affecting the perforin-dependent pathway, both in humans and animals. It has also been shown recently that in some murine models, PTX promotes tumor growth. Such a phenomenon, at least partially, could result from PTX-dependent inhibition of natural cytotoxicity. However, the detailed mechanism of PTX influence on cytotoxic activity in humans has not been established. We hypothesized that PTX-dependent inhibition of natural cytotoxicity could result from decrease in perforin expression. In this study, it was shown that pentoxifylline only moderately inhibits perforin expression at the mRNA level in human peripheral blood mononuclear cells (PBMC), and this effect seems to be independent of intracellular cAMP concentration. On the other hand, PTX did not significantly influence perforin expression at the protein level. These results suggest that in humans, contrary to murine models, inhibition of perforin-dependent natural cytotoxicity through pentoxifylline does not result from changes in perforin production. Presumably, influence of PTX on natural cytotoxicity could be caused by e.g. interference with lymphocyte degranulation. Moreover, also other possibilities, such as PTX influence on conformational changes of perforin molecules and/or its influence on susceptibility of target cells to pore-forming of polyperforins cannot be excluded.

Cells, Cultured↗

PubMedDate not supplied

An acute vasculitis resembling polyarteritis nodosa.

Peripheral vascular disease are structural and functional abnormalities of the peripheral blood vessels that produce blood flow irregularities. The signs and symptoms relate either to ischemia or inflammation of the involved vessels, or to both. A previously healthy 4.5-year-old girl was referred to our hospital with bruises on fingers and toes. She had no history of environmental causes, including drug intake. Symptoms of abdominal pain, fever, and a swollen face preceded the symptoms of her extremities. On physical examination, her blood pressure, which could be obtained only on the things, was high. There were no pulses on the upper extremities or on either the a. dorsalis pedis or the a. tibialis anterior dextra. There was massive necrosis on fingers which led to dry gangrene. A rise in acute phase reactants accompanied the physical findings, and a segmental obstruction was found proximally to a. brachiales, and distally to a. radialis dextra and a. dorsalis pedis dextra on digital subtraction angiography (DSA). High-dose methylprednisolone, cyclophosphamide, salicylates and dipyridamole were given; as these medications did not relieve the symptoms, a thoracal sympathatectomy was performed. The peripheral circulation improved, but a demarcation zone developed on the fingertips, leading to amputation.

Amputation, Surgical↗

PubMed1985

General pharmacological properties of cilostazol, a new antithrombotic drug. Part II: Effect on the peripheral organs.

The pharmacological effects of the new antithrombotic drug, cilostazol (6-(4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)-qui nolinone, OPC-13013) on the peripheral nervous system and miscellaneous organs were studied. Cilostazol produced a very slight increase in beating rate of the isolated atrium and a very slight increase in contraction of the papillary muscle of guinea pigs induced by cilostazol compared with that of isoproterenol (isoprenaline). The beating rate increasing effect was not antagonized by propranolol and it augmented isoproterenol's effect. When administered intravenously in anesthetized dogs, cilostazol increased blood flow in the coronary, internal carotid, vertebral and femoral arteries and transiently decreased blood flow in the renal and superior mesenteric arteries probably because of blood pressure fall. In anesthetized dogs, cilostazol decreased blood pressure by reducing the resistance in the peripheral blood vessels. An increase in heart rate, cardiac contractile force, myocardial oxygen consumption and respiration rate were also observed. In conscious rats, the drug increased heart rate. Cilostazol produced a slight relaxation of the smooth muscle of all organs except for blood vessels and slightly inhibited spontaneous motility of the isolated uterus of pregnant rats, the isolated ileum of rabbits and the ileum of rats in situ. It was considered that cilostazol had no specific effects against norepinephrine, serotonin, acetylcholine or histamine based on the results that the drug was only slightly antagonistic against the contraction of rabbit aorta induced by norepinephrine and serotonin, the contraction of isolated guinea-pig ileum induced by acetylcholine, histamine and barium chloride and the contraction of the isolated uterus of non-pregnant rats induced by oxytocin. The drug had little effect on the contraction of the nictitating membrane induced by stimulation of the preganglionic sympathetic nerve in the cat. These results suggest that cilostazol had little effect on the autonomic nervous system. Cilostazol slightly inhibited edema induced by carrageenin, but showed no diuretic effect and had little effect on neuromuscular transmission or the secretion of gastric juice, bile and pancreatic juice, and therefore it was considered to have no appreciable effect on the peripheral nervous system or organs except for its vasodilating and cardiac effects.

