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At least 883 records · Page 49Linked to original sources
PubMed1987

Responses of resistance and capacitance vessels in human nasal mucosa to beta-receptor agonists.

To investigate the responses of nasal vessels, divided into resistance and capacitance vessels, to a beta-receptor agonist in human, mucosal blood flow of the inferior turbinate and nasal airway resistance were measured when 1.5 mg terbutaline was applied topically. Mucosal blood flow was measured by the hydrogen clearance method just beneath the site where terbutaline in physiological saline (0.02 ml) was applied on an extremely localized area of the nasal mucosa. Nasal airway resistance of the ipsilateral and contralateral nasal cavities was measured separately by anterior rhinomanometry when terbutaline in normal saline (0.1 ml) was sprayed in the unilateral nasal cavity. Topical application of terbutaline elicited neither a significant increase of mucosal blood flow of the inferior turbinate nor an increase of nasal airway resistance. beta-Receptors seem not to be as densely distributed both in the resistance vessels and in the capacitance vessels as to cause vasodilatation by their activation in the nasal mucosa.

Adult↗
PubMed2002

Differential effects of antihypertensive drug therapy on arterial compliance.

Although vascular compliance, deltaV/deltaP, is abnormal in essential hypertension and can be improved by antihypertensive drug therapy, it is not clear whether drug-induced changes in compliance are attributable solely to lower achieved blood pressure (BP), and thus equally likely with different drugs possessing similar antihypertensive efficacy. Therefore, we used computerized arterial pulse waveform analysis (CAPWA) to measure capacitive (C1) and oscillatory (C2) components of arterial compliance in essential hypertensive subjects (n = 39) before, and 1 and 3 months after achieving normotensive BP values with administration of either dihydropyridine calcium channel antagonists (CaBl, n = 11), converting enzyme inhibitors (CEI, n = 9), angiotensin receptor blockers (ARB, n = 9), or beta-blockers (BBl, n = 10). Despite equivalent effects on BP (CABL: -19 +/- 4/-15 +/- 2 mm Hg; CEI: -12 +/- 3/-13 +/- 2 mm Hg; ARB: -10 +/- 3/-12 +/- 2 mm Hg; and BBl: -14 +/- 3/-12 +/- 2 mm Hg; P <.005 for each drug v pretreatment), CaBl, CEI, and ARB significantly increased arterial compliance (CaBl: %deltaC1 = 30.0 +/- 5.8, %Delta C2 = 43.7 +/- 23.3; CEI: %deltaC1 = 32.7 +/- 5.4, %deltaC2 = 26.7 +/- 7.1; ARB: %deltaC1 = 36.3 +/- 11.8, %deltaC2 = 43.6 +/- 23.1; P <.01 for CaBl, CEI, and ARB v pretreatment), but BBl did not (%deltaC1 = -3.9 +/- 7.6, %deltaC2 = -7.0 +/- 11.5, P = not significant v pretreatment, sig = 0.01 v other drugs). We conclude that for an equivalent effect on BP, arterial compliance improves after therapy with some, but not all antihypertensive drugs. We hypothesize that a greater clinical benefit may result from the preferential use of drugs that concomitantly improve arterial compliance.

Adrenergic beta-Antagonists↗
PubMed2000

Asynchronous Ca(2+) waves in intact venous smooth muscle.

The rabbit inferior vena cava (IVC) is a large-capacitance vessel that displays typical contractile dose-response curves for caffeine and phenylephrine (PE). Using confocal microscopy on the endothelium-denuded IVC, we undertook experiments to correlate these whole-tissue contractile dose-response curves with changes in subcellular [Ca(2+)](i) signals in the in situ vascular smooth muscle cells (VSMCs). We observed that both caffeine and PE initially elicited Ca(2+) waves in individual VSMCs. The [Ca(2+)](i) in cells challenged with caffeine subsequently returned to baseline whereas the [Ca(2+)](i) in cells challenged with PE exhibited repetitive asynchronous Ca(2+) waves. These [Ca(2+)](i) oscillations were related to Ca(2+) release from the sarcoplasmic reticulum as they were inhibited by ryanodine and caffeine. The lack of synchronicity of the [Ca(2+)](i) oscillations between VSMCs can explain the observed tonic contraction at the whole-tissue level. The nature of these Ca(2+) waves was further characterized. For caffeine, the amplitude was all-or-none in nature, with individual cells differing in sensitivity, leading to their recruitment at different concentrations of the agonist. This concentration dependency of recruitment appears to form the basis for the concentration dependency of caffeine-induced contraction. Furthermore, the speed of the Ca(2+) waves correlated positively with the concentration of caffeine. In the case of PE, we observed the same characteristics with respect to wave speed, amplitude, and recruitment. Increasing concentrations of PE also enhance the frequency of the [Ca(2+)](i) oscillations. We therefore conclude that PE stimulates whole-tissue contractility through differential recruitment of VSMCs and enhancement of the frequency of asynchronous [Ca(2+)](i) oscillations once the cells are recruited.

