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PubMed1975

The mean circulatory pressure, reproducibility of its measurements and the effect of phenylephrine with a note on the effect of pentobarbital.

With 7 repeated measurements of the mean circulatory pressure (MCP) over a course of 35 minutes in one and the same dog, and also with paired measurements of MCP 10 minutes apart in 6 other dogs, the MCP was shown to be stable and reproducible in anesthetized, open-chest and vagus-intact dogs. Administered to 7 dogs with initial mean arterial blood pressure as low as 64 mmHg in dose of 20 mug/kg intravenously, phenylephrine nearly doubled the mean arterial blood pressure, total peripheral resistance and the MCP, indicating a marked vasoconstrictor effect on the resistance and capacitance blood vessels of the systemic circulation. The effect was transient and there were signs of tachyphylaxis. Influence of a cardiotoxic dose of pentobarbital on the peripheal circulation was discussed.

Animals↗
PubMed1984

Short-term extrusion of isolated teeth of adult monkey (Macaca fascicularis).

By means of a variable capacitance device, the occlusal movements of 12 fully-developed teeth were recorded in 6 adult monkeys. Sustained extrusion was seen, with rhythmic pulsations due to the heart beat and to breathing. Extrusion varied from 10 to 138 micrometers over periods of 40-360 min, and became progressively slower with time. Because of the protracted nature of the extrusion, it is probable that these tooth movements were caused by forces generated in the periodontal ligament resulting from biochemical changes in the periodontium rather than by vascular alterations, and occurred as a result of the removal of intrusive loads from the opposing teeth.

Animals↗
PubMed1985

Negative effects of dihydroergotamine (Orstanorm) on central haemodynamics and aorto-coronary bypass blood flow. An intraoperative study.

Dihydroergotamine (DHE), Orstanorm, because of its strong constrictor action on capacitance vessels, is used in the treatment of hypotension caused by orthostatism or spinal or epidural anaesthesia. Lately Orstanorm has also been used in combination with heparin as prophylaxis against postoperative thromboembolism. In the present study, Orstanorm (0.01 mg/kg b.w.) was given intravenously to 20 patients after coronary bypass surgery. Coronary bypass blood flow, heart rate, systemic mean and systolic blood pressures, right and left atrial pressures, pulmonary artery pressure and cardiac output were measured. Stroke volume, cardiac index, stroke index, systemic and regional myocardial vascular resistance and cardiac work index were then calculated. The results showed that despite increased filling pressures there was no rise in cardiac output, and despite increased cardiac work the bypass flow significantly decreased. The significant increase in regional myocardial vascular resistance found after administration of DHE may explain the absence of expected increase of cardiac output and coronary bypass flow.

Adult↗
PubMed1985

[Venous distensibility in essential hypertension].

Using venous occlusive plethysmography, venous distensibility was examined in 85 hypertensive patients and in 21 normal men. Venous distensibility in the hypertensive versus normal subjects was significantly lower, being inversely depended on the blood pressure level. Venous distensibility depended directly on the blood flow in the forearm and inversely on the resistance of the resistive vessels at rest. This may indicate that the reduction of venous distensibility was caused by both functional and structural changes characteristic of both resistive and capacitance vessels. It appears that functional and structural alterations in the system of low pressure, along with an elevated resistance of the arterioles, were actively involved in changes of the peripheral resistance and the development of a hypertensive state.

Adult↗
PubMed1981

Extent of structurally reduced venous distensibility in rats.

1. Venous pressure--volume relations were studied in maximally vasodilated whole-body preparations after cardiac arrest, as well as in fully vasodilated, perfused hindquarter preparations of spontaneously hypertensive rats (SHR) and normotensive controls. Central venous pressures were measured also in the anaesthetized animals before cardiac arrest. 2. Central venous pressure in intact, anaesthetized SHR was 1.9 +/- 0.20 mmHg compared with 0.75 +/- 0.25 in controls (P less than 0.001). 3. In both preparations SHR showed a nearly 20% reduction in venous compliance, whereas calculated 'unstressed' volumes (volumes at zero transmural pressure) were largely equal in SHR and controls. 4. SHR capacitance vessels thus appear to have a structurally reduced wall distensibility of about 10% with no change in overall size. It probably reflects a structural adaptation to a modest increase of average transmural pressure that also affects the low-pressure side.