Anesthetics, Local↗

PubMed2001

Blood pressure-independent effect of angiotensin AT1 receptor blockade on renal endothelin-1 production in hypertensive uremic rats.

OBJECTIVE: We recently reported that treatment of uremic rats with reduced renal mass with the angiotensin II (Ang II) subtype 1 receptor (AT1) antagonist losartan reduces endothelin-1 (ET-1) levels in blood vessels and in glomeruli. Although this suggests an important role for Ang II in the modulation of ET-1 production, the concomitant decrease in blood pressure may also be involved. The present study was designed to investigate whether the modulation of ET-1 production in uremic rats is related to tissue-specific effects of AT1 receptor blockade or to the antihypertensive effect of losartan. DESIGN: One week after renal mass reduction, uremic rats were treated with the conventional triple therapy (TRx) [reserpine (5 mg/l), hydralazine (80 mg/l) and hydrochlorothiazide (25 mg/l)] or losartan (20 mg/kg per day) for 6 weeks. Immunoreactive-ET-1 (ir-ET-1) levels in plasma and urine, as well as in vascular and renal tissues were measured by a specific radioimmunoassay after sample extraction and purification. RESULTS: Before treatment, systolic blood pressure was significantly higher in uremic animals compared to sham-operated controls (165+/-4 versus 123+/-2 mmHg, respectively; P < 0.01). Treatment with the TRx or with losartan normalized systolic blood pressure in uremic rats, whereas it was further increased in untreated uremic animals. At week 6, serum creatinine, proteinuria and urinary ET-1 and transforming growth factor-beta1 (TGF-beta1) excretion, as well as vascular and glomerular ET-1 content were increased in uremic rats compared to the controls (P < 0.01). Treatment of uremic rats with the TRx or with losartan reduced ET-1 content in the thoracic aorta and the mesenteric arterial bed (P < 0.01). However, losartan, but not the TRx, significantly attenuated the rise of serum creatinine, proteinuria and urinary ET-1 and TGF-beta1 excretion, as well as ET-1 content in glomeruli of uremic rats. Compared with the controls, renal preproET-1 mRNA expression was also significantly higher in uremic rats. Treatment of uremic rats with losartan prevented renal preproET-1 mRNA overexpression, indicating that changes in glomerular ET-1 content and urinary ET-1 excretion were related to modulation of renal ET-1 production. CONCLUSIONS: These findings indicate that the effect of losartan on ET-1 production in peripheral blood vessels may be mediated, in part, by the reduction of blood pressure. In contrast, the reduction of renal ET-1 production is mediated by tissue-specific effects of AT1 receptor blockade, and may contribute to the renal protective effects of losartan.

Angiotensin Receptor Antagonists↗

PubMed1993

Newer concepts in the medical management of patients with congestive heart failure.

