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PubMed1992

The effect of FK664, a new cardiovascular drug, on systemic capacitance vessels in anesthetized dogs.

To characterize the cardiovascular effect of FK664, a compound developed for the treatment of heart failure, the mean circulatory pressure (MCP), cardiac output and other parameters were measured in open-chest anesthetized dogs. Milrinone, a cardiotonic agent, and nifedipine, a calcium channel blocker were used as reference substances. Nifedipine (10 micrograms/kg), FK664 (0.1 mg/kg) or milrinone (0.1 mg/kg) given intravenously reduced the total peripheral resistance in a similar extent (35-40%). Whereas nifedipine had no effect on MCP, FK664 produced a significant decrease in MCP. Milrinone caused a minimal decrease in MCP, but not significantly. These results indicate that FK664 dilates the systemic capacitance vessels. This action to reduce the pre-load would be beneficial in the treatment of heart failure.

Animals↗
PubMed1993

ACE inhibition with perindopril and atherogenesis-induced structural and functional changes in minipig arteries.

The effects of angiotensin-converting-enzyme (ACE) inhibition on atherosclerosis-induced changes in arterial function are unknown, as well as whether they are coupled to improvements of structural alterations in the arterial wall. An atherogenic (A) diet and the ACE inhibitor perindopril (P) were given concomitantly for 4 months to seven adult Pitman-Moore minipigs (7 months of age; A+P animals), which were compared with seven A and seven control (C) animals. Perindopril, at a daily dose of 4 mg PO that is commonly used in the clinical setting, induced a continuous 70% inhibition of serum ACE activity. At the end of the study, the atherosclerosis-induced impairment of arterial flow was investigated via the hemodynamics and vascular rheology of hindlimb arteries in non-barbiturate-anesthetized pigs. Structural alterations were evaluated from the histopathology of lesions in the arterial tree (abdominal aorta, left interventricular coronary artery [LIVCA], and brachiocephalic trunk [BCT]), with particular attention given to the analysis of the structure and composition of aortic elastic fibers. Atherosclerosis impaired the function of both capacitance and resistance arteries. Blood pressure (BP) rose significantly because of increased hindlimb peripheral resistance (HPR) and aortic input impedance (Zc), although blood flow was not affected. Altered aortic stress and elastic responses revealed that the stiffness of the aorta was markedly increased because of increased wall tension and reduced viscoelasticity, the viscous component being blunted in the arterial wall. Perindopril significantly opposed these alterations by reducing BP, HPR, and Zc and by returning parietal stiffness values to C values by increasing aortic compliance. ACE inhibition prevented the alteration of both stress and elastic responses. Major fibroproliferative fatty lesions were observed in the aorta and LIVCA, while moderate fibrosclerotic lesions were found in the BCT. Computerized densitometric analysis of orcein-stained elastin showed that elastic laminae fragmentation was prominent in the abdominal aorta, less in the LIVCA, and moderate in the BCT. Furthermore, the elastin content was reduced in the atherosclerotic aorta, although this loss of elastin was not associated with changes in the biochemical nature of alkali-insoluble elastin. Perindopril significantly prevented the development of atherosclerosis in the abdominal aorta, LIVCA, and BCT by decreasing the cross-sectional area of lesions as well as the number of lipid-laden cells in the abdominal aorta and LIVCA. In the abdominal aorta, ACE inhibition significantly prevented the alteration of elastic laminae by specifically preventing elastolytic fragmentation of dense elastic laminae, but it didn ot modify elastin content.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Mechanisms involved in the cellular calcium homeostasis in vascular smooth muscle: calcium pumps.