Animals↗
PubMed2000

Endothelium-derived nitric oxide contributes to the regulation of venous tone in humans.

BACKGROUND: Although nitric oxide (NO) is known to play an important part in the regulation of arterial tone, little is known about its role in veins. The aim of this study was to investigate the role of basal and stimulated NO activity in the regulation of tone of the human venous capacitance bed. METHODS AND RESULTS: We measured venous tone using radionuclide forearm venous plethysmography in 24 healthy subjects with no cardiovascular risk factors. In 13 subjects, basal NO activity was assessed by measuring the effects on venous tone of an intra-arterial infusion of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA). In the remaining 11 subjects, stimulated NO activity was evaluated by measuring the effects of an intra-arterial infusion of incremental doses of carbachol, followed in a subgroup by coinfusion with L-NMMA. Infusion of carbachol caused dose-dependent venodilation, with a maximal reduction in forearm venous tone of 40.1+/-12.5% (P<0.0001). Carbachol-induced venodilation was inhibited by L-NMMA (48.9+/-6.2% reversal of maximal venodilation, P<0.01). Infusion of L-NMMA alone caused venoconstriction (9.1+/-6.4% increase in venous tone, P=0.002). CONCLUSIONS: Human forearm capacitance veins exhibit both stimulated and basal NO activity, which indicates that NO contributes not only to the regulation of venous tone but also to resting venous tone in healthy human subjects.

Adult↗
PubMed1998

Increase in functional Ca2+ channels in cerebral smooth muscle with renal hypertension.

The hypothesis that availability of functional Ca2+ channels in vascular smooth muscle is augmented in hypertension was tested in basilar artery cells from Wistar rats exhibiting stable systolic blood pressure (BPsys) for 2 to 11 weeks after partial renal artery ligation (Goldblatt 2-kidney 1-clip [2K1C] model). Cells were freshly isolated and patch-clamped using a nystatin-perforated patch method. BPsys ranged from 110 to 280 mm Hg and correlated with normalized kidney mass. Macroscopic current-voltage curves were fit to a Boltzmann function to obtain maximum conductance (gmax), steepness and midpoint potential for the voltage dependence of activation (k and E1/2, respectively), and extrapolated reversal potential for the chord conductance (Erev). Linear regression of normalized conductance (ng(max)=g(max)/cell capacitance) versus BPsys for 103 cells indicated a strong relationship, with a slope of 0.0019 nS x pF(-1) x mm Hg(-1) (P<0.0001). Similar analysis of data from 35 other cells exposed to 500 nmol/L Bay K 8644 gave a slope of 0.0041 nS x pF(-1) x mm Hg(-1) (P=0.001). Voltage-dependent parameters, k, E1/2, and Erev, were not significantly related to BPsys. Single-channel measurements in cell-attached patches revealed that the number of channels in 32 patches was significantly related to BPsys (P=0.0024) but that slope conductance, open dwell times at 0 mV, and distribution between 2 open states were not. Finally, in a subgroup of 61 cells from animals made hypertensive (180 mm Hg<BPsys<200 mm Hg) for approximately 1/2 to 6 weeks, we found that elevation of ngmax depended on duration of hypertension (P=0.003), with no elevation at approximately 1/2 week. We conclude that in the 2K1C model, availability of functional Ca2+ channels increases with BPsys with no change in channel properties and that measurable BPsys elevation occurs before the increase in functional channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1981

Mechanism of action of IUDs: an ultrastructural view.