Animals↗
PubMed1984

Effects of vasodilators on the systemic capacitance vessels, a study with the measurement of the mean circulatory pressure in dogs.

There have been yet only a few studies on the action of vasodilators on the entire systemic capacitance vessels of the living body. In the present study, we studied the action of the vasodilators on the systemic capacitance vessels by measuring the mean circulatory pressure (MCP), introduced by Guyton, and that on the systemic resistance vessels from total peripheral resistance, in anesthetized open chest dogs. We also studied the venous return curves. Depending on vasodilators and the dosages used, resistance vessels could be dilated, but capacitance vessels could not be dilated. The reverse was never true. It was also found frequently that capacitance vessels could be dilated only when the tone of the capacitance vessels have been previously elevated by norepinephrine. Again, depending on vasodilators and their dosages, the venous return curves were changed in position and/or slope. We constructed a venous return curve by connecting 2 points on the venous return-right atrial pressure (VR-RAP) plane, one, VR-RAP plot, and the other, the point of VR = 0, RAP = MCP. Changes in the venous return curve caused by these vasodilators were classified into three types; (a) a clockwise rotation with a constant MCP, where one sees no change in MCP and decreased resistance to venous return (RVR), so that one may call this RVR-type, (b) a parallel shift of the venous return curve to the left, where one sees no change in RVR but a decreased MCP, so that one may call this MCP-type and (c) a shift to the left plus clockwise rotation, where one sees a decrease in MCP and decrease in RVR, so that this is a mixture of patterns (a) and (b). One may call this the mixed-type. The existence of the response of mixed-type is worth special attention, because, in this type, cardiac output (CO) was increased by the predominant decrease in RVR in spite of a decreased MCP, leading to an important condition that the CO does not necessarily decrease when systemic capacitance vessels were dilated by the vasodilators.

Animals↗
PubMed1996

Comparison of responses to histamine by constant-flow and constant-pressure perfusion methods in the rabbit isolated kidney preparation.

1. Reproducibility and sensitivity of responses of isolated perfused rabbit renal vascular bed to bolus administration of histamine was compared for the conditions of constant-flow and constant-pressure perfusion by Krebs-Henseleit solution. Two other vasoactive agents (noradrenaline and angiotensin II) were also tested in the same preparation for comparison with the effect of histamine. 2. In constant-pressure mode, different hydrostatic pressures were also employed for the analysis of time-effect phenomena. 3. Drug responses were recorded by computer and were evaluated as changes of perfusion pressure or flow, to correspond to drug activities at the resistance vessels and, also, change of organ weight, as effects on exchange and capacitance functions of the circulation. Both parameters were also recorded on a Grass polygraph. 4. Reproducibility and sensitivity of responses to vasoactive agents (histamine, noradrenaline, angiotensin II) were significantly low in the constant-flow conditions, compared to constant-pressure mode. 5. Responsivity also deviated for different perfusion pressures of constant-pressure mode and 80-100 mm H2O pressure was found to be the most convenient value. 6. It is concluded that constant-flow and constant-pressure conditions provide different hydrodynamic conditions. In constant-flow methodology, when the predetermined perfusion rate is not tolerated by the vascular bed, excessive flow in the circulation would lead to depression of vasoactivity, failing pharmacodynamic equilibria and loss of responsivity. Structural deviation of the vascular bed would also be expected due to differences of organ specimen and, probably, result in the variation of responsivity of constant-flow perfusion procedure.

Animals↗
PubMed1989

Lung edema increases transvascular filtration rate but not filtration coefficient.

To determine whether the accelerated rate of lobe weight gain during severe pulmonary edema is attributed to increased permeability of the microvascular barrier or a loss of tissue forces opposing filtration, the effect of edema on capillary filtration coefficient (Kf,C), interstitial compliance (Ci), and the volume of fluid filtered after a step increase in microvascular pressure (delta Vi) were determined in eight isolated left lower lobes of dog lungs perfused at 37 degrees C with autologous blood. After attaining a base-line isogravimetric state, the capillary pressure (Pc) was increased in successive steps of 2, 5, and 10 cmH2O. This sequence of vascular pressure increases was repeated three times. Edema accumulation was expressed as weight gained as a percent of initial lobe weight (% delta Wt), and Kf,C was measured by time 0 extrapolation of the weight gain curve. An exponential rate constant for the decrease in the rate of weight gain with time (K) was calculated for each curve. Ci was then calculated by assuming that the capillary wall and interstitium constitute a resistance-capacitance network. Kf,C was not increased by edema formation in any group. Between mild (% delta Wt less than 30%) and severe edema states (% delta Wt greater than 50%) respective mean Ci increased significantly from 3.54 to 9.12 ml.cmH2O-1.100 g-1, K decreased from 0.089 to 0.036 min-1, and delta Vi increased from 1.28 to 2.4 ml.cmH2O-1.100 g-1. The delta Vi during each Pc increase was highly correlated with Kf,C and Ci when used together as independent variables (r = 0.99) but less well correlated when used separately.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Clinical significance of mean circulatory filling pressure and cardiac preload under anesthesia.

