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At least 145 records · Page 8Linked to original sources

Tetraethylammonium-evoked oscillatory contractions of rat tail artery: a K-K model.

Spontaneously rhythmic contraction of peripheral blood vessels actively modulates the peripheral circulation and blood pressure. However, the underlying mechanisms for the complex rhythmic contraction patterns of various vascular tissues are not yet fully understood. In the present study, the tetraethylammonium (TEA)-induced spontaneously oscillatory contractions of isolated rat tail artery tissues were examined. It was found that TEA evoked arterial oscillatory contractions in a concentration-dependent, but endothelium-independent manner. The voltage-dependent K+ (Kv) channel specific blocker, 4-aminopyridine (4-AP), induced a sustained, but not oscillated, vascular contraction. The presence of 4-AP had no effect on the TEA-induced oscillatory contractions. The blockade of KCa channels with charybdotoxin or apamin did not affect the basal force of vascular tissues. Neither the TEA-induced oscillatory contraction was affected by these blockers. The opening of KATP channels by levcromakalim or their blockade by glybenclamide ceased or increased, respectively, the oscillation of TEA-induced contractions. The absence of Ca2+ or the presence of nifedipine in the bath solution completely abolished the effects of TEA. The inhibition of Ca2+-ATPase in the sarcoplasmic reticulum with micromolar concentrations of thapsigargin or cyclopiazonic acid either abolished or enhanced, respectively, the TEA-induced oscillatory contractions. Ryanodine did not affect the TEA-induced oscillatory contraction. In conclusion, the TEA-induced oscillatory contraction may be initiated by the blockade of the TEA-sensitive delayed rectifier K+ channels and maintained by the TEA-insensitive but ATP-sensitive K+ channels. This K-K model presents a novel mechanism for the depolarization-induced rhythmic contractions of small arteries.

Animals↗

Platelet adhesion and myointimal proliferation in canine pulmonary arteries.

Pulmonary arteries were studied by scanning and transmission electron microscopy in 15 preconditioned dogs. Five dogs were control animals, while 10 dogs were studied 4 and 30 days following transplantation of adult heartworms into the pulmonary arteries. Evan's blue dye was used to locate areas of vascular damage. Pulmonary arteries from control dogs exhibited no Evan's blue staining. The surface and ultrastructural characteristics of these blood vessels were comparable to normal peripheral blood vessels. Pulmonary arteries removed from dogs after 4 days of heartworm infection exhibited extensive staining with Evan's blue. These stained areas had disrupted endothelium with many platelets adhered to the exposed subendothelium. In addition, leukocytes were attached to adjacent areas of damaged endothelium. Pulmonary arteries of dogs infected with heartworms for 30 days also exhibited extensive staining with Evan's blue. The blue-stained areas in this group had two typical responses. On some portions the lesions were similar to those seen at 4 days (ie, loss of endothelium with platelet and leukocyte adhesion), while other stained areas had complex lesions that projected from the surface into the lumen of the blood vessel. These lesions were endothelialized, and transmission electron microscopy revealed that they consisted of large numbers of smooth muscle cells that had migrated through the internal elastic lamina. The findings in the 30-day infection group suggest that the proliferative lesion formation was a result of an ongoing active process of endothelial loss and plateletleukocyte adhesion. The characteristic response of canine pulmonary arteries to the presence of heartworms (endothelial loss, platelet-leukocyte adhesion, and development of myoproliferative intimal lesions) suggests that this condition is a potential model for study of the early vascular changes that produce myointimal proliferation.

Animals↗

[Diagnostic value of intravascular ultrasound diagnosis in peripheral arteriosclerotic blood vessel changes].

