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PubMed1989

[The effect of the ventral structures of the medulla oblongata on systemic arterial pressure and on the resistance and capacitance of the skeletal muscle vessels].

Following the isolation of ventral portions of the medulla oblongata from the dorsal ones and from the upper parts of the c. n. s. in cats, no changes were found in the initial level of systemic blood pressure, in perfusion pressure or in venous outflow in the m. gastrocnemius, vessels. Electrical stimulation of ventral portions of the lateral paragigantocellular nucleus under these conditions increased the systemic AP, regional vascular resistance and decreased the capacitance of the n. gastrocnemius' vessels, whereas after bilateral electrical coagulation of the nucleus the stimulation led to a stable and obvious decrease in the systemic AP and perfusion pressure in the muscle vessels. No changes of the regional vascular capacitance were noted. The significance of ventral structures of medulla oblongata in maintaining of initial AP level, formation of tonic neurogenic messages to arterial vessels of m. gastrocnemius and in actualization of the reflex neurogenic effects upon arterial and venous vessels of skeletal muscles, is discussed.

Animals↗

PubMed2001

[Hemodynamic mechanisms of blood flow regulation in the vena cava anterior].

A similarity of the blood flow shifts in response to every single pressor or depressor stimulus in the v. cava anterior in cats and a possibility of dissimilar changes of capacity of the vein's vascular basin under the effect of one and the same stimulus, are revealed. This dissimilarity is mainly due to a skin-muscular component of this vascular basin. An increase in the central venous pressure from 0 to 40 mm of water limits the extent of shifts in the capacity function of the v. cava anterior's basin. The blood flow changes in the v. cava anterior is mainly due to a relationship among regional components of the vessels' total peripheral resistance. A potential possible contribution of the v. cava anterior basin vessels capacitance's shifts constitutes 17.5%, whereas under the effect of neurogenic stimuli in the increase of the blood flow in the v. cava anterior may be completely (up to 100%) maintained by a drop of the capacitance of the vein's vascular basin.

Animals↗

PubMed1998

Determination of total effective vascular compliance in patients with sepsis syndrome.

Changes in capacitance vessels have important consequences on cardiac filling pressure and fluid volume distribution in patients with sepsis syndrome. Vascular compliance may be evaluated from the slope of the relationship between changes in total blood volume (deltaTBV) and changes in central venous pressure (deltaCVP) during acute volume expansion (450 ml of gelatin fluid over 6 min), i.e., from the deltaTBV/deltaCVP ratio. The mean ratio (ml x mm Hg-1 x kg-1) was 2.03 +/- 0.21 in control subjects, 1.43 +/- 0.25 in mechanically ventilated patients without sepsis syndrome, and 0.94 +/- 0.24 in mechanically ventilated patients with sepsis syndrome (p < 0.0001 versus the other two groups). Based on echocardiographic determinations, cardiac performance was constantly found within the normal range (cardiac output ranged from 5.6 +/- 1.2 to 6.7 +/- 2.0 L/min in nonseptic patients from 6.8 +/- 1.9 to 7.8 +/- 2.2 in septic patients). Effective compliance of the total vascular bed is therefore reduced in patients with sepsis syndrome, independently of the hemodynamic modifications due to mechanical ventilation.

Adolescent↗

PubMed2001

Vascular adrenoceptors: an update.