The regulation of cytosolic Ca2+ homeostasis is essential for cells, and particularly for vascular smooth muscle cells. In this regulation, there is a participation of different factors and mechanisms situated at different levels in the cell, among them Ca2+ pumps play an important role. Thus, Ca2+ pump, to extrude Ca2+; Na+/Ca2+ exchanger; and different Ca2+ channels for Ca2+ entry are placed in the plasma membrane. In addition, the inner and outer surfaces of the plasmalemma possess the ability to bind Ca2+ that can be released by different agonists. The sarcoplasmic reticulum has an active role in this Ca2+ regulation; its membrane has a Ca2+ pump that facilitates luminal Ca2+ accumulation, thus reducing the cytosolic free Ca2+ concentration. This pump can be inhibited by different agents. Physiologically, its activity is regulated by the protein phospholamban; thus, when it is in its unphosphorylated state such a Ca2+ pump is inhibited. The sarcoplasmic reticulum membrane also possesses receptors for 1,4,5-inositol trisphosphate and ryanodine, which upon activation facilitates Ca2+ release from this store. The sarcoplasmic reticulum and the plasmalemma form the superficial buffer barrier that is considered as an effective barrier for Ca2+ influx. The cytosol possesses different proteins and several inorganic compounds with a Ca2+ buffering capacity. The hypothesis of capacitative Ca2+ entry into smooth muscle across the plasma membrane after intracellular store depletion and its mechanisms of inhibition and activation is also commented.

Animals↗
PubMed1988

In situ analysis of alpha-adrenoceptors on arteriolar and venular smooth muscle in rat skeletal muscle microcirculation.

The purpose of this study was to determine whether both alpha 1- and alpha 2-adrenergic receptors exist on vascular smooth muscle of microvessels and whether adrenergic constriction of anatomically distinct microvascular segments is differentially subserved by either receptor subtype. The cremaster skeletal muscle of anesthetized rats was acutely denervated and suspended in a Krebs bath containing cocaine, normetanephrine, and propranolol to block uptake1, uptake2, and beta-receptors, respectively. Intravital microscopy was used to study large distributing arterioles (mean diameter, 100 microns), small precapillary arterioles (25 microns), and capacitance venules (140 microns). Concentration-response (diameter change) curves were obtained for bath-added agonists norepinephrine (mixed alpha 1/alpha 2), phenylephrine (alpha 1), and B-HT 933 (alpha 2) in the absence or presence of antagonists prazosin (alpha 1) and yohimbine (alpha 2). Apparent pD2(-log ED50) values for large arterioles and venules were, respectively, as follows: norepinephrine (7.41 and 7.15), phenylephrine (5.95 and 5.41), and B-HT 933 (5.05 and 5.06). Low concentrations of prazosin (10(-8) M) and yohimbine (10(-7) M) produced receptor subtype-selective antagonism and parallel, dextral displacement of norepinephrine curves for large arterioles and venules. The large arteriole pKB (-log KB) was 7.83 +/- 0.65 for prazosin and 7.36 +/- 0.46 for yohimbine. Higher concentrations of prazosin (10(-7) and 3 X 10(-7) M) and yohimbine (10(-6) M) produced further dextral but nonparallel displacement of norepinephrine curves. In contrast, receptor subtype-selective concentrations of only yohimbine inhibited adrenergic constriction of small, precapillary arterioles; but prazosin had no effect at receptor subtype-selective concentrations. These data suggest that adrenergic regulation of large arterioles and venules in skeletal muscle uses both alpha 1- and alpha 2-adrenoceptors. Precapillary arterioles, however, may be subserved predominantly by alpha 2-receptors.

Adrenergic alpha-Antagonists↗
PubMed1979

Comparative haemodynamic effects of dopamine and dobutamine in septic shock.

Septic shock associated with depressed myocardial function generally requires the use of catecholamine. Currently dopamine is often selected. Dobutamine is a newly developed catecholamine which has been shown to be of value in severe cardiomyopathic disease. The aim of this work was to determine the most appropriate drug by comparing haemodynamic responses to dopamine and dobutamine in 19 studies carried out in 11 patients with septic shock and heart failure. Cardiac index increased siliarly with dopamine and dobutamine (33%), as did stroke volume (respectively 26.4 and 25%). Arterial pressure increased by 17% with dopamine whereas it did not significantly change with dobutamine due to reduction in vascular resistance of 19%. Dobutamine decreased filling pressure, either right (14%) of left (28%) whilst they slightly but unsignificantly increased with dopamine. Pulmonary shunting increased more with dopamine (47%) than with dobutamine (16%), but PaO2 remained constant with both. Since septic shock is characterized by lowered arterial pressure and vasodilatation it is concluded that effects of dopamine on capacitance and resistance vessels make this drug more suitable. In addition it selectively increases renal blood flow. Nevertheless dobutamine could be appropriate, in case of very high filling pressures, severe peripheral vasoconstriction, marked pulmonary shunting and in some cases where dopamine becomes ineffective.