Endometrial samples from 64 women using different types of IUDs were used to study the ultrastructural changes of the human endometrium as influenced by nonmedicated and copper devices, using SEM and TEM in an attempt to explain the physiological mechanism of their actions. The absence of cytoplasmic macro-apocrine secretory granules with copper devices and their defective separation with nonmedicated IUDs support the theory that the IUD interferes with the carbohydrate metabolism and secretory function of the endometrial cells. It also indicates that IUDs may function through the interference with the blastocyst-endometrial interaction and blastocyst survival. The change in the intrauterine environment due to the absence of normal secretion may also affect sperm capacitation and/or the acrosomal reaction, with subsequent failure of fertilization. The absence of ciliated cells at the site of copper IUD contact zone and their defective ciliation away from it in the presence of normal steroid function may indicate an effect of the copper ions on the estrogen receptors. The asynchronous development of the endometrium and blastocyst mechanism of IUD function was not supported in this study. The occurrence of intermenstrual bleeding with IUDs is governed by 2 factors: 1) the pressure exerted by the IUD causing endothelial vascular injury and release of erythrocytes into endometrial stroma; and 2) the increased stromal hydrostatic pressure which acts as a force against the basal lamina and epithelial integrity. This was proven by the loss of normal microvillous pattern of the endometrial cells even away from the copper IUD, which support the rigidity of the cellular membranes.

Biology↗
PubMed2004

Mechanisms underlying enhanced cardiac excitation contraction coupling observed in the senescent sheep myocardium.

Ageing related stiffening of the vascular system is believed to be in part responsible for a number of clinical outcomes including hypertension and heart failure. In the present study, we sought to determine whether there are alterations in cardiac excitation contraction coupling that may help compensate for the increased vessel stiffness. Experiments were performed on single cardiac myocytes isolated from young (18 months) and aged (>8 years) sheep. Intracellular Ca(2+) concentration, action potentials, L-type Ca(2+) currents and SR Ca(2+) content were measured at 23 degrees C. With ageing, cell capacitance increased by 26% indicating cellular hypertrophy. Action potential duration (APD90) (590 +/- 21 vs. 726 +/- 36 ms), Ca(2+) transient amplitude (112 +/- 15 vs. 202 +/- 25 nmol l(-1)) and fractional cell shortening (by 37%) also increased in the aged hearts (all values P < 0.05). The larger Ca(2+) transient amplitude observed under current clamp conditions was maintained under voltage clamp control; however, SR Ca(2+) content was identical. Both the peak L-type Ca(2+) current (2.8 +/- 0.3 vs. 4.9 +/- 0.5 pA pF(-1)) and integrated Ca(2+) entry (5.1 +/- 0.7 vs. 7.9 +/- 0.8 micromol l(-1), all P < 0.01) were greater in aged cells. In this study we show that in the ageing ovine myocardium, the amplitude of the systolic Ca(2+) transient is increased. The larger Ca(2+) transients cannot simply be explained by changes in APD and we suggest that the greater inward L-type Ca(2+) current provides a more effective trigger for calcium-induced-calcium release from the SR whilst maintaining a stable SR Ca(2+) content. These changes in cardiac excitation contraction coupling may help maintain cardiac output in the face of increased great vessel stiffness.

Action Potentials↗
PubMedDate not supplied

Sex hormone replacement therapy reverses altered venous contractility in rats after pharmacological ovariectomy.