Congestive heart failure (CHF) remains a major cause of morbidity and mortality in the United States, especially among the elderly. Although an underlying disturbance in cardiac function can be identified in most patients, manifestations of the disease are greatly influenced by other factors, particularly neurohumoral and peripheral adaptive responses which occur secondary to impaired cardiac function. The renin-angiotensin system (RAS) is integrally involved in the pathophysiology of CHF. Originally considered a humoral system, the RAS is now known to exist and operate within cardiac and vascular tissues. The importance of tissue-specific renin-angiotensin systems in CHF is presently under investigation. Most patients with symptomatic CHF benefit from the administration of an ACE inhibitor. Certain asymptomatic patients, such as those with severe left ventricular (LV) dysfunction and those who are at high risk for LV remodeling after anterior wall myocardial infarction, may also benefit from ACE inhibitor therapy. Diuretics and nitrates improve symptoms and often cardiac output in many patients with CHF. Although many new inotropic agents have been tested in CHF patients, none appear clinically superior to digitalis glycosides. The efficacy of digitalis glycosides in CHF may in part result from sympathoinhibitory properties such as the activation of baroreceptor mechanisms. Despite the fact that many CHF patients die from arrhythmias, treatment of asymptomatic ventricular arrhythmias in these patients is not recommended. Patients with symptomatic or sustained ventricular arrhythmias are best treated by a physician experienced in cardiac electrophysiology. Therapy with beta-blocking drugs for CHF patients is controversial. Anticoagulants are recommended for selected patients with CHF. Finally, exercise therapy may improve functional capacity in some patients with CHF through its effects on peripheral blood vessels and skeletal muscle tissues.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

Hereditary hemorrhagic telangiectasis treated by the harmonic scalpel.

BACKGROUND: Hereditary hemorrhagic telangiectasis (HTT) is a familial autosomal dominant genetic disorder that causes abnormalities of the wall of peripheral blood vessels. Severe nosebleed often is the dominant symptom. A variety of therapies have been proposed for epistaxis control in HHT but with limited success. METHODS: We report two cases of HHT in which recurrent nasal bleeding was successfully controlled using the Harmonic Scalpel. RESULTS: Use of the Harmonic Scalpel avoids the carbonization and incrustation of the nasal mucosa that commonly results from electrocautery and laser irradiation. Even during active bleeding, hemostasis can be achieved by repeated applications of the scalpel blade. CONCLUSION: This method can be performed quick and reliably on an outpatient basis. The Harmonic Scalpel may be the treatment of choice for recurrent epistaxis in HHT.

Blood Coagulation↗

PubMed1987

Review of tissue welding applications in neurosurgery.

New technical advances have made feasible the utilization of low-powered laser energy for constructive applications. Experience with laser bonding of blood vessels, peripheral nerves, and dura has been obtained. These studies are summarized, and the future potential of laser bonding of tissues of the central nervous system is discussed.

Animals↗

PubMed1994

Effect of erythropoietin on DNA synthesis, proto-oncogene expression and phospholipase C activity in rat vascular smooth muscle cells.

The administration of recombinant human erythropoietin (rHuEpo) to anemic chronic renal failure patients may be associated with an increase in blood pressure, possibly by direct effects on peripheral blood vessels. The experiments of the present study were designed to explore the hypothesis that rHuEpo might exert mitogenic effects on vascular smooth muscle cells (VSMCs), and that pre-existing hypertension might be a predisposing condition. Cultured aortic VSMCs from spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied for DNA synthesis, phospholipase C activity, and cell growth related proto-oncogene expression in the presence of rHuEpo. In cells from both rat strains, rHuEpo dose-dependently increased DNA synthesis and stimulated phospholipase C activity, as indicated by 3H-thymidine incorporation and inositol phosphate formation, respectively. Exposure of VSMCs to rHuEpo for various periods gradually increased the levels of c-myc and JunB mRNAs and transiently induced c-fos mRNA expression as determined by Northern analysis. The hormone-induced DNA synthesis was markedly enhanced in VSMCs from SHR compared to those from WKY. In contrast, rHuEpo-induced phospholipase C activity and proto-oncogene expression did not differ between the two strains. Taken together, these results suggest that rHuEpo may function as a vascular smooth muscle cell growth promoting factor through activation of the phospholipase C cascade and a modulation of proto-oncogene expression. It could thereby contribute to vascular hypertrophy and arterial hypertension.

Animals↗

PubMed1996

Ischemia-induced peripheral arterial vasospasm role of alpha 1- and alpha 2-adrenoceptors.