Intravascular ultrasound is an adjunct for the diagnosis of atherosclerotic peripheral vessels. In this in-vitro study, 69 segments of human peripheral arteries were fixed in formalin, examined with intravascular ultrasound and pathomorphologically evaluated. Sensitivity, specificity, both positive and negative predictive value and accuracy of intravascular ultrasound for the detection of irregular lumen contours, intraarterial structures and intimal thickening were determined for each of four quadrants. Sonographic features (echogeneity, homogeneity, shadowing of echoes) were compared to the architecture of lesions. Intravascular ultrasound detected regular (normal) lumen contours with high specificity (96.5%), a sensitivity of 65.0%, and an accuracy of 88.4%; intraluminal structures were detected with a sensitivity of 88.6%, a specificity of 97.8%, and an accuracy of 96.4%. Most atherosclerotic lesions could be localized with a sensitivity of 86.1%, a specificity of 99.1%, and an accuracy of 86.9%. Slight intimal thickening was detectable with a sensitivity of 85.9%, a specificity of 87.8%, and an accuracy of 86.2%. Comparison of sonographic features and the pathomorphological architecture of atherosclerotic lesions revealed that fibrous, atheromatous, and complex lesions without calcification did not show shadowing of echoes. The majority of fibrous or atheromatous lesions presented with homogeneous echoes; these lesions showed hypo-, hyper- and normodense echoes. The homogeneity of echoes did not help to identify the different components of combined atherosclerotic lesions. Thus, intravascular ultrasound is able to detect irregular lumen contours, intraluminal structures, and intimal thickening, but further sonographic criteria are needed to identify the architectural structure of combined lesions.

Aorta, Abdominal↗

A method for MR quantification of flow velocities in blood and CSF using interleaved gradient-echo pulse sequences.

The aim of this study was to establish a rapid method for in vivo quantification of a large range of flow velocities using phase information. A basic gradient-echo sequence was constructed, in which flow was encoded along the slice selection direction by variation of the amplitude of a bipolar gradient without changes in sequence timings. The influence of field inhomogeneities and eddy currents was studied in a 1.5 T interleaved sequences for calibration and in vivo flow determination were constructed, and flow information was obtained by pairwise subtraction of velocity-encoded from velocity non-encoded phase images. Calibration was performed in a nongated mode using flow phantoms, and the results were compared with theoretically calculated encoding efficiencies. In vivo flow was studied in healthy volunteers in three different areas using cardiac gating; central blood flow in the great thoracic vessels, peripheral blood flow in the popliteal vessels, and flow of cerebrospinal fluid (CSF) in the cerebral aqueduct. The results show good agreement with results obtained with other techniques. The proposed method for flow determination was shown to be rapid and flexible, and we thus conclude that it seems well suited for routine clinical MR examinations.

Aorta↗

Effects of nifedipine on resistance vessels, arteries and veins in man.

1 The effect of nifedipine on peripheral blood vessels has been studied in man. 2 Nifedipine induced dilatation of the forearm resistance vessels when given either by local intra-arterial infusion or sublingually (10 mg). 3 Local infusion of the drug did not relax hand veins preconstricted by infusion of noradrenaline and neither local infusion nor sublingual administration prevented constriction mediated by the sympathetic nervous system. Nifedipine was, however, a potent inhibitor of hand vein contractions induced by high concentrations of potassium provided that the noradrenergic component of the response was suppressed by simultaneous infusion of phentolamine. 4 Sublingual nifedipine (10 mg) did not dilate the elbow collateral arteries. 5 The effects of nifedipine on peripheral blood vessels are similar, but not identical, to those of verapamil. The pattern of action, with dilatation of resistance vessels but not capacitance, resembles that of hydralazine rather than glyceryl trinitrate and this suggest that nifedipine may prove useful in the treatment of hypertension.

Adult↗

Characterization of sumatriptan-induced contractions in human isolated blood vessels using selective 5-HT(1B) and 5-HT(1D) receptor antagonists and in situ hybridization.