OBJECTIVE: Female sex hormones have several important effects on the venous system. We earlier found that hormone replacement has a significant effect on venous distensibility, but effects of menopause and hormone replacement on venous contractility have never been studied. Therefore, and because the changes we found earlier in distensibility were most likely caused by alterations of contractility, we examined the changes in contractility of saphenous vein caused by depletion and replacement of sex hormones in female rats. DESIGN: Twenty Sprague-Dawley rats were pharmacologically ovariectomized by triptorelin. Ten of these rats received combined sex hormone replacement (HRT) with estradiol propionate and medroxyprogesterone acetate. The rest were given vehicle. Ten animals without ovariectomy served as controls. After 3 months of treatment, segments of the saphenous vein were dissected. Pressure-diameter curves were recorded in relaxed, contracted, and control states. RESULTS: Venous diameter, adjusted for body weight, was significantly decreased after pharmacological ovariectomy. HRT increased the diameter. The presence of sex hormones augmented norepinephrine contraction measured at physiological pressures (control: 19.2 +/- 2.3%; pharmacological ovariectomy: 15.2 +/- 1.4%, p < 0.05 and 17.8 +/- 2.2% following HRT). Myogenic (spontaneous) tone of the saphenous vein did not change after ovariectomy, but it was lowered by hormone replacement (control: 8 +/- 1.1%; ovariectomy: 6.9 +/- 2.5%; ovariectomy + HRT: 2.7 +/- 1.1%, p < 0.05). CONCLUSIONS: Sex hormone depletion induces significant alterations in contractility of the saphenous vein, which could perturb venous capacitance function and distensibility. This effect has a potential role in the development of hypertension and venous varicosity, and these changes could possibly be prevented by HRT.

Animals↗
PubMed1995

Endothelin ETA and ETB receptors cause vasoconstriction of human resistance and capacitance vessels in vivo.

BACKGROUND: The role of endothelin ETB receptors in mediating vasoconstriction in humans is unclear. As yet, there have been no in vivo studies in resistance vessels, and in vitro data have been contradictory. We therefore investigated the function of ETB receptors in vivo in human forearm resistance and hand capacitance vessels using endothelin-1 as a nonselective agonist at ETA and ETB receptors and endothelin-3 and sarafotoxin S6c as selective agonists at the ETB receptor. METHODS AND RESULTS: A series of single-blind studies were performed, each in six healthy men. Brachial artery infusion of endothelin-1 and endothelin-3 caused slow-onset dose-dependent forearm vasoconstriction. Although endothelin-3 caused significantly less forearm vasoconstriction than endothelin-1 at low doses, vasoconstriction was similar to the two isopeptides at the highest dose (60 pmol/min). Endothelin-3 caused transient forearm vasodilatation at this dose, whereas endothelin-1 showed only a nonsignificant trend toward causing early vasodilatation. Intra-arterial sarafotoxin S6c caused a progressive reduction in forearm blood flow, although less than that to endothelin-1 (P = .04). Dorsal hand vein infusion of sarafotoxin S6c caused local venoconstriction that was also less than that to endothelin-1 (P = .002). CONCLUSIONS: Selective ETB receptor agonists cause constriction of forearm resistance and hand capacitance vessels in vivo in humans, suggesting that both ETA and ETB receptors mediate vasoconstriction. Hence, antagonists at both ETA and ETB receptors, or inhibitors of the generation of endothelin-1, may be necessary to completely prevent vasoconstriction to endogenously generated endothelin-1.

Adult↗
PubMed1975

[The effect of acidic metabolic products on the capacitance and resistance vessels of the skeletal muscles and intestines].

Under conditions of the resistography of the skeletal muscle and intestinal vessels intraarterial injections of the acetic and lactic acid solutions in 75% cases evoked significant dilatation of the resistance vessels. Simultaneously enhancement of the venous outflou takes place, which is determined mainly by venous constriction and partly by the transfer of liquid from tissues into the blood. The rise of the venous outflow was lasted for 45 sec. and for 90 sec. in several experiments. This was not observed by the intraarterial injection of hypertonic solutions of NaCl Glucose, MgSO4 and others. The reactions of capacitance vessels was not dependent on the reactions of resistance vessels since the rise of the venous outflow took place also when only constriction of the resistance vessels (8 experiments) or when constrictor-dilatator reactions of the resistance vessels were observed.

Acetates↗
PubMed1989

[Prostaglandin E1, as a vasodilator therapy, for low output syndrome after cardiac surgery].