Catecholamines↗
PubMed1988

Vascular responses to hypercapnia in anesthetized dogs.

To evaluate the vascular responses to systemic acute mild hypercapnia (Pa(CO)(2) = 65 mmHg), we determined the vascular compliance with the relation between the change in circulating blood volume and the change in central venous pressure during and after fluid infusion in dogs anesthetized with halothane in normocapnia and hypercapnia. Circulating blood volume was measured continuously by (51)Cr-labeled erythrocyte dilution method together with hemodynamic variables. Small reduction in vascular compliance (8.1 +/- 1.0 ml.mmHg(-1).kg(-1) in normocapnia, 5.8 +/- 0.5 ml.mmHg(-1).kg(-1) in hypercapnia), large reduction in delayed compliance, which were quantitated by computer simulation using Maxwell's viscoelastic model, and significant increase in blood volume in central circulation were observed in hypercapnia. The essential change in hypercapnia was concluded as the vasoconstriction in capacitance vessels. Simultaneously, the reduction of total peripheral resistance (1.09 +/- 0.08 mmHg.min.kg.ml(-1) in normocapnia, 0.98 +/- 0.07 mmHg.min.kg.ml(-1) in hypercapnia) with no change in transvascular filtration coefficient (0.14 +/- 0.02 ml.mmHg(-1).min(-1).kg(-1)) suggests the increase in shunt flow in peripheral circulation.

Journal Article↗
PubMed2003

Norepinephrine induces slow calcium signalling in murine brown preadipocytes through the beta-adrenoceptor/cAMP/protein kinase A pathway.

The mechanism of adrenergically activated calcium signalling in isolated murine brown preadipocytes (stromal-vascular fraction) was studied with Fura-2. Norepinephrine (NE) generated in preadipocytes a slow Ca(2+)-response ( approximately 10 nM/min) without a burst and a maximum, whereas in mature brown adipocytes, the quick burst reached 1.5 microM [Ca(2+)](i). Thapsigargin, which is known to discharge Ca(2+) ions from the IP(3)-sensitive stores, initiated a huge capacitative calcium entry in mature brown adipocytes but failed to stimulate a response in preadipocytes. The beta-selective antagonist nadolol almost completely prevented the effect of NE on [Ca(2+)](i), while the antagonist of alpha-adrenoceptors phentolamine caused only a approximately 25% reduction of the cellular response. Forskolin or the cell-permeable Br-cAMP caused [Ca(2+)](i) rise, which were even higher than with NE. The protein kinase A (PKA) inhibitor N-[2-(p-bromocynnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89) reduced and the phosphodiesterase inhibitors 3-isobutyl-1-methylxanthine (IBMX), N-cyclohexyl-N-(2-hydroxyethyl)-4-(6-(1,2-dihydro-2-oxoquinolyloxy))butyramide (OPC-3911), 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidone (Ro 20-1724) or the protein phosphatase inhibitor okadaic acid enhanced the NE-, isoproterenol- or forskolin-initiated cellular calcium responses. It was concluded that (i) brown preadipocytes lacked a trigger mechanism of initiation of [Ca(2+)](i) rises and (ii) the cAMP- and protein kinase A-mediated phosphorylation played an important role in the beta-adrenoceptor-initiated calcium signalling in these cells. All these features distinguish brown adipocyte precursors from differentiated brown adipocytes, where calcium signalling is initiated exclusively via alpha(1)-adrenoceptors and the trigger mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed2002

Characterization of hypoxia-induced [Ca2+]i rise in rabbit pulmonary arterial smooth muscle cells.