The total and regional peripheral resistance and capacitance of the vascular system is regulated by the sympathetic nervous system, which influences the vasculature mainly through changes in the release of catecholamines from both the sympathetic nerve terminals and the adrenal medulla. The knowledge of the targets for noradrenaline and adrenaline, the main endogenous catecholamines mediating that influence, has recently been greatly expanded. From two types of adrenoceptors (alpha and beta), we have now nine subtypes (alpha1A, alpha1B, alpha1D, alpha2A/D, alpha2B, alpha2A/D, beta1, beta2, and beta3) and two other candidates (alpha1L and beta4), which may be conformational states of alpha1A and beta1-adrenoceptors, respectively. The vascular endothelium is now known to be more than a pure anatomical entity, which smoothly contacts the blood and forms a passive barrier against plasma lipids. Instead, the endothelium is an important organ possessing at least five different adrenoceptor subtypes (alpha2A/D, alpha2C, beta1, beta2, and beta3), which either directly or through the release of nitric oxide actively participate in the regulation of the vascular tone. The availability of transgenic models has resulted in a stepwise progression toward the identification of the role of each adrenoceptor subtype in the regulation of blood pressure and fine-tuning of blood supply to the different organs: alpha2A/D-adrenoceptors are involved in the central control of blood pressure; alpha1-(primarily) and alpha2B-adrenoceptors (secondarily) contribute to the peripheral regulation of vascular tone; and alpha2A/D- and alpha2C-adrenoceptors modulate transmitter release. The increased knowledge on the involvement of vascular adrenoceptors in many diseases like Raynaud's, scleroderma, several neurological degenerative diseases (familial amyloidotic polyneuropathy, Parkinson disease, multiple-system atrophy), some kinds of hypertension, etc., will contribute to new and better therapeutic approaches.

Animals↗

PubMed1987

Organization of lumbar spinal outflow to distal colon and pelvic organs.

The lumbar sympathetic outflow projects through the lumbar splanchnic, lumbar colonic, and hypogastric nerves (and to a lesser degree through the sacral sympathetic chain and pelvic nerves). It is thought to be involved in the regulation of the storage and evacuation functions of the following three organ systems: lower urinary tract, hindgut, and reproductive organs. In addition, it controls vascular resistance and capacitance. Thus the target tissues of the postganglionic neurons are vascular smooth muscle, visceral smooth muscles, probably secretory epithelia, and also neurons in the enteric nervous system and the pelvic ganglia. The preganglionic neurons are situated in the caudal part of the spinal representation, neurons associated with the colon being located rostral to those associated with the pelvic organs. Most lie medial to the classical intermediolateral cell column that may contain mainly vasoconstrictor neurons. Most (if not all) preganglionic neurons are cholinergic; some also contain an identified peptide. Most of the postganglionic neurons are situated in the inferior mesenteric ganglion (or equivalent structures); again, those projecting to the colon lie rostral to those projecting to the pelvic organs. Others lie in intercalated prevertebral ganglia, in the pelvic plexus, and in sacral paravertebral ganglia. The majority is noradrenergic, and most also contain one or several peptides, the topographical distribution of which appears to characterize functional subgroups of neurons. The terminations of noradrenergic axons in many pelvic organs probably make close contact with both vascular and nonvascular effectors. In the colon, most endings are located in the enteric plexuses. The responses of these organs to electrical stimulation of visceral nerves, and their reflex responses (together with those observed in the efferent axons of visceral nerve trunks) to electrical and natural stimulation of afferent fibers, lead to the general conclusion that several distinct classes of pre- and postganglionic neurons exist. 1) Vasoconstrictor neurons demonstrate ongoing activity with cardiac rhythm and appropriate reflexes to stimulation of cardiovascular afferent receptors and respond only weakly to natural stimulation of visceral receptors. 2) MR neurons respond to visceral stimuli but are not influenced from arterial baro- and chemoreceptors. These show at least two different response patterns consistent with their separate involvement in the reciprocal behavior of the colon and bladder. 3) Other neurons are silent in anesthetized animals and do not respond to any stimuli used thus far.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1975

Parasympathetic control of blood circulation and secretion in the nasal mucosa.