Ischemia produces functional and structural alterations in peripheral blood vessels. Our study was designed to investigate alpha-adrenoceptor modifications induced by prolonged ischemia and their role in enhancing the contractile response during reperfusion in canine femoral arteries. Unilateral vessel ischemia was created by double crossclamping a femoral artery and was maintained for 3 hr. Reperfusion was allowed for 1 hr. The contralateral femoral artery was utilized as a control. The vessels were harvested for contractile and binding studies. Isometric tension studies revealed that the magnitude of the maximum contractile response to norepinephrine (NE), potassium chloride (KCl), and methoxamine was 671 +/- 82 mg/mm2 versus 245 +/- 43 mg/mm2 (P < 0.01), 485 +/- 46 mg/mm2 versus 229 +/- 62 mg/mm2 (P < 0.05), and 486 +/- 88 mg/mm2 versus 126 +/- 38 mg/mm2 (P < 0.01), respectively for ischemic and nonischemic femoral arteries. EC50 values showed that ischemic vessels were more sensitive to NE, KCl, and methoxamine (P < 0.05). Sodium nitroprusside induced concentration-dependent and complete relaxation in all arterial rings (100% relaxation) but the ischemic femoral artery showed less sensitivity (P < 0.05). Binding studies showed that the number of binding sites (Bmax) for [3H]Prazosin and [3H]Rauwolscine were significantly increased in ischemic versus nonischemic vessels (1261 +/- 95 fmole/mg versus 704 +/- 113 fmole/mg, P < 0.03, and 490 +/- 86 fmole/mg versus 175 +/- 15 fmole/mg, P < 0.04, respectively). Furthermore, a significant decrease in affinity (Kd) for [3H]Prazosin and [3H]Rauwolscine was observed in ischemic versus nonischemic tissues (9.4 +/- 1.7 nM versus 4 +/- 0.2 nM, P < 0.02, and 6.4 +/- 1.5 nM versus 1.8 +/- 0.6 nM, P < 0.01, respectively). The increase in canine femoral artery vasoreactivity, following prolonged ischemia, seems to be also due to an increased density and functional activity of alpha-adrenoceptors expressed by the ischemic arterial smooth muscle cells.

Animals↗

PubMed1994

Functional morphology of the light yellow cell and yellow cell (sodium influx-stimulating peptide) neuroendocrine systems of the pond snail Lymnaea stagnalis.

Neuroendocrine light yellow cells of the pond snail Lymnaea stagnalis express a neuropeptide gene encoding three different peptides. The morphology of the cell system has been studied by in situ hybridization, using two synthetic oligonucleotides encoding parts of light yellow cell peptides I and III, and by immunocytochemistry with antisera to synthetic light yellow cell peptide II and to two fragments of light yellow cell peptide I. One large cluster of light yellow cells was observed in the ventro-lateral protrusion of the right parietal ganglion, smaller clusters lying in the posterior dorsal part of this ganglion and in the visceral ganglion. The cells had an extended central neurohaemal area. Immunopositive axons projected into all nerves of the ganglia of the visceral complex, into the superior cervical and the nuchal nerves, and into the connective tissue surrounding the central nervous system. Axon tracts ramified between the muscle cells of the walls of the anterior aorta and of smaller blood vessels. Peripheral innervation by the light yellow cell system was only found in muscular tissue of the ureter papilla. The antisera to the two peptide fragments of light yellow cell peptide I not only stained the light yellow cells, but also the identified yellow cells, which have previously been shown to produce the sodium influx-stimulating neuropeptide. The latter cells were negative to the in situ hybridization probes and antisera specific to the light yellow cell system. It is therefore unlikely that the yellow cells express the light yellow cell neuropeptide gene. Nevertheless, the cells contain a neuropeptide sharing antigenic determinants with light yellow cell peptide I.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMedDate not supplied

PY 108-068, a dihydropyridine derivative, and verapamil interact differently with the ouabain effects on the heart and the peripheral circulation.

