Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vascular Capacitance”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMed1995

Hyperglycemia alters cytoplasmic Ca2+ responses to capacitative Ca2+ influx in rat aortic smooth muscle cells.

Concentrations of free cytoplasmic Ca2+ in rat aortic smooth muscle (RASM) cells were monitored using the ratiometric Ca2+ indicator fura 2-acetoxymethyl ester (AM). In RASM cells cultured in 5 mM Glc, incubation with angiotensin II, ATP, or thapsigargin [a selective inhibitor of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase] depleted SR Ca2+ stores and initiated a capacitative Ca2+ influx through the plasma membrane. This influx was resistant to verapamil, a selective inhibitor of L-type voltage-gated Ca2+ channels, but was sensitive to SKF-96365, an inhibitor of the receptor-operated Ca2+ entry pathway. RASM cells cultured in 25 mM Glc exhibited a significant decrease in cytoplasmic Ca2+ responses to agonist-induced Ca2+ release from SR stores and to subsequent capacitative Ca2+ entry. In addition, the cytoplasmic response to thapsigargin-induced release of Ca2+ from the SR in hyperglycemic cells peaked more sharply than in control cells and returned to baseline more rapidly. The effects of hyperglycemia were not overcome by myo-inositol supplementation.

Adenosine Triphosphate↗
PubMedDate not supplied

Cardiovascular disease in chronic renal failure: pathophysiologic aspects.

Cardiovascular complications are the leading cause of mortality in patients with end-stage renal disease (ESRD). The excess cardiovascular risk and mortality is already demonstrable in early renal disease and in patients with chronic renal failure (CRF), with the highest relative risk of mortality in the youngest patients. The high risk for cardiovascular disease (CVD) results from the additive effect of multiple factors, including hemodynamic overload and several metabolic and endocrine abnormalities more or less specific to uremia. CVD includes disorders of the heart (left ventricular hypertrophy [LVH], cardiomyopathy) and disorders of the vascular system (atherosclerosis, arteriosclerosis), these two disorders being usually associated and interrelated. LVH is the most frequent cardiac alteration in ESRD, resulting from a combined pressure and volume overload. LVH in general is an ominous prognostic sign and an independent risk factor for arrhythmias, sudden death, heart failure, and myocardial ischemia. Regression of LVH needs a combined intervention to reduce hemodynamic overload and is associated with improved prognosis and survival. Clinical studies have shown that damage of large conduit arteries is a major contributing factor for the high incidence of congestive heart failure (CHF), LVH, ischemic heart disease (IHD), sudden death, cerebrovascular accidents, and peripheral artery diseases. Damage to large conduit arteries is principally related to highly calcified occlusive atherosclerotic lesions and to stiffening of large capacitive arteries. These two complications are independent risk factors for survival, and improvement of arterial stiffness is associated with better prognosis and survival. The present review summarizes the most recent works dealing with the pathophysiology of CVD and some aspects of the therapeutic approach.

Anemia↗
PubMedDate not supplied

Evaluation of the clinical pharmacological activity of a phlebotonic agent. Application to the study of Daflon 500 mg.

Provided certain methodological precautions are observed, mercury strain gauge venous occlusion plethysmography represents one of the best available function tests in phlebology to evaluate the efficacy of a phlebotonic agent. All physiological and environmental parameters liable to affect venous tone must be determined and controlled before and during the procedure, which is to be carried out in controlled and fully reproducible conditions. Intra and inter-observed reproducibility of results must be checked regularly in each laboratory. The objective character of the parameters assessed (Hmax, delta Vmax, T50, T2p...) does not spare the need for randomized, crossover or comparative, double-blind placebo-controlled trials, as plethysmographic results may show wide variations from one subject to another, and even from one moment to another, in chronic venous insufficiency, depending on the subject's environment and occupation. Furthermore, knowledge of treatment by the observer may affect the validity of the results. Taking into account all of these methodological pre-requisites, the phlebotonic activity of a single dose of Daflon 500 mg in lower limb chronic venous insufficiency was assessed in placebo-controlled clinical pharmacological studies. The following characteristics emerged: (1) significant improvement of venous capacitance, distensibility, and emptying times, as from the 2nd hour following Daflon 500 mg administration; (2) dose-response relationship, with an optimal dose of 2 tablets per day; (3) rapid onset and long duration of action; (4) significant hemodynamic effect on the venous system, whatever the type of venous insufficiency: organic, functional or gestational.