We have investigated the effects of hypoxia on the intracellular Ca2+ concentration ([Ca2+]i) in rabbit pulmonary (PASMCs) and coronary arterial smooth muscle cells with fura-2. Perfusion of a glucose-free and hypoxic (PO2<50 mmHg) external solution increased [Ca2+]i in cultured as well as freshly isolated PASMCs. However it had no effect on [Ca2+]i in freshly isolated coronary arterial myocytes. In the absence of extracellular Ca2+, hypoxic stimulation elicited a transient [Ca2+]i increase in cultured PASMCs which was abolished by the simultaneous application of cyclopiazonic acid and ryanodine, suggesting the involvement of sarcoplasmic reticulum (SR) Ca2+ store. Pretreatment with the mitochondrial protonophore, carbonyl cyanide m-chlorophenyl-hydrazone (CCCP) enhanced the [Ca2+]i rise in response to hypoxia. A short application of caffeine gave a transient [Ca2+]i rise which was prolonged by CCCP. Decay of the caffeine-induced [Ca2+]i transients was significantly slowed by treatment of CCCP or rotenone. After full development of the hypoxia-induced [Ca2+]i rise, nifedipine did not decrease [Ca2+]i. These data suggest that the [Ca2+]i increase in response to hypoxia may be ascribed to both Ca2+ release from the SR and the subsequent activation of nifedipine-insensitive capacitative Ca2+ entry. Mitochondria appear to modulate hypoxia induced Ca2+ release from the SR.

Animals↗
PubMed1992

Effects of milrinone on systemic capacitance vessels in relation to venous return and right ventricular pump function.

To investigate the effect of milrinone (MIL) on systemic capacitance vessels, we measured the mean circulatory filling pressure (MCP) in anesthetized open chest dogs. We measured hemodynamic parameters (a) at baseline blood volume (BV), (b) immediately after bloodletting (5 ml/kg), and (c) immediately after dextran injection (5 ml/kg). These measurements were taken in a control group (n = 8) and in a MIL group (n = 8), where MIL (100 + 2.5 micrograms/kg/min) was administered i.v. The extra volume (EV) was obtained by extrapolating the straight line that was fit to the MCP-BV plot. MIL significantly decreased the EV, from 22.8 +/- 1.0 to 19.1 +/- 0.4 ml/kg, indicating that MIL dilates the systemic capacitance vessels. MIL shifted the right ventricular output curve to the left and upward and shifted the venous return curve to the left and rotated it clockwise. Thus, venous return was increased by decreasing the resistance to venous return and by improving right ventricular pump function. Next we evaluated the effects of MIL (100 micrograms/kg) on systemic capacitance and resistance vessels from changes seen in the MCP and the total peripheral resistance (TPR), respectively. In the untreated dogs, MIL decreased TPR significantly without affecting MCP. In dogs pretreated with total spinal anesthesia or phenoxybenzamine, MIL significantly decreased both MCP and TPR. This suggests that the intrinsic venodilator action of MIL is modified by the baroreflex in untreated animals. MIL decreased the MCP and TPR elevated previously by norepinephrine. One would, therefore, predict that MIL would dilate the systemic capacitance vessels in patients with congestive heart failure.

Anesthesia, Spinal↗
PubMed1988

In vivo pharmacological studies with SK&F 94836, a potent inotrope/vasodilator with a sustained duration of action.

1. SK&F 94836 (racemate) was studied in vivo for its cardiovascular properties in cats and dogs. 2. In anaesthetized cats and dogs SK&F 94836 administered intravenously caused increases in left ventricular contractility and decreases in peripheral vascular resistance at similar doses, thus demonstrating the compound to be a mixed acting positive inotropic/vasodilator agent. 3. In conscious instrumented dogs SK&F 94836 was active via the oral as well as intravenous route. 4. The inodilator activity of SK&F 94836 in conscious and anaesthetized animals occurred in association with minimal changes in either blood pressure or heart rate. 5. Detailed studies carried out on anaesthetized cats indicated that SK&F 94836 caused a balanced dilatation of both resistance and capacitance blood vessels. 6. Haemodynamic studies in anaesthetized cats indicated that as a consequence of the inotropic/vasodilator actions, SK&F 94836 caused significant increases in cardiac output and stroke volume. 7. Detailed studies in anaesthetized dogs indicated that significant inodilator activity occurred in the absence of an increase in myocardial oxygen consumption. 8. The duration of action of SK&F 94836 was sustained following both i.v. and oral administration. 9. We conclude that SK&F 94836, as an orally active inotropic/vasodilator agent with a sustained duration in vivo, has potential utility in the treatment of congestive heart failure.

