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PubMed1979

Whole body transvascular filtration coefficient and interstitial space capacitance.

Infusion experiments with Ringer's solution were performed on 5 splenectomized dogs with continuous monitoring of blood volume and hematocrit. The plasma volume was calculated from these data and followed during the infusion and also during the recovery period. Applying electrical equivalent simulation analysis to the result of the plasma volume, the capacitance of the interstitial fluid space and the transvascular filtration coefficient of water in the whole body were determined simultaneously. The mean values of the capacitance and the coefficient were 5.91 ml/kg-mmHg and 0.314 ml/min-kg-mmHg, respectively. From this simulation study, a transfer function which predicts the fluid shift between the vascular system and the interstitial fluid space was also derived. Using the transfer function, predictions of the changes in plasma volume are possible from any given rate of infusion.

Animals↗
PubMed1994

Intra-arterial pressure wave parameters modeled using electrical analogs.

An Electrical Model was developed to help identify parameters obtained from dynamic pressure data on the in vitro rat aortic artery. The data was obtained using a Multifunction Pressure Generator (MPG) and recording MPG Input Pressure (Pi) and Intraarterial Pressure (Po). Transfer functions of the form Po/Pi = (A1S+Ao)/(B2S2 + B1S+Bo) were obtained and it is necessary to link A1, Ao, B2, B1 and Bo to the Biological Parameters of Inertance (M), Vascular Resistance (R) and Compliance (C). Using the Electrical Analogs to P, M, R and C which are Voltage (V), Inductance (L), Resistance (Re), and Capacitance (Ce), an Electrical Model was built. The Electrical Model has the form Vo/Vi = (Re1S + 1/Ce)/[LS2 + (Re1 + Re2)S + 1/Ce]. Since Ao = Bo = 1 from our experimental data we multiplied the denominator and numerator by Ce to obtain Vo/Vi = (CeRe1S + 1)/[CeLS2 + Ce(Re1 + Re2)S + 1]. We then transformed our Electrical Model to its Pressure Equivalent and obtained Po/Pi = (CR2S + 1)/[CMS2 + C(R1 + R2)S + 1]. Since R2 is less than R1 + R2 we theorize that total R is composed of two viscoelastic or resistive elements R1 and R2. Using measured values of compliance it should be possible to obtain reasonable values for R1, R2 and Inertance.

Animals↗
PubMedDate not supplied

Central nervous control of venous tone. III. Responses of capacitance and resistance vessels of skin to bulbar and hypothalamic stimulation.

Electrical stimulation of 350 points in the bulbar formation of 35 dogs under chloralose anaesthesia demonstrated the presence of sites producing increase or decrease of systemic arterial pressure (SAP) in the same general morphological limits of bulbar pressor and depressor regions as described by earlier authors. Simultaneous recording of pressure changes in the cutaneous vessels however demonstrated that pressure changes in these vessels did not correspond to the pressor or depressor effects of the SAP. Instead, responses were obtained in which pressures in cutaneous capacitance and resistance vessels followed a trend which was opposite in direction and magnitude to that of SAP. Thus there were 30 depressor sites which produce increase in cutaneous vessel pressure and 23 pressor sites which produced a fall in cutaneous vessel pressure. For a marked rise in the SAP, only 62 sites elicited equally marked increase in both capacitance and resistance vessel pressure, while another 52 elicited only a small increase of equivalent magnitude in the capacitance and resistance vessels. Stimulation of 84 points produced dissimilar effects on capacitance and resistance vessels out of which 38 elicited moderate increase in resistance vessel tone with minimal changes in the capacitance vessel tone, while 46 points elicited moderate increase in capacitance vessel tone with only a small increase in the resistance vessel tone. These points were diffusely admixed in the bulbar reticular formation. Effects which were exclusive to the capacitance and resistance vessels of skin, singly or in combination, without affecting the SAP were elicited from 12 points while another 28 points produced marked rise or fall of systemic arterial pressure without affecting the cutaneous vessels. These observations suggest that the neuronal organisation regulating cardiovascular activities at the bulbar level is quite complex having the capacity to generate varying activities in different components of the vascular circuits by differentially altering the discharge of the efferent sympathetic fibres on the one hand, and marked selectivity of action on any particular vascular bed or circulatory component on the other hand. Stimulation of 93 points in the hypothalamus produced similar patterns of response as obtained from medulla oblongata. In addition, stimulation of 6 points in the anterior hypothalamus produced a distinctive response accompanied by dilatation of cutaneous resistance and capacitance vessels with marked increase in respiratory rate and minimal changes in the SAP. This type of response which resembled the physiological response employed for heat loss was not obtained from any stimulation site in the medulla oblongata.