Adult↗
PubMed1983

Intravenous bolus nitroglycerin--hemodynamic effects and clinical implications.

Intravenous bolus nitroglycerin has been used routinely in our cardiac catheterization laboratory during the past three years. Observations on more than 1500 patients suggest that in the supine properly hydrated patient intravenous nitroglycerin produces an initial rapid fall in arterial pressure (systolic, diastolic, and mean). This is followed by gradual return of arterial pressure toward but not to baseline during the subsequent 30-60 seconds. There is a concomitant fall in left ventricular end-diastolic pressure (LVEDP), which appears to be biphasic. Initially, LVEDP falls concomitantly with aortic pressure; subsequently, there is further decrease in LVEDP at a time when aortic pressure is nearly back to baseline. These observations suggest that bolus nitroglycerin, as opposed to continuous nitroglycerin infusion, may act primarily on resistance vessels (systemic arteries), and secondarily on capacitance vessels (systemic veins). A series of experiments was designed to test this hypothesis. During routine right and left heart catheterization of patients with suspected coronary artery intravenous bolus nitroglycerin (.1 mg-.8 mg) was injected into inferior vena cava, pulmonary artery, left ventricle, aortic root, distal aorta, and coronary aorta. The time course of bolus nitroglycerin effect on central venous pressure, pulmonary artery pressure, left ventricular end-diastolic pressure, and arterial pressure was observed for the various injection sites. These time courses of effect were compared to appearance times of indocyanine green injected into the various injection sites, and sampled from the various measuring sites. Initial data suggest that the initial rapid fall in blood pressure is secondary to a primary decrease in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1994

Influence of compression stockings on lower-limb venous haemodynamics during laparoscopic cholecystectomy.

Lower-limb venous haemodynamics were studied prospectively in 40 patients (24 women, 16 men of median age 52 years) undergoing laparoscopic cholecystectomy. Patients were randomized to wear compression stockings during surgery or no stockings. All received subcutaneous heparin prophylaxis. Venous capacitance and outflow were measured non-invasively before, during and after pneumoperitoneum. In the group without compression stockings (20 patients) venous capacitance and outflow decreased during pneumoperitoneum in most patients. In the group wearing stockings (20 patients) the changes were less pronounced or abolished. There was a significant difference between the groups in venous capacitance and outflow ratios at mid-operation: median (interquartile range) 0.89 (0.56-1.16) and 0.89 (0.56-1.15) respectively in the group without stockings versus 1.48 (1.09-2.19) and 1.71 (1.20-2.19) respectively in that with stockings (P < 0.001). Pneumoperitoneum creates a significant resistance to venous return. Compression stockings counteract the changes observed.

Adult↗
PubMed1986

Application of the medical anti-shock trouser (MAST) increases cardiac output and tissue perfusion in simulated, mild hypovolaemia.

We have studied the haemodynamic effects of the application of the medical anti-shock trouser (MAST) in 10 healthy subjects in the semi-upright position in order to simulate mild hypovolaemia. Left ventricular end diastolic dimension (EDD) was measured by M-mode echocardiography and cardiac output (CO) by the Doppler ultrasound technique. Forearm blood flow (FBF) was measured by plethysmography and blood pressure (BP) by the standard cuff technique. Systematic increases in MAST pressure of up to 80 mm Hg were applied. EDD increased to a maximum of 9.3% (p less than or equal to 0.01) which was associated with a maximum increase in CO of 31.7% (p less than or equal to 0.05). FBF increased by a maximum of 54.2% (p less than or equal to 0.001) whilst BP increased by a maximum of 12% (p less than or equal to 0.001). These results demonstrate that the application of the MAST is an effective means of transferring blood to the central circulation by compression of the capacitance vessels resulting in significant increases in cardiac output and tissue perfusion. At high pressures there was evidence of compression of resistance vessels, which may be useful in reducing blood loss. The ease and rapidity with which his suit can be applied suggests that it may be useful in the short term treatment of hypovolaemia.