Anesthesia↗
PubMed1989

Clinical pharmacotherapeutics of doxazosin.

Doxazosin is the latest in a series of highly selective postsynaptic alpha 1-adrenoceptor inhibitors. It is readily absorbed, with high bioavailability and a relatively long plasma half-life, neither of which property is influenced by age. This accounts for the prolonged pharmacologic activity of doxazosin following a single oral dose. Its prime pharmacodynamic activity resides in its ability to counter sympathetic vasoconstriction of the systemic arteriolar resistance vessels and venous capacitance system, which enables the drug to target the major pathophysiologic abnormality in hypertension, i.e., the generalized systemic arteriolar constriction. The widespread vasodilation induced by doxazosin relieves both cardiac preload and afterload and, consequently, reduces left ventricular wall stress and myocardial oxygen consumption. In hypertension, doxazosin reduces blood pressure both at rest and during exercise by reduction of systemic vascular resistance without precipitating substantial reflex cardiac stimulation. The effects are maximal on the standing blood pressure between two and four hours after ingestion; due to doxazosin's relatively slow absorption, postural hypotension is infrequent. Its antihypertensive activity is maintained over 24 hours following a single oral dose, and the optimal dose range is 2 to 8 mg once daily. The antihypertensive efficacy of doxazosin has been shown to be comparable with that of other alpha-adrenoceptor inhibitors, beta-blocking drugs, diuretics, calcium antagonists, and angiotensin-converting enzyme inhibitors. In contrast to other conventional antihypertensive drugs, a unique feature of alpha-adrenoceptor-inhibiting drugs, including doxazosin, is their ability to reduce the plasma concentrations of triglycerides, total cholesterol, and low-density lipoprotein cholesterol and to increase high-density lipoprotein cholesterol concentration. This contrasts with the opposite effect on lipid levels induced by hydrochlorothiazide and atenolol seen in comparative studies. Side effects show no predilection for any organ system, and the overall incidence of such effects compares well with those of other commonly used antihypertensive drugs. This unique combination of antihypertensive efficacy and favorable effect on blood lipid levels indicates that once-daily treatment with doxazosin holds considerable promise in the treatment of hypertension, both from the point of view of its antihypertensive efficacy and also from its primary preventative potential.

Adrenergic alpha-Antagonists↗
PubMed1991

Reduced orthostatic tolerance following 4 h head-down tilt.

The cardiovascular responses to a 10-min 1.22 rad (70 degrees) head-up tilt orthostatic tolerance test (OST) was observed in eight healthy men following each of a 5-min supine baseline (control), 4 h of 0.1 rad (6 degrees) head-down tilt (HDT), or 4 h 0.52 rad (30 degrees) head-up tilt (HUT). An important clinical observation was presyncopal symptoms in six of eight subjects following 4 h HDT, but in no subjects following 4 h HUT. Immediately prior to the OST, there were no differences in heart rate, stroke volume, cardiac output, mean arterial pressure and total peripheral resistance for HDT and HUT. However, stroke volume and cardiac output were greater for the control group. Mean arterial pressure for the control group was less than HDT but not HUT. Over the full 10-min period of OST, the mean arterial pressure was not different between groups. Heart rate increased to the same level for all three treatments. Stroke volume decreased across the full time period for control and HDT, but only at 3 and 9 min for HUT. There was a higher total peripheral resistance in the HDT group than control or HUT. The pre-ejection period to left ventricular ejection time ratio was less in HDT than for control or HUT groups. These data indicate a rapid adaptation of the cardiovascular system to 4 h HDT that appears to be inappropriate on reapplication of a head to foot gravity vector. We speculate that the cause of the impaired orthostatic tolerance is decreased tone in venous capacitance vessels so that venous return is inadequate.