Prostaglandin E1 (PGE1) has a direct vasodilating effect to smooth muscles of resistant vessel much more than that of capacitance one. In afterload mismatch, vasodilator which acts on resistant vessel mainly should be selected. We used PGE1 for vasodilator therapy to two patients with low cardiac output syndrome (LOS) in intensive care unit. One patient undergoing coronary artery bypass grafting developed LOS and disseminated intravascular coagulation which derived from post-transfusional anaphylactoid reaction. Another patient undergoing mitral valve replacement, tricuspid valve annuloplasty and coronary artery bypass grafting also developed LOS with massive thrombosis caused by cold agglutinin during cardio-pulmonary bypass. In both patients, PGE1 decreased systemic vascular resistance index and pulmonary arterial resistance index, and increased cardiac output. PGE1 inhibits release of lysosomal enzymes from polymorphonuclear leukocytes and increases splanchnic blood flow. These effects lead to inhibit production of myocardial depressant factor and might relate to the improvement of LOS partially. We suggest that PGE1 was effective for LOS after cardiac surgery, especially in afterload mismatch.

Aged↗
PubMed1994

Controlled studies of Daflon 500 mg in chronic venous insufficiency.

Although great advances have been made in the operative treatment of vascular disorders, the management of most venous problems is still nonsurgical. Daflon 500 mg* is a micronized flavonoid mixture of 90% diosmin and 10% hesperidin that has phlebotonic properties. The efficacy of Daflon 500 mg has been investigated in three double-blind, randomized trials using strain gauge plethysmography to provide quantitative information on venous hemodynamics in patients with chronic venous insufficiency. In total, 183 patients were treated with Daflon 500 mg versus a control group of equal number of patients. Daflon 500 mg produced a significant decrease in venous capacitance, venous distensibility, and venous emptying time (P < 0.001). In addition, these changes were accompanied by improvement in clinical symptoms and a decrease in the supramalleolar circumference. Clinical side effects were rare and led to treatment withdrawal in only 3 patients. It is concluded that Daflon 500 mg is of benefit to patients with chronic venous insufficiency.

Diosmin↗
PubMed1998

Muscle metaboreceptor modulation of cutaneous active vasodilation.

PURPOSE: Isometric handgrip exercise in hyperthermia has been shown to reduce cutaneous vascular conductance (CVC) by inhibiting the cutaneous active vasodilator system. METHODS: To identify whether this response was initiated by muscle metaboreceptors, in seven subjects two 3-min bouts of isometric handgrip exercise in hyperthermia were performed, followed by 2 min of postexercise ischemia (PEI). An index of forearm skin blood flow (laser-Doppler flowmetry) was measured on the contralateral arm at an unblocked site and at a site at which adrenergic vasoconstrictor function was blocked via bretylium iontophoresis to reveal active cutaneous vasodilator function unambiguously. Sweat rate was measured via capacitance hygrometry, CVC was indexed from the ratio of skin blood flow to mean arterial pressure and was expressed as a percentage of maximal CVC at that site. In normothermia, neither isometric exercise nor PEI affected CVC (P > 0.05). RESULTS: The first bout of isometric handgrip exercise in hyperthermia reduced CVC at control sites and this reduction persisted through PEI (pre-exercise: 59.8 +/- 5.4, exercise: 49.8 +/- 4.9, PEI: 49.7 +/- 5.3% of maximum; both P < 0.05), whereas there were no significant changes in CVC at the bretylium treated sites. The succeeding bout of isometric exercise in hyperthermia significantly reduced CVC at both untreated (pre-exercise: 59.0 +/- 4.8, exercise: 47.3 +/- 4.0, PEI: 50.1 +/- 4.1% of maximum; both P < 0.05) and bretylium treated sites (pre-exercise: 61.4 +/- 7.3, exercise: 50.6 +/- 5.1, PEI: 53.9 +/- 6.0% of maximum, both P < 0.05). At both sites, CVC during PEI was lower than during the pre-exercise period (P < 0.05). Sweat rate rose significantly during both bouts of isometric exercise and remained elevated during PEI. CONCLUSIONS: These data suggest that the reduction in CVC during isometric exercise in hyperthermia, including the inhibition of the active vasodilator system, is primarily mediated by muscle metaboreceptors, whereas central command or muscle mechanoreceptors have less influence.