Adult↗
PubMed1998

Left coronary pressure-flow relations of the beating and arrested rabbit heart at different ventricular volumes.

OBJECTIVE: To study the effect of cardiac contraction on left coronary artery pressure-flow relations at different vascular volumes and to compare these relations in the beating heart with those in the heart arrested in systole and diastole. METHODS: Maximally vasodilated, Tyrode perfused, rabbit hearts (n = 6) with an intra-ventricular balloon were used. The left coronary artery was separately perfused via a cannula in the left main coronary artery. The slopes and the intercepts of left coronary pressure-flow relations were determined in the beating and arrested heart at different chamber volumes. A 3-factor design with repeated measures was used to compare the effect of three factors: phase of contraction (systole and diastole), chamber volume (V0 and V1, left ventricular end-diastolic pressure 1.4 and 20 mm Hg, respectively) and the type of contraction (beating and arrested; a measure of capacitive effects). RESULTS: The phase of contraction has a significant effect on the intercepts (> 40 mmHg, p = 0.00032) but not on the slopes of the pressure-flow relations. Chamber volume had a small effect on the intercepts (< 5 mm Hg, p = 0.037), but not on the slopes of the pressure-flow relations. The type of contraction has a significant effect on the slopes (approximately 10%, p = 0.00021) but not on the intercepts of the pressure-flow relations. CONCLUSIONS: In the isolated Tyrode perfused rabbit heart left coronary pressure-flow relations are mainly determined by contraction, while left ventricular chamber volume and capacitive effects contribute little.

Animals↗
PubMed1999

Pharmacological evidence for a KATP channel in renin-secreting cells from rat kidney.

1. Openers of the ATP-sensitive potassium channel (KATP channel) increase and blockers decrease renin secretion. Here we report the effects of levcromakalim (LCRK, a channel opener) and glibenclamide (GBC, a blocker) on membrane potential, whole-cell current and the cytoplasmic Ca2+ concentration of renin-secreting cells (RSC). Studies were performed on afferent arterioles from the kidney of Na+-depleted rats. 2. As monitored with the fluorescent oxonol dye DiBAC4(3), LCRK (0.3 and 1 microM) induced a hyperpolarization of approximately 15 mV which was abolished by GBC (1 microM). 3. Whole-cell current-clamp experiments showed that RSC had a membrane potential of -61 +/- 1 mV (n = 16). LCRK (1 microM) induced a hyperpolarization of 9.9 +/- 0.2 mV (n = 16) which, in the majority of cells, decreased slowly with time. 4. Capacitance measurements showed a strong electrical coupling of the cells in the preparation. 5. At -60 mV, LCRK induced a hyperpolarizing current in a concentration-dependent manner with an EC50 of 152 +/- 31 nM and a maximum current of about 200 pA. 6. Application of GBC (1 microM) produced no effect; however, when applied after LCRK (300 nM), GBC inhibited the opener-induced hyperpolarizing current with an IC50 of 103 +/- 36 nM. 7. LCRK (0.3 and 1 microM) did not significantly affect the cytoplasmic Ca2+ concentration either at rest or after stimulation by angiotensin II. 8. The data show that LCRK induces a GBC-sensitive hyperpolarizing current in rat RSC. This current presumably originates from the activation of KATP channels which pharmacologically resemble those in vascular smooth muscle cells. The stimulatory effect of KATP channel opening on renin secretion is not mediated by a decrease in intracellular Ca2+ concentration.