Animals↗
PubMed1990

Regional distribution of vasoconstrictor tone in acute spinal rats.

Rats, chronically instrumented with an electromagnetic flow probe around the carotid, superior mesenteric, or renal artery, or the terminal aorta as well as having an arterial and venous catheter, were anesthetized with either and submitted to high spinal cord transection. One hour later, when the rats had recovered consciousness and the arterial pressure had recovered partially, hexamethonium was intravenously injected for ganglionic blockade. Peripheral resistance (arterial pressure/regional flow) was decreased significantly by ganglionic blockade in the carotid and renal areas but not in the superior mesenteric and hindquarter (terminal aortic) areas. This suggests the presence of sizable vasoconstrictor tone to resistance vessels in the carotid and renal areas but not in the superior mesenteric and hindquarter areas in the acute spinal rat. This distribution of vasoconstrictor tone is similar to that in intact conscious rats in the resting state and suggests the possibility that the vasoconstrictor tone for resistance vessels in intact rats is also for the most part generated in the spinal cord. Spinal transection decreased blood flow in all the four regions, suggesting a decrease in cardiac output due to dilation of capacitance vessels. It is possible that, in intact rats at rest, the so-called medullary vasomotor center is sending tonic impulses for the most part to capacitance vessels.

Animals↗
PubMed1993

In-vivo effects of endothelin-1 and ETA receptor blockade on arterial, venous and capillary functions in skeletal muscle.

Results from in vitro studies have indicated that endothelin-1 is a main candidate for endothelium-derived contracting factors. The aim of this in vivo study was to describe in quantitative terms the effects of endothelin-1 (ET-1), and of ETA receptor blockade, on vascular tone (resistance) in large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns) and the veins, as well as on capillary pressure and fluid exchange in cat gastrocnemius muscle. Endothelin-1 (100-1600 ng kg-1 min-1, i.a.) elicited, after an initial transient dilation, a strong dose-dependent constrictor response in all three consecutive vascular sections, yet with a preferential action on the small arterioles and the veins. The vasoconstriction developed very slowly over about 1 h and was also long-lasting after cessation of the infusion. Our main quantitative analysis refers to effects elicited by 20 min long i.a. infusions of ET-1 at a dose of 400 ng kg-1 min-1. At the end of this period, the peptide caused, on average, a three-fold increase in total regional vascular resistance, in turn explained by a 70% increase in large-bore arterial resistance, a 280% increase in arteriolar resistance and a 220% increase in venous resistance. The latter effect was also manifested as a pronounced capacitance response, and as a decrease in the pre- to post-capillary resistance ratio leading regularly to a rise in capillary pressure, net transcapillary fluid filtration and oedema formation which is unusual for a vasoconstrictor. The new specific competitive ETA receptor antagonist FR 139317 was found to be fully effective in vivo, insofar as it abolished the constrictor response to endothelin-1. ETA receptor blockade, or administration of phosphoramidon, an inhibitor of ET-1 production, did not influence the level of basal vascular tone, indicating no significant endogenous release of ET-1 under resting conditions. This contrasts to the established pronounced endogenous release of endothelium-derived nitric oxide. Finally, vascular myogenic regulation was found not to be mediated by ET-1. The results, taken together, suggest a possible role of ET-1 in long-term, rather than short-term, regulation of vascular tone in vivo, perhaps especially during pathophysiological conditions.