The effects of selective parasympathetic nerve activation on the secretory response and the vascular exchange and capacitance sections in the cat nasal mucosa were studied. The vascular events were investigated by measuring the local disappearnce of 125I- and changes in gross pulse rate from 131I- labelled serum albumin as monitored over the nose. A frequency-dependent increase in nasal secretion and local blood content occurred in the range 0.5-12 imp/sec: an increase in disappearance rate was observed at the same time. This indicates that the vascular and secretory responses are activated simultaneously. The secretory responses, but not the vascular events, were shown to be blocked by atropine. The results thus shown that the postganglionic parasympathetic mediator of nasal secretion is cholinergic, whereas the vasodilatation appears to be due to a different mechanism, which is not sensitieve to atropine. The beneficial effect of some antihistamines in vasomotor rhinitis may thus be due to their anticholinergic properties.

Animals↗

PubMed1995

Acute hemodynamic effects of drugs acting on the renin-angiotensin system in acute heart failure.

OBJECTIVE: To determine the role of the renin-angiotensin system in a model of acute heart failure. METHODS: Placebo or drugs (Ro 44-9375, a renin inhibitor; captopril, an angiotensin-converting enzyme [ACE] inhibitor; or DuP 532, an angiotensin II receptor [AT1] antagonist) were given to anesthetized splenectomized dogs (n = 12 for each group) for 50 mins after a volume load (dextran 70, 25 mL/kg over 10 mins) during rapid right ventricular pacing at 250 beats/min. Total vascular compliance and capacitance were determined from mean circulatory filling pressure-blood volume curves during transient circulatory arrests induced by acetylcholine. Cardiac index was measured by thermal dilution. RESULTS: Compared with the untreated group, all three drugs significantly reduced systemic pressure and total peripheral resistance while increasing arterial compliance. Captopril alone increased cardiac index (25 +/- 11 versus -23 +/- 13 mL/kg/min) and reduced pulmonary capillary wedge pressure (16.6 +/- 0.7 versus 21.9 +/- 1.0 mmHg). None of the drugs altered the mean circulatory filling pressure, total vascular compliance or capacitance, stressed or unstressed blood volumes, or central blood volume. CONCLUSION: The renin-angiotensin system is not strongly implicated in the hemodynamic manifestations of this model of acute heart failure. These drugs had effects on the arterial but not the venous side of the circulation. Captopril alone reduced pulmonary capillary wedge pressure, perhaps by nonangiotensin effects.

Acute Disease↗

PubMed1990

Unresponsiveness of forearm hemodynamics to omega-3 polyunsaturated fatty acids and aspirin.

Prostaglandin synthesis has been reported to change with aspirin ingestion via cyclooxygenase enzyme inhibition and with marine oil supplementation via an increase in the metabolism of 3-series eicosanoids. This study investigated the effects of pharmacological manipulations of prostaglandin metabolism on forearm hemodynamics and blood pressure. The agents studied were omega-3 fatty acids and aspirin. In the omega-3 fatty acid study, two groups of normal volunteers (N = 10/group) supplemented their diets with either marine oil capsules or placebo. Hemodynamic variables (Mercury-in-Silastic forearm plethysmography) were measured initially and weekly for 4 weeks. There were no significant differences between the two groups in blood pressure, forearm blood flow, venous capacitance, or forearm vascular resistance. Parallel changes occurred for forearm blood flow and venous capacitance. Six normal volunteers took daily dosages of aspirin, increasing from 162 to 2600 mg. Hemodynamic measurements, ADP-induced platelet aggregation, and serum salicylate levels were obtained daily. Maximum inhibition of platelet aggregation occurred after 162 mg. (serum salicylate = 17.7 +/- 6.4 mg/l). Though serum salicylate levels rose to 165.0 +/- 20.0 mg/l, no significant changes occurred in blood pressure or forearm blood flow. Even at aspirin levels 16-fold greater than those required to impair platelet aggregation, the changes in forearm vascular resistance were not found to be significant. These results suggest that under resting conditions in normotensive males, neither pharmacological inhibition nor stimulation of vascular prostaglandin metabolism alters forearm vascular resistance or arterial blood pressure.

