Blood vessels最新文献

Measurements of coronary microvascular parameters in situ are difficult because of the thickness of the heart muscle and cardiac contraction. Both of these problems hamper the visualization of the coronary microcirculation. We have refined methodological approaches that enable the study of the coronary microcirculation in situ. In the first approach, microvessels can be visualized in the beating heart using a preparation that compensates for cardiac motion by creating an illusion that the heart is motionless. This is accomplished by flashing a stroboscopic light source once per heart cycle at the same point in each cycle and synchronizing a ventilator with the cardiac cycle. Images of microvessels can be obtained using standard intravital video-microscopic techniques. To visualize the intramural and subendocardial microcirculation, studies are completed in isolated hearts. In this preparation, measurements of microvascular diameters and pressures can be performed in both the subepicardial and subendocardial microcirculations. This latter approach allows insight into transmural differences of coronary microvascular regulation.

The cerebral circulation is supplied with two vasodilator systems: the parasympathetic system storing vasoactive intestinal peptide, peptide histidine isoleucine, acetylcholine and in a subpopulation of nerves neuropeptide Y, and the sensory system, mainly originating in the trigeminal ganglion, storing substance P, neurokinin A and calcitonin gene-related peptide (CGRP). Recent knowledge of the innervation and effects of the dilator neuropeptides in the cerebral circulation is reviewed. Their role in the pathophysiology of subarachnoid hemorrhage and migraine has now received attention, with documentation of a clear linkage with the release of CGRP. In subarachnoid hemorrhage, other perivascular peptides are, to a lesser extent, involved.

Postganglionic sympathetic cotransmission by noradrenaline (NA) and adenosine 5'-triphosphate (ATP) was studied in isolated arteries from rabbits using as tools alpha-adrenoceptor antagonists and alpha, beta-methylene-ATP which first activates and then desensitizes purine P2X receptors. In the pulmonary artery, NA was the only chemical signal responsible for neurogenic vasoconstriction. In sharp contrast, ATP was the only signal eliciting electric as well as mechanical postjunctional responses in small jejunal arteries. Mixed adrenergic and purinergic transmission was found in the largest ramus caecalis of the ileocolic artery. The purinergic component prevailed in short pulse trains and early in long trains, whereas the adrenergic component prevailed in the late phases of long (20 s) trains. Prejunctional alpha 2-adrenergic autoinhibition markedly depressed purinergic as well as adrenergic transmission as soon as a latency of about 2 s was exceeded.

Previous studies have demonstrated that vein storage in normal saline leads to significant mechanical morphological, and biochemical aberrations. However, little information is available regarding the functional damage that occurs. The purpose of this study was to evaluate the effect of saline storage on venous smooth muscle and endothelial function. Segments of ten external jugular veins from male New Zealand White rabbits were placed nondistended in either modified Krebs solution at 37 degrees C (Krebs-stored, KS) or heparinized normal saline at room temperature (saline-stored, SS) for 1 h. Segments 4 mm in length were then simultaneously studied in vitro under isometric tension. There was no difference in maximum tension or sensitivity to either bradykinin or histamine. Acetylcholine-induced relaxation in KS segments was not significantly different from relaxation in a historical cohort of nonstored segments (nonstored 87.4 +/- 1.0% vs. KS 84.5 +/- 2.0%; p = NS). However, there were significant attenuations in SS segment endothelium-dependent relaxation in response to both acetylcholine (KS 84.5 +/- 2.0% vs. SS 76.4 +/- 2.7%, p less than 0.02) and adenosine diphosphate (KS 47.9 +/- 2.9% vs. SS 40.6 +/- 3.7%, p less than 0.002). Relaxant responses to sodium nitroprusside (endothelium-independent) were not significantly different in the two groups (KS 94.6 +/- 1.6% vs. SS 95.7 +/- 2.2%; p = NS). Electron microscopic evaluation of SS segments revealed endothelial cell disruption with cellular edema and loss of intact junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Conditioned medium from cultured aortic smooth-muscle cells from rat aorta yielded neurite-extending effects on sensory and sympathetic ganglia of chick embryos. These effects were blocked by adding specific antiserum against 2.5S nerve growth factor (NGF), suggesting that NGF might be released from vascular smooth-muscle cells.