Angiotensin II↗
PubMed1995

Splanchnic venous pressure-volume relation during experimental acute ischemic heart failure. Differential effects of hydralazine, enalaprilat, and nitroglycerin.

BACKGROUND: Vasodilator drugs have variable effects on veins and arteries. However, direct measurements of their effects on the splanchnic veins, perhaps the most important volume reservoir, have not been reported. We assessed the effect of acute heart failure and the subsequent administration of hydralazine, enalaprilat, and nitroglycerin on the splanchnic venous pressure-volume relation in intact dogs. METHODS AND RESULTS: Experimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure-volume relation was determined by radionuclide plethysmography during the control stage, after acute heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86 +/- 2% and an increase in LVEDP from 6 +/- 1 to 21 +/- 1 mm Hg (P < .001). There was a parallel leftward shift of the splanchnic vascular pressure-volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88 +/- 3%, 96 +/- 3%, and 113 +/- 3%, respectively (P = NS, P < .01, and P < .001, respectively, versus heart failure). After drug administration, the LVEDPs were 18 +/- 2, 16 +/- 1, and 13 +/- 1 mm Hg (P = NS, P < .05, and P < .001, respectively, versus heart failure). CONCLUSIONS: Acute heart failure was associated with a parallel leftward shift of the splanchnic venous pressure-volume relation (venoconstriction). Splanchnic (systemic) venoconstriction may in part explain the increased LVEDP during acute heart failure by displacement of blood to the central compartment. Subsequently administered enalaprilat and, to a greater degree, nitroglycerin produced splanchnic venodilation, thereby lowering LVEDP. Hydralazine had no significant effect on the splanchnic veins and only a modest effect on LVEDP. In this model, splanchnic capacitance changes appear to modulate change in left ventricular preload.

Animals↗
PubMed1990

[The capacitive function of the spleen during electrical stimulation of the structures of the ventral section of the medulla oblongata].

In acute experiments on cats under perfusion with constant blood expenditure of hemodynamically isolated spleen the authors studied the reactions of its vessels in the electrical stimulation of ventral brainstem. It was shown that the stimulation of the rostral zone of these structures increased vein outflow from the spleen. It was shown the deterioration of the parametres which characterize a capacitance function of the spleen by stimulation of a causal depressor zone of the brainstem by means of the current of threshold size and its increase by irritation of the brain structures with a 2 threshold current size. There have been made a supposition has been made about the participation of the pointed structures of the brain in the regulation of a vasomotion tonus of the spleen vessels.

Animals↗
PubMed1988

Estimation of intramyocardial pressure and coronary blood flow distribution.

To characterize the intramyocardial pressure (IMP) and coronary blood flow distribution in a stenosed coronary circulation, we compared four analog circuits for modeling coronary impedance. The resistor (R)-diode (D) model simulates vascular collapse, and the capacitor (C) simulates compliance effect. Identification of the best model and magnitudes of the endocardial and epicardial IMPs (IMPendo and IMPepi) was done retrospectively using data from studies in 28 anesthetized swine. Performance evaluation was based on comparison of model predicted vs. observed coronary distal pressure (DP) waveforms and endocardial-to-epicardial (endo-epi) flow ratios as determined by radiolabeled microspheres. The R-D-C model gave the best performance at IMPendo = 1.1 times left ventricular pressure (LVP), and IMPepi = 0.1.LVP + 15 mmHg; with good fit to DP (r = 0.98, slope of regression line = 1.0) and estimates of endo-epi flow ratio (r = 0.78, slope = 1.01, P less than 0.02, SEE = 0.21, n = 139). The R-D model gave comparable results even though capacitance was omitted. Although R-C and R models predicted distal coronary pressure well, they failed to predict endo-epi flow ratios (r less than 0.50). The R-D-C and R-D models were applied in seven prospective studies. Both models generated reasonable estimates of endo-epi flow distribution (r = 0.78, n = 50). Thus the R-D-C or R-D models of the stenosed coronary circulation can be used to provide reliable estimates of transmural blood flow distribution.