Adult↗

PubMed2006

Pulmonary artery smooth muscle cells from normal subjects and IPAH patients show divergent cAMP-mediated effects on TRPC expression and capacitative Ca2+ entry.

Pulmonary vascular remodeling due to overgrowth of pulmonary artery smooth muscle cells (PASMC) is a major cause for the elevated vascular resistance in patients with idiopathic pulmonary arterial hypertension (IPAH). Increased cytosolic Ca(2+) concentration, resulting from enhanced capacitative Ca(2+) entry (CCE) and upregulated transient receptor potential (TRP) channel expression, is involved in stimulating PASMC proliferation. The current study was designed to determine the impact of cAMP, a second messenger that we hypothesized would blunt aspects of PASMC activity, as a possible contributor to IPAH pathophysiology. Short-term (30 min) pretreatment with forskolin (FSK; 10 muM), a direct activator of adenylyl cyclase, in combination with the cyclic nucleotide phosphodiesterase inhibitor isobutylmethylxanthine (IBMX; 200 muM), attenuated CCE in PASMC from normal subjects, patients without pulmonary hypertension (NPH), and patients with IPAH. The FSK-mediated CCE inhibition was independent of protein kinase A (PKA), because the PKA inhibitor H89 negligibly affected the decrease in CCE produced by cAMP. By contrast, longer (4 h) treatment with FSK (with IBMX) attenuated CCE in normal and NPH PASMC but enhanced CCE in IPAH PASMC. This enhancement of CCE was abolished by PKA inhibition and associated with an upregulation of TRPC3. In addition, cAMP increased TRPC1 mRNA expression in IPAH (but not in normal or NPH) PASMC, an effect blunted by H89. Furthermore, iloprost, a prostacyclin analog that increases cAMP, downregulated TRPC3 expression in IPAH PASMC and FSK-mediated cAMP increase inhibited IPAH PASMC proliferation. Although a rapid rise in cellular cAMP decreases CCE by a PKA-independent mechanism, sustained cAMP increase inhibits CCE in normal and NPH PASMC but increases CCE via a PKA-dependent pathway in IPAH PASMC. The divergent effect of cAMP on CCE parallels effects on TRPC expression. The results suggest that the combined use of a PKA inhibitor and cAMP-elevating drugs may provide a novel approach for treatment of IPAH.

Adult↗

PubMed1991

Action of propofol on resistance and capacitance vessels during cardiopulmonary bypass.

The peripheral vascular action of propofol on the resistance and the capacitance vessels was investigated in 16 patients during cardiopulmonary bypass. The venous reservoir (RV) and mean arterial pressure (MAP) were used as indices of the changes in venous capacitance and systemic vascular resistance (SVR), respectively. Propofol 2 mg.kg-1 produced a decrease in MAP without a significant change in RV, suggesting that propofol preferentially decreases SVR without a significant change in venous capacitance.

Adult↗

PubMedDate not supplied

Structural changes in resistance and capacitance vessels in borderline hypertension.

Vascular resistance at rest may be normal in humans with borderline or mild hypertension. However, this finding is a facade which can obscure the presence of vascular structural alterations that may have an important influence on resistance and capacitance functions of the circulation. This paper reviews several studies regarding vascular structural changes in borderline hypertension (BHT). First, forearm vasodilator capacity is limited in BHT and in normotensive young men with a family history of hypertension; this suggests the presence of structural changes in forearm resistance vessels. Second, forearm venous distensibility is decreased in BHT. Most of this decrease is caused by nonadrenergic mechanisms--which suggests that there may be structural changes in veins in BHT. Third, the studies of Takeshita and colleagues suggest that sodium intake may influence vascular structural changes. In hypertensive patients who responded to salt loading with increased blood pressure and vascular resistance, salt loading limited vasodilator responses to 10 minutes of ischemia. This effect of salt loading on vasodilator responses occurred in some patients (salt-responders), but not in others (salt-nonresponders). Functional studies support the concept that structural changes in resistance and capacitance vessels occur during the early stages of human hypertension. These changes may not be entirely adaptive responses to elevated arterial pressure, since they occur in capacitance as well as resistance vessels. In addition, the structural changes appear to be responsive to factors such as sodium intake. These observations suggest that vascular structural changes in human hypertension may be related in part to neurohumoral influences or to primary vascular abnormalities.