The 5-HT(1B/1D) receptor agonist sumatriptan is effective in aborting acute attacks of migraine and is known to cause constriction of cranial arteries as well as some peripheral blood vessels. The present study set out to investigate whether 5-HT(1B) and/or 5-HT(1D) receptors mediate contractions of the human isolated middle meningeal and temporal arteries (models for anti-migraine efficacy) and coronary artery and saphenous vein (models for side-effect potential). Concentration-response curves were made with sumatriptan (1 nm-100 microm) in blood vessels in the absence or presence of selective antagonists at 5-HT(1B) (SB224289) and 5-HT(1D) (BRL15572) receptors. SB224289 antagonized sumatriptan-induced contractions in all blood vessels, although the antagonism profile was different amongst these blood vessels. In the temporal artery, SB224289 abolished contraction to sumatriptan, whereas in the middle meningeal artery and saphenous vein sumatriptan-induced contractions were blocked in an insurmountable fashion. Moreover, SB224289 acted as a weak surmountable antagonist in the coronary artery (pK(B): 6.4 +/- 0.2). In contrast, BRL15572 had little or no effect on sumatriptan-induced contractions in the four blood vessels investigated. In situ hybridization revealed the expression of 5-HT(1B) receptor mRNA in the smooth muscle as well as endothelial cells of the blood vessels, whereas the mRNA for the 5-HT(1D) receptor was only very weakly expressed. These results show that the 5-HT(1B) receptor is primarily involved in sumatriptan-induced contractions of human cranial as well as peripheral blood vessels.

Adult↗

Ultrastructural changes in blood vessels of peripheral nerves in leprosy neuropathy. I. Tuberculoid and borderline-tuberculoid leprosy patients.

Radial or superficial peroneal nerve biopsies of 6 patients with tuberculoid or borderline-tuberculoid leprosy and 6 control nerve biopsies were examined by electron microscopy. Endoneurial blood vessels showed histopathology in all the leprosy patients. Changes, in particular, involved the basement membrane in postcapillary venules and venules. Multilayered parellel basement membranes, with collagen and ground substance, formed a thick coat ("hyaline zone") around the vessels. It is suggested that the zone inhibits passage of nutrients and metabolites and, thus, contributes to or is the main cause of the local destruction of (unmyelinated) nerve fibres and the lack of nerve fibre regeneration observed in this type of leprosy. The perivascular zone, presumably, is produced by pericytes in response to defects in the "blood-nerve barrier" of endoneurial vessels. In granulomata of leprosy skin lesions, a perivascular zone was not present. The endothelium of endoneurial vessels, in affected nerves, generally was normal. Occasionally, however, gaps and fenestrations were seen and there were histological indications that leakage of blood plasma had occurred through the gaps and through the basement membrane of the endothelium. Occlusion of endoneurial vessels was found only in the oldest patient and the degeneration of nerve fibres generally observed thus is considered not to be caused by ischaemia. Histopathology in epi-and perineurial vessels was definitely less pronounced than in endoneurial vessels.

Adolescent↗

Histological examination of blood vessels in peripheral gangrene among patients with sporadic outbreak of ergotism.

During the academic year 1985-1986 at Gondar College of Medical Sciences Hospital gangrenous ergotism was clinically diagnosed in seven patients (5 males, 2 females) ranging in age from 20 to 45 years. Amputation and subsequent histological examination of the blood vessels revealed occluded tibial arteries by acute thrombosis without cellular reaction or inflammatory lesion of the arterial wall in 3 patients. Endangitis with organized arterial thrombosis and focal recanalization of the vessels was noted in the remaining four patients. The smaller arterial branches including the dorsal pedal artery appeared to be contracted with knobby projections into the lumen. The latter was occluded by chronic, organized thrombosis in all patients. The present finding indicates that thrombosis and its organization could be another pathogenic factor in the development of gangrene due to ergotism, which is a histological picture similar to that of thrombangitis obliterans.

Adult↗

Distribution of adrenergic innervation of blood vessels in peripheral nerve.

The distribution of adrenergic innervation of microvessels in the extrafascicular and endoneurial compartments of rat tibial nerve was examined with glyoxylic acid-induced and formaldehyde-induced histofluorescence methods. Periarterial and arteriolar adrenergic nerves were present in the epineurium-perineurium suggesting that blood flow in the extrafascicular connective tissue is under neurogenic influence. In contrast, blood vessels in the nerve endoneurium were not associated with histofluorescent nerve fibers. The absence of perivascular adrenergic innervation in the endoneurium suggests that regulation of vascular function within the endoneurium is not under neurogenic control.