Animals↗
PubMed1995

Intervessel (arteries and veins) and heart/vessel selectivities of therapeutically used calcium entry blockers: variable, vessel-dependent indexes.

The intervessel selectivity indexes of the calcium entry blockers amlodipine, felodipine, isradipine, nicardipine, nifedipine, nitrendipine, diltiazem and verapamil were assessed by determining the potency of these compounds [concentration decreasing tension developed by KCl in blood vessels by 50% (bvlC50)] to relax several KCl-precontracted blood vessels (femoral, jugular and saphenous veins and left anterior descending and left circumflex coronary and renal arteries) precontracted with KCl. The concentrations of KCl (25 mM for arteries and 50 mM for veins) used gave a similar response in these vessels. Intervessel selectivity indexes are the ratios of the bvlC50 determined in two different vessels. The negative inotropic potency (hlC50) was ascertained in paced (2 Hz), isoproterenol-(10 nM) supported atrial strips, and for three of the compounds, in papillary muscles. This allowed calculation of heart/vessel selectivity or vasoselectivity (ratio of hlC50 and bvlC50). All compounds overcame almost entirely (85-100%) the vessel contractile response to KCl and strongly reduced (65-90%) the tension developed by myocardial preparations. The rank order for vasorelaxant potency (bvlC50 from approximately 1 to approximately 700 nM) was generally as follows: isradipine > or = nifedipine > or = nitrendipine > or = amlodipine > or = verapamil > or = felodipine > or = nicardipine > or = diltiazem. However, the rank order for negative inotropic potency (hlC50 spanning from approximately 200 to approximately 6000 nM) was isradipine > or = nifedipine > or = verapamil > or = diltiazem > or = amlodipine > or = nitrendipine > or = felodipine > or = nicardipine. All compounds were generally more potent in relaxing capacitance than conductance vessels. Furthermore, of the capacitance vessels, the jugular vein was the least susceptible to relaxation; among the conductance vessels, five of the eight compounds relaxed renal arteries with greater potency than coronary arteries. Consequently, the value of the heart/vessel selectivity index is intrinsically dependent on the vessel used to calculate it. Overall, nitrendipine was the most vasoselective calcium entry blocker studied, with selectivity indexes ranging from 28 to 523. In conclusion, 1,4-dihydropyridine calcium entry blockers generally have a much greater affinity for calcium channels present in micropig veins than in heart muscle myocytes. This is possibly due to tissue-specific features of L-type calcium channels. Finally, comparing the vasoselectivity index of various compounds has validity only if this index is calculated by using the same experimental procedure applied to the same vascular tissue and the same heart preparation taken from the same species.

Animals↗
PubMed1993

Effect of tetanic myocardial contraction on coronary pressure-flow relationships.

Cardiac contraction causes a decrease in coronary flow. Despite many studies, it is still not clear what mechanism or mechanisms are responsible for this flow decrease. The phasic nature of myocardial contraction and the complexities intrinsic to intact heart preparations make it difficult to elucidate the mechanisms. We therefore studied coronary pressure-flow relationships during steady-state (tetanic) contractions in the maximally vasodilated isolated canine interventricular septum to see whether waterfall-type behavior is present. Using ryanodine and electrical stimulation allowed the production of reproducible and reversible tetani. This preparation minimizes the difficulties associated with transmural variations and also the effects of intramyocardial capacitance. Two separate protocols were performed to delineate the pressure-flow relationships in the passive and tetanized states. The first compared diastolic and tetanized pressure-flow relationships. In the second protocol, 2,3-butanedione monoxime was added to obtain an intermediate contractile level, thus allowing the comparison of two contractile states. Both the diastolic and tetanized pressure-flow relationships were curvilinear in the low-pressure range. Linear and nonlinear fits to the data showed that the primary effect of contraction was a shift of the pressure-flow relationships to higher pressures at a given flow. This effect was graded by the level of contractility and was independent of developed stress. Although other mechanisms may also be operative, these results support the presence of waterfall behavior in the coronary vascular bed.

