Blood vessels最新文献

This study investigated the release of nitric oxide (NO) from glyceryl trinitrate (GTN) and SIN-1 in Langendorff rabbit hearts. Infusion of either GTN (10-40 microM) or SIN-1 (0.45-4.5 microM) into the coronary inflow tract resulted in a decrease in coronary perfusion pressure and NO release (oxyhemoglobin technique) into the coronary effluent. NO release from SIN-1 occurred spontaneously whereas passage through the coronary circulation, i.e. active metabolism, was required for NO release from GTN. Removal of the coronary endothelium and blockade of endothelial NO formation did not affect NO release from GTN and SIN-1. In GTN-tolerant hearts, there was a considerable inhibition of GTN- but not SIN-1-induced NO formation and coronary vasodilation. These data suggest (1) that metabolic NO release from GTN occurs during passage of the coronary circulation and is independent of the presence of endothelium, and (2) reduced NO release is a major cause of nitrate tolerance.

The present study investigates the question of capillary recruitment and reserve capillaries in the brains of awake rats. Perfused capillaries were marked by intravenous globulin-coupled fluorescein isothiocyanate (FITC) and cerebral blood flow was measured autoradiographically. During hypercapnia, the density of perfused capillaries was unchanged compared to normocapnia, although blood flow was markedly increased. This shows the lack of capillary recruitment in the brain during the high flow that occurs during hypercapnia. In additional studies using fluorescent staining both of morphologically existing and of perfused capillaries, perfusion of all capillaries during normal, normocapnic conditions was found. These experiments show the lack of any capillary reserve in the rat brain.

The effect of buflomedil on postischemic reperfusion injury was studied in the dorsal skin fold chamber preparation of awake hamsters. Microvascular events were investigated in the striated skin muscle by means of intravital fluorescence microscopy prior to 4 h of pressure-induced ischemia and 30 min, 2 and 24 h after reperfusion. In untreated control animals, ischemia and reperfusion provoked marked leukocyte sticking and macromolecular leakage while functional capillary density was reduced. Treatment with buflomedil (3 mg/kg b.w. in 0.3 ml saline, administered as bolus of 0.1 ml 10 min prior to release of ischemia followed by i.v. infusion of 0.2 ml during the first 20 min of reperfusion) significantly reduced leukocyte sticking and macromolecular leakage, while functional capillary density was effectively preserved. No differences in macro- and microhemodynamic parameters were observed between buflomedil-treated and untreated animals. These findings support the concept that activated leukocytes are involved in the microvascular manifestation of reperfusion injury and indicate that leukocyte sticking and its sequelae can be efficiently prevented by treatment with buflomedil.

The effects of renal arterial pressure change on renal output of sodium and volume were measured during water diuresis in 25 chloralose-anesthetized dogs. Conditions included a minimal invasive stress, limited sodium administration, and mean renal arterial pressures varied suprarenally, by aortic balloon inflation to lowermost levels of 82-106 mm Hg. Group A dogs received no aldosterone; group B, C and D dogs were given aldosterone. Dogs of group C also received (1-Sar, 8-Ile)-angiotensin II. Group D dogs received phenylephrine which elevated arterial and right atrial pressures moderately without decrease in renal blood flow. In groups A, B and C, mean changes in sodium output, volume output, fractional excretions and free water clearances were not detectable with mean renal arterial pressure reductions, which averaged 29 +/- 2.9, 22 +/- 2.8 and 27 +/- 5.2 mm Hg, respectively. Right atrial pressures, effective renal blood flows and glomerular filtration rates did not change with the renal arterial pressure changes in these groups. In the group D dogs, during the larger pressure reductions of 54 +/- 6.6 mm Hg from higher values of 158 +/- 7.0 mm Hg, mean urine flow and effective renal blood flow remained constant while glomerular filtration rate and sodium output decreased only slightly. Output efficiency ratios related to perfusion pressure were calculated. With no more than modest pressure-induced excretory changes, it is concluded that excretory sodium and urinary volume autoregulation in concert with nearly perfect circulatory autoregulation were demonstrated with regionally varied mean renal arterial pressure. The same preglomerular myogenic responses to transvascular pressure, which restrict glomerular and transcapillary pressures, are viewed dominantly responsible for both circulatory and excretory autoregulation under normal conditions of minimal stress and low fractional sodium excretions. Homeostatic implications are discussed concerning likely relevance to the Guyton-Coleman theory for the long-term control of arterial blood pressure.