Blood Vessels↗

PubMed1985

The treatment of resistant hypotension with ornipressin. A case report.

A 50-year-old man underwent emergency aortic valve replacement. He had been treated with five antihypertensive agents before the procedure; this contributed to the development of profound hypotension after induction of anaesthesia. The hypotension did not respond to conventional treatment with an incremental intravenous infusion of phenylephrine HCl, probably due to the direct vasodilator action of the hydralazine group of drugs which renders the peripheral vascular smooth muscle unresponsive to sympathomimetic stimulation. The hypotension did, however, respond rapidly to low-dose infusion of a synthetic vasopressor, ornipressin (POR 8; Sandoz), a drug with a direct action on vascular smooth muscle, especially the capacitance vessels. Ornipressin thus restores vascular smooth-muscle tone even when the integrity of the adrenergic pathways is no longer intact.

Anesthesia, General↗

PubMed1991

[Dynamics of body fat mass and blood circulation in young men with obesity].

The body fat mass (BFM), central and peripheral hemodynamics was studied in 112 adipose males (age: 18-32 years) after a 18-24 days hospital treatment and 3-3.5 years later. It was found that an increase of the BFM was accompanied by a distinct increase of the AP level, a tendency to reduction of the cardiac ejection, volume rate of the arterial blood flow, increase of the peripheral vascular resistance, venous capacitance, venous tone. The dynamics of circulation indices in reduction of the BFM reflect normalization of the cardiac and vascular function. Obtained data evidence diverse changes of the hemodynamic indices in progression, regress and stable course of adiposity in young males.

Adolescent↗

PubMed1986

Effect of veratridine injected into the aortic root on resistance and capacitance in the abdominal circulation in anaesthetized dogs.

In dogs anaesthetized with chloralose, cardiac receptors were stimulated by injections of veratridine into the aortic root and the effects studied on resistance and capacitance in the vascularly isolated and perfused abdominal circulation. Unless carotid sinus pressure was high, veratridine injections consistently resulted in dilatation of resistance and capacitance vessels. However, at high carotid pressures, the resistance response to veratridine was inhibited and the capacitance response was usually reversed. These results indicate that stimulation of cardiac receptors can affect resistance and capacitance in the abdominal circulation. Further experiments are required to evaluate the physiological role of these responses.

Abdomen↗

PubMed2003

Diverse effects of monensin on capacitative Ca2+ entry and release of stored Ca2+ in vascular smooth muscle cells.

The effects of monensin, an activator of Na(+)/H(+) exchanger (NHE), on capacitative Ca(2+) entry (CCE) were investigated using A7r5 cells. Capacitative Ca(2+) entry was induced by elevation of extracellular Ca(2+) concentrations of A7r5 cells in which stored Ca(2+) had been depleted by previous administration of thapsigargin. Capacitative Ca(2+) entry was abolished by pretreatment of the cells with SKF-96365 (1-[beta-(3-[4-methoxyphenyl]propoxy)-4-methoxyphenethyl]-1H-imidazole hydrochloride) but was not affected by pretreatment with verapamil. Monensin significantly increased capacitative Ca(2+) entry. On the other hand, 5-hydroxytryptamine-induced inositol monophosphate accumulation and subsequent intracellular Ca(2+) release from its stores were significantly inhibited by monensin, while thapsigargin-induced Ca(2+) release was not affected by monensin. These results suggest that monensin has diverse actions on capacitative Ca(2+) entry and agonist-induced release of stored Ca(2+) in vascular smooth muscle cells.

Animals↗

PubMedDate not supplied

Influence of venous function on exercise tolerance in chronic heart failure.