Animals↗
PubMed1990

Effects of alpha 1- and alpha 2-adrenoceptor antagonists on venous tone in conscious rats.

The dose-response effects of hexamethonium, prazosin and rauwolscine - a ganglionic blocker, alpha 1- and alpha 2-adrenoceptor antagonists, respectively - on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of body venous tone, were examined in conscious and unrestrained rats. Prazosin and rauwolscine were also administered to rats after venous tone was elevated by drug-induced hypotension via the infusion of the vasodilator drug hydralazine. The effects of these drugs were compared with those of the vehicle, acidified glucose solution, administered to control rats. In intact rats, i.v. infusions of prazosin and rauwolscine dose dependently decreased MAP; the highest dose of rauwolscine, but not prazosin slightly reduced MCFP. The i.v. infusion of hexamethonium reduced MAP and caused a marked dose-dependent decrease in MCFP. After venous tone was raised by hydralazine, both prazosin and rauwolscine dose dependently decreased MCFP. The decrease in MCFP caused by rauwolscine was significantly greater than that caused by prazosin. Our results show that in the basal condition, the capacitance vessels are somewhat resistant to the effects of alpha-adrenoceptor antagonists in contrast to the effects of ganglionic blockers. After venous tone was raised by reflex mechanisms, both alpha-adrenoceptor antagonists were effective in lowering venous tone, however, the effect of alpha 2-adrenoceptor antagonist is significantly greater than that of alpha 1-adrenoceptor antagonist.

Adrenergic alpha-Antagonists↗
PubMed1989

Lumbar sympathetic ganglia in man: an electrophysiological study in vitro.

A method has been developed for the removal, preservation and electrophysiological study 'in vitro' of sympathetic lumbar chains (L1-L3) from subjects undergoing lumbar ganglionectomy in the treatment of peripheral vascular diseases. Extracellular recordings from interganglionic trunks, and intracellular recordings from single sympathetic neurons, were performed. The extracellular experiments substantiated the concept, hitherto deduced from animal experiments, that the preganglionic fibres in the sympathetic lumbar chain are mainly of a descending nature. In fact, stimulation of the interganglionic trunk cranial to ganglia is always much more effective in driving ganglion neurons to fire than stimulation of the interganglionic trunk caudal to ganglia. The intracellular experiments produced a good definition of the main electrical characteristics of human sympathetic neurons. The results can be summarized as follows: the resting membrane potential ranged from 50 to 75 mV (63.4 +/- 9.2 mV; 21 neurons); action potential amplitude from 62 to 93 mV (74.3 +/- 8.1 mV; 27 neurons); membrane input resistance was 42.3 +/- 12.6 m omega (8 neurons) and total membrane capacitance 83.7 +/- 15.3 pF (8 neurons).

Action Potentials↗
PubMed2002

Impaired mechanisms of leukocyte adhesion in vitro by the calcium channel antagonist mibefradil.

PURPOSE: Enhanced adhesion to the vascular endothelium and excessive trafficking to extravascular locations can lead to serious tissue injury and destruction. Therefore, interfering with molecular mechanisms of leukocyte adhesion to the vascular endothelium is an important goal to block diseases like chronic inflammations and atherosclerosis. METHODS: We studied the influence of the calcium antagonists mibefradil (T-type channel blocker), amlodipine and verapamil (both L-type channel blockers) on mechanisms related to leukocyte adhesion using isolated peripheral human blood leukocytes. RESULTS: Mibefradil but not amlodipine and verapamil attenuated leukocyte adhesion in vitro. Regarding the mechanisms we found that mibefradil reduced the surface expression of beta2 integrins and L-selectin. The immobilization of the beta2 integrin subunit to the cytoskeleton that was inducible by receptor cross linking was impaired. Mibefradil was able to significantly inhibit the formyl-methionyl-leucyl-phenylalanine (fMLP) induced calcium rise, which suggests that mibefradil interfered with integrin signaling through blocking the intracellular calcium rise. SK&F 96365, a blocker of the capacitative calcium entry had no effect on cell adhesion and was less effective to influence integrin mediated mechanisms than mibefradil. CONCLUSION: Our data suggest that mibefradil or chemically related substances are promising to serve as potent drugs to prevent excessive adhesion of leukocytes.