Adult↗
PubMed1980

Effects of changes in the aortic input impedance on systolic pressure-ejected volume relationships in the isolated supported canine left ventricle.

We examined the effects of aortic input impedance alteration on left ventricular pressure, aortic flow and ejected volume (integral value of aortic flow), in an isolated blood perfused ejecting canine heart, with special reference to end-systolic values. A hydraulic model which stimulates an aortic input impedance was attached to the aortic root of an excised heart. Left ventricular end-diastolic pressure was kept constant by electrical pacing. Three coronary arteries were perfused with arterial blood from support dogs. When the peripheral resistance in the hydraulic model was changed, there were inverse linear relationships between stroke volume and mean left ventricular systolic pressure and between ejected volume and pressure at end-systole. Time interval from the onset of contraction to end-systole did not change. Thus the relation between stroke volume and mean left ventricular pressure obtained by changes in peripheral resistance is governed by a source resistance, which can be considered as the contractile state of the ventricle. When the capacitance (arterial compliance) was changed, there was no inverse linear relation between stroke volume and mean systolic pressure. In many cases, there was an inverse linear relationship between ejected volume and pressure at end-systole. However, an increase in capacitance prolonged the time interval from the onset of contraction to end-systole. We conclude that the end-systolic pressure-ejected volume relationship in the ejecting heart is governed not only by contractility but also by arterial capacitance.

Animals↗
PubMed1982

Internal capacitance and resistance allow prediction of right ventricle outflow.

The relationship between right ventricle afterloading pressure (P) and outflow (Q) was studied in three isolated canine right ventricle (RV) preparations. Right atrial pressure was held constant while graded elevations in P were induced with stepwise occlusions of the right and left branches of the pulmonary artery. P and Q signals were collected and analyzed using a digital computer system. Data were analyzed by assuming a model structure for the RV and comparing resultant model predictions of Q with actual observations. The model structure was modified in accordance with the discrepancy between prediction and observation to improve the model's predictive capability. The initial model tested was the time-varying linear relationship between ventricular volume and pressure. Utilizing this model, accurate predictions of RV outflow in the face of varying pressure afterloads could not be made. The addition of a series resistance to this elementary model resulted in marked improvement in predictive performance. The addition of greater complexity to the model gave only marginal improvement to the model's predictive capability. It was concluded that a time-varying capacitance and series resistance adequately model internal properties of the RV that relate outflow to afterloading pressure.

Animals↗
PubMedDate not supplied

The influence of smoking cessation on hemodynamics and arterial compliance.

Cigarette smoking is associated with consistent changes in small arteries and arterioles. Recently, arterial compliance was determined in smokers; however, the effect of smoking cessation on arterial compliance has not yet been investigated. The objective of the study was to assess how smoking cessation, achieved with use of behavioral and pharmacologic therapy, influences vascular compliance and arterial stiffness in smokers. In an open-label study, 60 habitual smokers were treated for 2 months with buproprion 300 mg per day and personal and group conversations in order to facilitate smoking cessation. Hemodynamic variables, including vascular compliance and augmentation index (AI), were measured twice, at the beginning of the study and after 6 months. Of the 60 smokers, 35 stopped smoking and 25 failed at the end of the 2-month treatment period. Of the 35 who were initially successful, 12 went back to smoking, and thus only 23 remained nonsmokers at the end of 6 months. Smoking cessation was accompanied by significantly lower arterial pressure and heart rate but by weight gain. Among the 23 subjects who stopped smoking for 6 months capacitive compliance (C(1)) did not change but oscillatory compliance (C(2)) rose significantly (from 5.1 +/-2.3 to 6.3 +/-3.0 p<0.01), and AI decreased significantly (from 63.1 +/-22 to 50.6 +/-17 p<0.05), whereas in smokers who still smoked after this period, both C(1) and C(2) and augmentation index did not change significantly from their basal values. The authors conclude that smoking cessation improves arterial stiffness as assessed by the augmentation index, owing mainly to increasing the small artery compliance, which is known to be an early index of endothelial damage.