In previous experiments PY 108-068 (PY) has been found to have more potent calcium antagonistic effects on vascular smooth muscle than on myocardial tissue. We now investigated the effects of PY and verapamil (V) on the increases in myocardial contractile force (measured with a strain gauge) and regional vasoconstriction (measured with tracer microspheres) effected by an infusion of 40 micrograms/kg ouabain into anaesthetized cats. Ouabain significantly increased contractile force of the left ventricle and caused vasoconstriction in the heart, stomach, small intestine, pancreas, spleen and skin, but not in the kidneys, brain, adrenals and liver. PY (30 micrograms/kg i.v.) and V (0.3 mg/kg i.v.) antagonized the vasoconstrictor effects of the glycoside in all organs except the skin, i.e. also in organs, where the calcium antagonists normally do not cause vasodilatation. However, PY did not affect the increase in contractile force, whereas V attenuated both the cardiac and peripheral vascular effects of ouabain. The results demonstrate the preferential action of PY on peripheral blood vessels as opposed to left ventricular myocardial tissue. Heart rate was decreased by both PY and V but the PQ-interval was lengthened only by V suggesting that PY in contrast to V preferentially acts on the sinus node rather than A-V conduction. A combination of PY with a glycoside might be beneficial in the treatment of cardiac failure, since this calcium antagonist apparently does not antagonize the positive inotropic action of ouabain on the heart while reducing afterload and reversing the undesirable vasoconstriction induced by cardiac glycosides.

Animals↗

PubMedDate not supplied

Basal blood pressure variability and reactivity of blood pressure to emotional stress in essential hypertension.

Blood pressure variability under basal conditions and blood pressure reactivity to emotional stress were studied in 38 hypertensives and 13 normotensives. Systolic basal blood pressure variability correlated with systolic blood pressure reactivity. Variability increased with higher basal blood pressure. Thus in the hypertension group the blood pressure variability was greater than in the normotension group. Besides, the hypertension group showed a greater reactivity of systolic blood pressure to emotional stress, too. An influence of age on basal blood pressure, blood pressure variability, and reactivity could be evaluated; but no influence of sex on these parameters was detected. The results indicate that variability and reactivity of blood pressure can be referred to a common central nervous blood-pressure-regulating mechanism. As both parameters are increased in hypertension, a greater lability of blood pressure must be assumed. This greater lability may be attributed to a stronger neurogenic influence or to structural changes of peripheral blood vessels.

Adult↗

PubMed1982

Fatal atheromatous embolization during coronary angiography.

Multiple fatal embolism following left heart catheterization is described in two patients. Postmortem examination showed friable atheromatous aortic plaques as the likely source of emboli that clinically involved the heart, peripheral blood vessels, brain, gastrointestinal system and solid organs. Histologic examination showed widespread arterial embolism by atheromatous material.

Angiography↗

PubMed2006

Oral oxymetholone reduces mortality induced by gamma irradiation in mice through stimulation of hematopoietic cells.

Oxymetholone is a 17alpha -alkylated anabolic-androgenic steroid. This drug can stimulate bone marrow cells and increase the blood cells in the peripheral blood vessels. It has been used for the treatment of anemia caused by low red cell production. Since oxymetholone has hematopoietic effect, we studied radioprotective effects of this drug in mice. In this study, we determined percentage of survival, dose-reduction factor (DRF) and hematological parameters in irradiated mice which treated with or without oxymetholone. Oxymetholone administrated at different doses 80, 160, 320, 640 mg/kg by gavages at 24 h before 8 Gy gamma irradiation. At 30 days after treatment, the following percentage of animals survival in each group was as: 80 mg/kg, 50%; 160 mg/kg, 50%; 320 mg/kg, 55%; 640 mg/kg, 75% and vehicle, 15%. Percentage of survival increased in all of treated groups statistically compared with irradiated-vehicle group. In the groups treated by oxymetholone, maximum protection was realized at 640 mg/kg. In order to calculate the DRF for oxymetholone, mice were exposed to whole-body gamma irradiation with dose ranges between 5.83 and 11.23 Gy. The probit line for oxymetholone-treated mice was shifted to the right with a DRF of 1.14. In mice exposed to whole-body gamma-irradiation (4 Gy), an oral administration of 640 mg/kg oxymetholone ameliorated radiation-induced decreases in circulating platelets and erythrocytes, but had a less effect on total number of WBC. These results demonstrate that oxymetholone stimulates myelopoiesis and thrombocytopenia and enhances survival in mice after ionizing radiation.