Adult↗
PubMedDate not supplied

5-HT, alpha-adrenoceptors, and blood pressure. Effects of ketanserin in essential hypertension and autonomic insufficiency.

The serotonin (5-hydroxytryptamine, 5-HT) antagonist, ketanserin, has a high affinity for 5-HT2-receptors but it also binds to alpha 1-adrenoceptors. The compound (10 mg i.v.) lowered mean arterial pressure by 22% +/- 2% (mean +/- SEM, p less than 0.001) in 30 patients with essential hypertension. Measurements of heart rate, cardiac output, cardiac filling pressures, forearm blood flow, renal blood flow, and glomerular filtration rate revealed a hemodynamic pattern compatible with vasodilation of both resistance and capacitance vessels. This was accompanied by moderate reflex cardiostimulation. Ketanserin did not alter the pressor effect of bolus injections of (-)-phenylephrine hydrochloride (25, 50, 100, and 200 micrograms i.v.). Ketanserin also had a distinct hypotensive effect in four normotensive patients with autonomic insufficiency due to an efferent sympathetic lesion, who were unresponsive to phentolamine (20 mg i.v.). Thus, ketanserin in the dose we have used appears to lower blood pressure independently of alpha 1-adrenoceptor blockade. On the other hand, in patients with essential hypertension the antihypertensive effect of ketanserin was blunted by pretreatment with prazosin (12 mg/day). Therefore, a certain degree of alpha 1-adrenergic tone seems to be required for the compound to exert its full antihypertensive action. The findings are indirect evidence for a role of 5-HT in the maintenance of increased vascular resistance in essential hypertension. This may be related, at least in part, to the alleged amplifying effect of 5-HT on alpha 1-adrenoceptor-mediated vasoconstriction.

Adult↗
PubMed2000

Clinical experience with cerebral oximetry in stroke and cardiac arrest.

OBJECTIVE: To address the ability and reliability of the INVOS 3100A (Somanetics, Troy, MI) cerebral oximeter to detect cerebral desaturation in patients and the interpretation of cerebral oximetry measurements using the INVOS 3100A in stroke and cardiac arrest. DESIGN: Case reports of two patients. SETTING: Neurologic Intensive Care Unit of a University Hospital. PATIENTS: Two patients suffering occlusive strokes of the middle cerebral artery. One later suffered a cardiac arrest. RESULTS: The first case, a patient who suffered cardiac arrest while undergoing continuous cerebral oximetry, clearly demonstrated the ability of the INVOS 3100A to detect rapid tissue vascular oxyhemoglobin desaturation in the brain during circulatory arrest. In the second case, oximetry readings were obtained in a patient with a right internal carotid artery occlusion and an infarct in the middle cerebral artery territory. The circulation of the anterior cerebral artery (ACA) territory was intact. Stable xenon-computed tomography of local cerebral blood flow showed no perfusion in the infarct, and oximetry readings were between 60 and 65. In the border zone between the middle cerebral artery and the ACA, readings of 35 to 40 were obtained, and over the ACA territory, the readings were in the 60s. CONCLUSIONS: Oximetry by near infrared spectroscopy reflects the balance between regional oxygen supply and demand. In dead or infarcted nonmetabolizing brain, saturation may be near normal because of sequestered cerebral venous blood in capillaries and venous capacitance vessels and contribution from overlying tissue. In regionally or globally ischemic, but metabolizing brain, saturation decreases because oxygen supply is insufficient to meet metabolic demand. These observations are supported by previously reported "normal" readings in unperfused or dead brains.

Aged↗