Adrenergic Fibers↗

Characterization of substances which promote or repel sympathetic fiber growth in vitro.

To determine whether a recognition mechanism is involved in determination of sympathetic innervation patterns of various tissues, tissue-derived substances were applied to a restricted test surface region of dishes and the responses of cultured sympathetic neurites were examined. Sympathetic fibers exhibited a turning or ramifying response, resulting in a dense fiber growth on test regions coated with particulate (adheron) fractions of a conditioned-medium (CM) from expansor secundariorum, heart, peripheral blood vessel or abdominal aorta, whereas on test regions coated with those from lung, skeletal muscle or dorsal aorta the neurite growth was repelled and sparse fiber growth was observed. Particulate fractions of brain- or gizzard-CM had no effect. These patterns in vitro were in parallel with the dense sympathetic innervation in expansor secundariorum, heart, peripheral blood vessel and abdominal aorta, but little or no sympathetic innervation in lung, skeletal muscle and dorsal aorta in vivo. These results suggest that adheron particles may participate in determination of sympathetic innervation patterns. Activity which repels or promotes the sympathetic fiber growth was inactivated by pronase E or trypsin but not by DNase or neuraminidase. Repelling activity was lost after treatment with heparinase or heparitinase but not with chondroitinase ABC or hyaluronidase. Promoting activity was retained after treatment with these glycosidases. These results suggest that the factor(s) possessing a repellent effect is a heparan sulfate proteoglycan and one(s) possessing a promoting effect is a protein.

Adrenergic Fibers↗

Effects of noise on some autonomic system activities.

Experiments were conducted on the effects of various expected noise conditions upon autonomic system activity in men during rest and work (bicycle ergometer). Skin temperature and heart rate were not appreciably, if at all, affected by any of the noises. Wide-band, predominantly low-frequency noise, at a level of 92 dB, A-weighted, generally caused a decrease in pulse amplitude (indicative of constriction of peripheral blood vessels) during either work or rest, whereas an equally intense one-third octave band of random noise, center frequency of 3150 Hz, had no appreciable effect on pulse amplitude. Repeated exposures to the wide-band noise showed some adaptation or habituation of the pulse amplitude response during conditions of either work or rest. The results were the same for fast rise time (impulsive) bursts of wide-band noise as for bursts with slow, gradual onsets. Rapid interruptions of wide-band noise caused less of a decrease in average pulse amplitude than did uninterrupted noise. It is suggested that constriction of peripheral blood vessels in response to expected intense low-frequency or wide-band noises is more related to auditory, reflexive protective mechanisms than to autonomic system responses generally considered to be stressful to the organism.

Adaptation, Physiological↗

[Observations of capillary fluid flow rate by vibration on the small vessel model].

The vibration hazards in peripheral blood vessels as an occupational origin is caused by using pneumatic vibrating tools. In order to know that the major part of causes is whether due to the direct effects of the physical vibration or due to the effects depended on the excitations of peripheral nervous system, an model experiment was employed to estimate the direct effect of the physical vibration. In our experiments, water as fluid was used instead of blood. The silicon capillary tube as same the physical qualities and conditions as blood vessels was vibrated by oscillator. The silicon capillary tube was exposed by following three type of vibration mode to flow axis; i) sine wave of transverse vibration, ii) rectangular wave of transverse vibration, and iii) sine wave of longitudinal vibration. The range of vibration frequency covered 1-2000 Hz. The averaged acceleration by oscillating vibration and the vibration strength level were estimated about 1-200 G and 150 dB, respectively. The observed decreases of water flow rate due to vibration extremely depend on frequency. The decrease ratio of water flow rate by vibration was at maximum 12% down compare with the cases of non vibration. In these observed results by this model experiment, it should be concluded that the direct effect of the physical vibration to the blood flow was not too strong to cause the actual vibration hazards.

Blood Circulation↗