The intracellular pH (pHi) of basilar artery rings was determined with 2',7'-bis-(carboxyethyl)-5,(6)-carboxyfluorescein (BCECF) by measuring the ratio of emitted (540 nm) fluorescence intensities (FI) at excitation wavelengths of 500 and 440 nm. There was a dye loss from the rings in 90 min (39.3 +/- 3.6%, p less than 0.001). We found that the ratio of fluorescence intensities does not adequately correct for dye loss; hence, we derived a method to correct for dye loss during pHi determinations. Calibration curves of the ratio versus pHi were constructed for the artery rings. The slope and intercept of the calibration curves depended on FI440. Linear regression lines for the slope and intercept versus FI440 were: [formula; see text] In solutions with different pH and different concentrations of free BCECF, the slope of the ratio versus pH of the solution was steeper at high concentrations of BCECF. Thus, pHi was calculated from a calibration curve in which the slope and intercept were determined from FI440 with the above formula. The corrected pHi was 7.37 +/- 0.05 (n = 25) at pHo 7.4 and 37 degrees C.

Smooth muscle tone and 'holding economy' depend on the rate constants governing the cross-bridge cycle. Thus, calcium activation via calmodulin-dependent myosin light chain phosphorylation may determine the apparent rate constant ('f') at which cross-bridges enter the force-generating state, forming actin-attached, strongly bound cross-bridges. This phosphorylation of the light chain may be inhibited in skinned fibers by a peptide mimic of the calmodulin recognition site of the myosin light chain kinase (RS 20) that relaxes smooth muscle. In smooth muscle, the apparent cross-bridge detachment rate constant ('g') also seems to be variable, a low constant allowing for a high holding economy and low shortening velocity in the 'latch state'. It may also account for force maintenance at low levels of myosin phosphorylation. Additionally, cross-bridge attachment may, however, be also controlled by other regulatory proteins such as calponin and caldesmon.

The amount of oxygen actually supplied to the ischemic muscle tissue of patients with intermittent claudication was quantified before and after a standardized pedal ergometric test. Muscle tissue pO2 was measured with micro-platin needle electrodes directly in the lower limb muscles at rest and 3, 10, 20 and 60 min after a 4-min work load. Time-dependent variations in the behavior of pO2 values as well as changes in the shapes of pooled pO2 histograms make it possible to monitor the effect of therapeutic measures. In claudicants (stage IIb) with ascertained occlusions or stenosis of the femoral artery or the pelvis region, it was demonstrated that the delayed increase in tissue pO2 after exercise could be improved by the infusion of 400 mg buflomedil. Comparison between the time-related pooled histograms confirmed improvement of oxygen supply under the influence of this drug.

Whether vasospasm results from smooth muscle contraction or from arterial wall infiltration by cells and other material is subject to debate. Computer-assisted image analysis was used to measure lumen area, total wall area, and area of tunica media plus tunica intima of cross-sections of monkey right middle cerebral arteries (MCAs), exposed in vivo for 6 days to whole blood (n = 4), oxyhemoglobin (OxyHb, n = 5), methemoglobin (MetHb, n = 5), bilirubin (n = 5), mock cerebrospinal fluid (CSF, n = 6), and supernatant fluid from an incubated mixture of autologous blood and mock CSF (n = 5). Five control (left) MCAs from each group and 4 MCAs contracted in vitro with potassium chloride were measured. Significant angiographic vasospasm occurred in groups receiving whole blood, supernatant fluid, and OxyHb (p less than 0.05). There was significant correlation (r = 0.58, p less than 0.05) between right MCA diameter on angiography and diameter calculated from lumen area. When compared to effects of mock CSF, OxyHb significantly increased total wall area. When right and left MCAs were compared within groups, total wall area increased in every group with significant increases in groups exposed to mock CSF, OxyHb, and bilirubin (p less than 0.05). No changes developed in area of tunica media plus tunica intima, whether comparing right versus left MCAs within groups or right MCAs between groups. Contraction in vitro did not significantly increase total wall area or area of tunica media plus tunica intima. Light microscopy demonstrated inflammatory debris in the tunica adventitia of arteries from every group. This study shows that whole blood, OxyHb, and supernatant fluid, which contains OxyHb, cause vasospasm. Increases in total wall area are not sufficient to account for luminal narrowing, and therefore, changes such as cell proliferation and arterial wall fibrosis in the intima or media apparently do not contribute primarily to arterial narrowing of vasospasm but could be related to persistence of narrowing. Vessel wall thickening, which does occur, is caused by increased tunica adventitia area only and is nonspecific in that it develops after injection of substances not associated with vasospasm. The data are consistent with the hypothesis that oxyHb causes vasospasm (both angiographic and morphologic) by inducing muscle contraction in the media.