Adult↗
PubMed1998

Reflex control of splanchnic blood volume in anaesthetized dogs.

1. In chloralose-anaesthetized, artificially ventilated dogs, the splenic pedicle was tied and the carotid sinuses were vascularly isolated and perfused at controlled pressures. In Series 1 experiments, the hepatosplanchnic circulation was perfused through the abdominal aorta with a tie on the aorta separating it from the caudal circulation, which was perfused through the femoral arteries. The two circulations were drained from cannulae in the inferior vena cava and the femoral veins, with a tie on the inferior vena cava separating the two. In Series 2, the splanchnic circulation drained from the portal vein. In both series, inflows and outflows were measured and integrated to derive volume changes. Capacitance responses were assessed during constant flow, and capacitance plus passive responses were obtained during constant pressure perfusion. 2. In Series 1, an increase in carotid sinus pressure (from 8 to 26 kPa) during constant flow and constant pressure perfusion increased hepatosplanchnic volume by 2.5 and 5.7 ml (kg body weight)-1, respectively. The volume of the subdiaphragmatic circulation did not increase during constant flow, but during constant pressure it increased by 2.0 ml (kg body weight)-1. 3. In Series 2, increasing carotid pressure during constant flow and constant pressure increased the volume of the splanchnic circulation by 0.5 and 4.2 ml (kg body weight)-1, respectively. 4. These results confirm that carotid baroreceptor stimulation causes larger volume changes during constant pressure perfusion than during constant flow perfusion. Also, the active capacitance change in the splanchnic circulation is small in relation to the passive response. We propose that in dogs (following splenic ligation), the major active capacitance control is from the liver. However, large passive changes in splanchnic volume occur due to changes in flow.

Anesthesia↗
PubMed2000

Models of the venous system.

Cardiac output is largely controlled by venous return, the driving force of which is the energy remaining at the postcapillary venous site. This force is influenced by forces acting close to the right atrium, and internally or externally upon the veins along their course. Analogue models of the venous system require at least three elements: a resistor, a capacitor and an inductor, with the latter being of more importance in the venous than in the arterial system. Non-linearities must be considered in pressure/flow relations in the small venules, during venous collapse, or low flow conditions. The venous capacitance is also non-linear, but may be considered linear under certain conditions. The models have to include time varying pressure sources created by respiration and skeletal muscles, and if the description includes the upright position, the partly unidirectional flow through the venous valves has to be considered.

Blood Flow Velocity↗
PubMedDate not supplied

Hemodynamic and myocardial effects of long-lasting venodilation in the conscious dog: analysis of molsidomine in comparison with nitrates.

The effect of molsidomine-induced venodilation on cardiac preload was studied in conscious resting dogs, instrumented to analyze left ventricular function and myocardial perfusion. Direct effects on veins were studied during chloralose anesthesia by measuring regional venous capacitance changes with an induction angiometer. Kinetics of molsidomine-induced effects were compared to those induced by nitroglycerin and isosorbide dinitrate. This comparison was restricted to low i.v. dosages, causing only transient threshold effects on peripheral resistance and heart rate. During molsidomine-induced venous pooling, neither any direct effect on the coronary circulation nor any direct cardiac depressant activity of the drug was detected. 100 microgram/kg molsidomine caused a reduction of left ventricular preload by 5 mm Hg, lasting at least 4 hours. This effect was significantly more pronounced than that induced by 1 microgram/kg nitroglycerin or by 25 microgram/kg isosorbide dinitrate, lasting 2 min or 20 min, respectively. However, in raising regional venous capacitance, these nitrate dosages were equi-effective to 100 microgram/kg molsidomine, the effect of which was persistent and with a greater delay in onset. These results indicate that the lasting persistance of venodilation is a decisive factor for the amount of volume pooled in the capacitance system and, consequently, for the extent of preload reduction obtained. It is concluded, that lasting vasodilation, restricted to the veins, is beneficial for ventricular performance in ischemic heart disease.

Animals↗