Animals↗

PubMed1987

Pharmacologic aspects of cardioselectivity in a beta-blocking drug.

Beta 2 adrenoceptors have been subdivided into beta 1 and beta 2 receptors, both by the varying response of different tissues to sympathomimetic amines and, more recently, by radioligand-binding techniques. It would appear that beta 1 receptors occur predominantly in the heart, whereas beta 2 receptors are found in lungs, peripheral blood vessels and uterus, and are also involved with glycogenolysis and glucagon and insulin secretion. In addition, the distribution of beta 1 receptors appears to relate to the density of sympathetic innervation of an organ or tissue, but tissues without sympathetic innervation are found to contain beta 2 receptors. Thus, beta 1 adrenoceptors may be considered as physiologically innervated receptors mediating responses to neuronally released norepinephrine, and beta 2 receptors as mediating responses to circulating catecholamines, particularly epinephrine. Radioligand-binding studies have also shown that the heart contains beta 2 receptors and the lung beta 1 receptors, but these are in the minority, and their role has not been identified. For many years, cardioselective beta 1-adrenoceptor antagonists have been available. This was considered to be a dose-dependent phenomenon but recent evidence has cast doubt on the concept that cardioselectivity is lost during dose increases within the therapeutic range. Nevertheless, even small doses of cardioselective drugs may show some beta 2-receptor antagonism, and may have adverse effects on patients with obstructive airways disease. Finally, nonselective drugs may result in a diastolic pressor effect in the presence of circulating catecholamines in contrast to the "vascular sparing" seen with cardioselective drugs.

Adrenergic beta-Antagonists↗

PubMed1976

Conversion of angiotensin I to angiotensin II.

The angiotensin I converting enzyme has two important functions: it inactivates bradykinin and converts angiotensin I to angiotensin II. Inhibition of the enzyme blocks the renin-angiotensin system and decreases systemic blood pressure if the pressure is maintained or increased by renin. The enzyme occurs in a variety of tissues and cell forms. The vascular endothelial cells of the lung and of peripheral blood vessels, and the epithelial cells of the kidney tubules are major sources of the enzyme. In addition to inactivating hypotensive peptides and activating a hypertensive one in the systemic circulation, the enzyme may affect organ functions by hydrolyzing peptides that are formed and released locally.

Angiotensin II↗

PubMed1985

Catecholamine-containing neurons and lymphoid cells in a lacrimal gland of the pigeon.

The Harderian gland of birds, a major lacrimal gland, contains a large population of lymphoid cells that produce IgA, a significant component of tears. Using histochemical techniques, we have examined the innervation of the gland. There was an extensive acetylcholine-esterase positive fiber network throughout the gland. However, catecholamine positive fibers were seen mainly associated with peripheral blood vessels and the lymphoid cell population which contained autofluorescent plasma cells. Ultrastructural examination showed that vesicle filled nerve varicosities were often seen near plasma cells and that some of these varicosities reacted positively for catecholamines. These anatomical data suggest that the lymphoid cell population may be affected by the autonomic nervous system.

Acetylcholinesterase↗

PubMed1988

L-glutamate stimulation of the zona incerta in the rat decreases heart rate and blood pressure.

Microinjections of L-glutamate into the zona incerta of pentobarbital anesthetized rats caused decreases in blood pressure and heart rate. The bradycardic response was reduced by approximately 70% after i.v. administration of atropine methyl nitrate. After combined muscarinic and beta-adrenergic blockade the bradycardic response was reduced to 90% of the control value. This suggests that the bradycardia was mediated primarily by activating the vagal outflow. Blood pressure decreases elicited after pharmacological blockade of the heart with both atropine and timolol were approximately 50% of the control values. This indicates that the zona incerta is also capable of altering stroke volume and/or inhibiting the sympathetic outflow controlling the peripheral blood vessels. By using an injectate containing L-glutamate mixed with [3H]L-glutamate and subsequent analysis of autoradiographic tissue sections, we have determined that the most reactive site is the region of the ventral zona incerta.

Animals↗