PURPOSE: The clinical phase of chronic heart failure (HF) includes a marked decline in exercise tolerance, in part due to impaired skeletal muscle blood flow delivery. Interestingly, the role of the venous system on exercise tolerance in patients with HF has not received much attention, despite evidence of changes in venous structure and function. The purpose of this study was to examine the relationship between forearm arterial and venous function, and exercise tolerance in patients with HF and age-matched controls. METHODS: Vascular function and exercise tolerance was examined in 20 patients with HF (age 59 +/- 13 years) and 10 control subjects (age 51 +/- 16 years). Nondominant forearm arterial inflow, vascular resistance, venous capacitance, and venous outflow were evaluated at rest and after 5 minutes of upper arm occlusion, using strain gauge plethysmography. Exercise tolerance was measured as the maximum walking distance achieved on a 6-minute walking test. RESULTS: Maximum walking distance (HF: 178 +/- 65 m; controls: 562 +/- 136 m, P=.0001), and forearm vascular function after occlusion were significantly different between groups (forearm arterial inflow: HF 15.3 +/- 6; controls 22 +/- 6.7; forearm venous capacitance: HF 1.4 +/- 0.5; controls 2.0 +/- 0.4; forearm venous outflow: HF 24.5 +/- 9.4; controls: 33 +/- 10 mL x 100 mL tissue(-1) x min(-1); and forearm vascular resistance: HF 7.8 +/- 3; controls 4.6 +/- 1.4 U). Correlation analysis revealed significant associations between all forearm vascular measurements after occlusion and maximum walking distance. CONCLUSION: These data confirm previous studies indicating the importance of arterial reactivity on exercise tolerance in patients with HF. Additionally, the results suggest the importance of venous function as a contributing factor to exercise performance.

Adult↗

PubMed1981

Forearm plethysmography in normotensive and hypertensive pregnant women.

Forearm plethysmography affords a simple noninvasive method of studying dynamic changes in the microcirculation. This technic was used to study the peripheral circulation of normotensive nongravid women and normotensive and untreated hypertensive pregnant women during the third trimester. The variables of forearm blood flow, vascular resistance, venous capacitance, and capillary filtration coefficient were measured in the resting state and during and after exercise. The pregnant women demonstrated an increase in forearm blood flow over the nonpregnant women. As expected, vascular resistance was higher in the hypertensive pregnant patients than in normotensive pregnant women. The possible predictive value of these findings is discussed.

Female↗

PubMedDate not supplied

Effects of capacitative calcium entry on agonist-induced calcium transients in A7r5 vascular smooth muscle cells.

OBJECTIVE: The purpose of this study was to evaluate the contribution of capacitative calcium influx to intracellular calcium levels during agonist-induced stimulation of vascular smooth muscle cells. METHODS: Aortic vascular smooth muscle cells (A7r5) were loaded with Indo-1 and intracellular calcium transients were measured. Cells were challenged with either arginine vasopressin (0. 5 microM) or thapsigargin (1 microM). Lanthanum (1 mM) was used to block capacitative calcium influx through store-operated channels. Calcium traces were analyzed for basal, peak and plateau responses. Recordings were derivatized and integrated to gain additional information. Nonlinear regression provided a time constant that describes restoration of ionic equilibrium involving both sequestration and extrusion pathways. RESULTS: Stimulation of cells with thapsigargin produced a non-L-type calcium influx that was attenuated by lanthanum. Cells excited with vasopressin exhibited a rapid calcium increase followed by a gradual decrease to a plateau level. Lanthanum pretreatment prior to stimulation caused no significant change in baseline, peak or plateau calcium levels as compared to control. Lanthanum caused no significant change in maximal calcium release rate, calcium integrals or time constant as compared to control. CONCLUSIONS: Capacitative calcium entry can occur in vascular smooth muscle cells, but does not appear to contribute significantly to the vasopressin response.

Animals↗