The circulatory effects of a rapid infusion of plasma substitute with intravenous administration of nitroglycerine (TNG) were investigated in low pressure systems of anesthetized patients by measuring various hemodynamic parameters. Measurements were made when the systolic blood pressure reached 70-80% of the control value after intravenous administration of TNG at 1-2 microg/kg/min and a 3.5% modified gelatin solution (Haemaccel) at a rate of 0.5 ml/kg/min. After the TNG was administered, the mean circulatory filling pressure (Pms) decreased, and the venous to arterial capacitance ratio (CV/CA) increased; however, they returned to control values after a rapid Haemaccel infusion. Changes in the pressure gradient between the X and Y valley of the right atrial pressure wave decreased to 70 +/- 14% of the control value when TNG was given and recovered to 106 +/- 22% by infusion. Pulmonary vascular resistance (PVR) decreased to 70 +/- 24% of the control value when TNG was administered and was restored to 96 +/- 40% by a rapid infusion. In the left ventricle, the mean velocity of myocardial circumferential fiber shortening (VCF) decreased in all cases when TNG was given and it recovered by a rapid infusion. In the right ventricle, VGF did not always decrease, and in a few case increased, but all cases recovered by a Haemaccel rapid infusion. We conclude that the augmentation of the right ventricular preload reserve is achieved by administration of TNG and infusion of a plasma substitute.

Journal Article↗
PubMed1986

Capacitance of the rabbit portal vein and inferior vena cava.

1. We used vessel strips and whole vessels in vitro to determine the length-tension and pressure-volume relationships of two veins with similar diameter and wall thickness, the portal vein and inferior vena cava of rabbits. 2. Length-tension studies indicate that longitudinal and circular strips of the portal vein have significantly smaller elastic moduli than similar strips of the inferior vena cava (P less than 0.05). 3. Pressure-volume relationships of intact vessels indicate that pressures greater than 5 mmHg do not produce significant increases in volume of the inferior vena cava, whereas volume of the portal vein increases significantly over a range of pressures from 2 to 15 mmHg. 4. Activation of smooth muscle with noradrenaline reduces the volume of the vena cava at distending pressures less than or equal to 5 mmHg. In contrast, noradrenaline reduces the volume of the portal vein at pressures up to 10 mmHg. During inactivation in calcium-free solution and activation with noradrenaline, the portal vein is more compliant than the inferior vena cava (P less than 0.05). 5. Morphometric studies demonstrate more collagen in the inferior vena cava than in the portal vein. Differences in capacitance of the vessels may be related, in part, to greater collagen content in the inferior vena cava.

Animals↗
PubMed1976

Compliance of the peripheral capacitance vessels in patients with congestive heart failure.

A method for measuring compliance of the peripheral capacitance vessels is reported, and the values of compliance in patients with congestive heart failure are compared with those in normal subjects. Peripheral venous compliance and right brachial venous pressure in both patients with congestive heart failure and in normal subjects, when plotted graphically, showed a relationship described by many hyperbolic curves. The mean value of compliance of the peripheral capacitance vessels in patients with congestive heart failure was only half that in normal subjects. This difference was statistically significant (P less than 0.001). After the congestion in the patients with congestive heart failure disappeared following treatment with digitalis and other drugs, the values of compliance became nearly the same as in normal subjects. It seems that the increase of compliance of the peripheral capacitance vessels is not due to an organic change but to a functional change of the vessels caused by distention.

Blood Vessels↗
PubMed1994

[Interferences between angiotensin-converting enzyme inhibitors and spinal anesthesia].

To determine whether angiotensine converting enzyme inhibition (ACEI) therapy should be continued up to the time of the surgical procedure, a standard practice for other modern antihypertensive agents, it should be known whether stopping the treatment does or does not lead to a hypertensive episode before surgery or at intubation and whether continuing treatment is or is not associated with an unacceptable fall in blood pressure at induction. Data from the literature obtained in patients chronically treated for essential hypertension with captopril or enalapril demonstrate that withdrawal of ACEI therapy before surgery does not result in a higher incidence of hypertensive episodes both preoperatively and at intubation. In contrast, an increased need for ephedrine to maintain blood pressure at induction is observed in patients who receive ACEI together with their premedication. This exaggerated hypotensive response to induction is in agreement with previous studies in anaesthetized subjects which have shown that angiotensin II contributes to hemodynamic regulation during general and epidural anaesthesia. It might also be the consequence of the specific effects of ACEI therapy on the loading conditions of the heart and/or the autonomic nervous system. It must be emphasized that both ACEIs and epidural anaesthesia dilate large arteries as capacitance vessels and increase vagal tone. The decreased tone in capacitance vessels accentuates the drops in blood pressure provoked by general or epidural anaesthesia through an increase in blood pooling at the expense of cardiac filling. This mechanism is enhanced by the presence of either a preoperative hypovolemia or a disturbed left ventricular diastolic function, which are two abnormalities frequently seen in hypertensive vascular surgical patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Epidural↗