Antidepressive Agents↗
PubMedDate not supplied

Peripheral vascular effects of a new dopamine analog: 5-6-dihydroxy-2-methylaminotetralin (M-8).

It has been reported that the cyclic dopamine analog 5,6-dihydroxy-2-methylaminotetralin (M-8) in an adrenergic agonist in the dog. In this study, the effects of M-8 on hindlimb vascular responses was determined in the dog. In group I (n = 10), hindlimb vascular responses to ipsilateral femoral artery injections of M-8 before and after adrenergic blockade were determined. Mean femoral artery and peripheral venous pressures and heart rate responses to intra-arterial injections of M-8 were recorded. Mean femoral artery flows were measured by an electromagnetic flowmeter. Low doses of M-8 (0.0001-01 micrograms/kg) elicited transient dilatory responses, while higher doses (1-10 micrograms/kg) produced a biphasic response consisting of a dilation followed by constriction. The dilatory responses were attenuated following pretreatment with propranolol and were augmented by pretreatment with phenoxybenzamine. The constrictor responses were attenuated by pretreatment with phenoxybenzamine. The constrictor responses were attenuated by pretreatment with pehnoxybenzamine and augmented by pretreatment with propranolol. These responses were not reflex-mediated, since the hemodynamic parameters in the contralateral limb were not altered during the depressor or pressor phases. In group II (n = 5), the effects of intra-arterially infused M-8 (0.01 micrograms/kg/min) on plethysmographically determined hindlimb venous capacitance were determined. Intra-arterial infusion increased venous capacitance through beta-adrenergic mechanisms without altering mean arterial pressure and heart rate or contralateral limb mean femoral artery flows. M-8 is a potent peripherally acting adrenergic agent.

Animals↗
PubMed1992

Pulmonary capillary pressure: a review.

OBJECTIVES: To demonstrate the importance of a) measuring effective pulmonary capillary pressure and b) evaluating the longitudinal distribution of pulmonary vascular resistance relative to pre- and postcapillary resistances. To review the development of methods used to determine pulmonary capillary pressure in experimental animal and clinical studies. DATA SOURCES: Human, animal, and modeling studies published since 1966 identified through MEDLINE and a review of bibliographies of relevant articles. STUDY SELECTION AND DATA EXTRACTION: All studies identified were reviewed with an emphasis on recent studies and those studies identifying various methodologies used to determine capillary pressure. Experimental studies were selected for their historical value and applicability to the clinical setting. DATA SYNTHESIS: Different models of the pulmonary circulation have been proposed. The electrical circuit model, which incorporated capacitance elements and two or four resistive elements, has been the basis for the determination of pulmonary capillary pressure in isolated lungs and in situ lungs in animals and patients. Methods used to determine pulmonary capillary pressure from a pulmonary arterial pressure tracing after balloon occlusion are: a) division of waveform into two components and logarithmic extrapolation of the slow component to occlusion time; b) visual determination of the pressure inflection point of the pulmonary arterial pressure tracing; and c) computer processing of the total arterial pressure transient. Both ease of calculations and difficulties can arise when each method is used. CONCLUSIONS: Pulmonary capillary hydrostatic pressure is an important determinant of pulmonary edema especially in the setting of pulmonary hypertension and adult respiratory distress syndrome. Hypoxia, sepsis, cardiac valvular disease, and inflammatory mediators produce variable changes in the longitudinal distribution of pulmonary vascular resistance so that an increased capillary pressure cannot be predicted by the pulmonary arterial or occlusion pressure. For proper therapy aimed at decreasing pulmonary vascular resistance, it is important to determine whether or not the particular therapy increases capillary pressure. Pulmonary capillary pressure is the most important determinant of lung fluid balance and is the major physiologic parameter that should be measured when various forms of plasma volume expansion and pulmonary vasodilators are used in the critically ill patient.

Animals↗