Analysis of flux motion by the laser Doppler technique in the forefoot of healthy controls and patients with peripheral arterial occlusive disease was performed by establishing computerized frequency histograms. It was found that the low frequency components (1-10 cycles/min) are caused by local vasomotion. The prevalence of high frequency flux waves (15-25 cycles/min) is significantly increased in peripheral ischemia compared to normal conditions. After successful reopening of large arteries by angioplasty the prevalence decreases (p less than 0.001). Preliminary results indicate that these high frequency rhythmic fluctuations might by induced by respiration.

Excised canine carotid arteries held at constant physiologic length were cycled from -13 to +27 kPa with a constant-flow infusion pump, and the pressure-volume curves were recorded. The change in diameter on reducing the pressure from 16 to 0 kPa was determined and the strain of recoil [(diameter16--diameter0)/diameter16] calculated. Diameter recoil was reduced from 51% (fresh tissue) to 5% after 3 h pressure fixation in 4% formaldehyde and to 9% after 15 min in 2% glutaraldehyde with little further change. Lengthwise recoil was reduced from 37 to 10% after 5 min in 2% glutaraldehyde. Photographs were taken to measure outer diameter during pressure fixation. There was no change in diameter in either fixative from the first minute up to 3 days at the constant pressure of 16 kPa.

Many endogenous and pharmacological vasodilators hyperpolarize vascular smooth muscle and this response appears to be due to an increased conductance to potassium ions. The hyperpolarization may contribute to the mechanism of dilation by causing voltage-dependent calcium channels to close. Recent evidence indicates that the response to hyperpolarizing vasodilators is mediated through activation of ATP-sensitive potassium (KATP) channels. Single KATP channels on isolated vascular smooth muscle cells are activated by cromakalim and calcitonin gene-related peptide (CGRP). This response is inhibited by glibenclamide. Cromakalim, CGRP and other vasodilators hyperpolarize and relax arteries in vitro and these responses are reversed by glibenclamide. The hypotensive effects of these agents in vivo are antagonized by glibenclamide. We propose that activation of KATP channels and the associated membrane hyperpolarization represents an important general mechanism of vasodilation.

Inhibitors of angiotensin-converting enzyme, renin and angiotensin II receptor lower the blood pressure of spontaneously hypertensive rats (SHRs) used as a model of essential hypertension. Since their plasma renin levels were normal or subnormal, renin in the vascular tissue was considered to play a key role in the maintenance of the hypertension. To clarify the source and localization of vascular renin in SHRs, the effects on blood pressure of antirenin antibodies, the converting enzyme inhibitors delapril and enalapril, and the angiotensin II receptor antagonist DuP 753 were examined in intact and bilaterally nephrectomized SHRs and their normotensive controls. The efficient hypotensive action of the renin antibody indicated that renin of the renal origin is a dominant factor. The gradual but complete disappearance of the antihypertensive action of these inhibitors of the renin-angiotensin system upon bilateral nephrectomy indicated the importance of membrane-associated renin of the renal origin and angiotensin-converting enzyme in the maintenance of the spontaneous hypertension.

Vascular endothelial cells produce a variety of substances known to modulate the tone of surrounding smooth muscle, but the initial steps involved in receptor-response coupling are poorly characterized in these cells. Because the stimulated release of endothelium-derived relaxing factor depends on the presence of external calcium, ion channel-mediated calcium influx might represent an essential first link. Furthermore, agonist-induced endothelial cell hyperpolarization has been widely described, although the ion channels involved and the functional significance of this response remain uncertain. A review of the available literature to date concerning voltage-dependent and agonist-activated ionic currents obtained using patch clamp techniques in vascular endothelial cells is presented here. A discussion of the possible functional roles of the underlying ion channels is included.