Animals↗
PubMed1995

Optimisation of gene transfer into vascular endothelial cells using electroporation.

OBJECTIVES: We have examined the conditions required to obtain optimum transfection efficiencies for human umbilical vein endothelial cells by transduction with a plasmid conferring neomycin resistance. MATERIALS AND METHODS: Preliminary studies examined the effects of electric discharges using the Biorad Gene Pulser on endothelial cells. Post-electroporation, there was a significant decrease in cell survival with increasing voltages (100-400 volts; p = 0.03), capacitances [125-960 microFarads (microF); p = 0.02], number of electric pulses (1-2; p = 0.03) and decreasing cell concentrations (p = 0.01). The optimal cell concentration was 3 x 10(6) cells/ml. Transfection studies utilised the neomycin resistance expressing plasmid, pTCF; transfectants were selected with the neomycin analogue G-148. RESULTS: Electro-transfection was optimised with increasing voltages (p = 0.02) and capacitances (p = 0.01) using a single pulse. Optimal transfection was obtained using 400 volts with a capacitance of 960 microF using a single pulse; the median transfection efficiency was 10%. Transduced endothelial cells stably expressed the plasmid for 12 days and at least two cell passages. CONCLUSIONS: The results indicate that endothelial cells can be efficiently transduced by electroporation to stably express an introduced gene. This may have important implications in vascular surgery.

Cell Survival↗
PubMed1986

Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog.

The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously. Hypercapnic gas challenge (8% CO2, 30% O2 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance. Hypoxic gas challenge (6% O2 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.

Airway Resistance↗
PubMed2004

Remifentanil induces systemic arterial vasodilation in humans with a total artificial heart.

BACKGROUND: To assess intrinsic vascular effects of remifentanil, increased concentrations were infused in critically ill patients with a total artificial heart. METHODS: In the early postoperative period after implantation of a total artificial heart, nine ventilated patients requiring short general anesthesia were included in this study. After anesthesia was induced with 0.3 mg/kg intravenous etomidate, the artificial heart settings were modified to render cardiac output "preload-independent." While maintenance of anesthesia was ensured by a continuous infusion of etomidate, increased concentrations of remifentanil (from 0.1 to 1 microg x kg(-1) x min(-1)) were infused in steps of 5 min under hemodynamic monitoring, including left and right atrial pressures, systemic and pulmonary arterial pressures, and left and right cardiac indices. The invasive procedure was started under the highest concentration of remifentanil tolerated by the patient. Infusion of remifentanil was stopped at the end of the invasive procedure, while etomidate infusion was maintained. New hemodynamic measurements were performed at the end of the 12-min recovery period. RESULTS: Remifentanil produced a dose-dependent and significant decrease in systemic arterial pressure and vascular resistances (n = 9) from a concentration of 0.25 microg x kg(-1) x min(-1). No significant changes were observed on pulmonary vascular resistances (n = 6). Neither right (n = 9) nor left (n = 6) atrial pressures were affected by remifentanil infusion. Hemodynamic variables returned to baseline value over the 12-min recovery period. CONCLUSIONS: In humans with a total artificial heart, remifentanil induces a systemic arterial vasodilation without significant effect on the capacitance vessels.

Adult↗
PubMed1986

Analysis of vascular responses in rat hindquarters arterial resistance vessels and veins in situ.

The venous compartment plays a critical role in circulatory control. The present series of experiments was conducted to assess simultaneously effects of vasoactive drugs on arterial resistance and venous capacitance vessels of the rat hindquarters perfused with physiological salt solutions (SS). Retrograde infusion of SS into rat hindquarters via the vena cava resulted in an increase in hindquarters venous pressure (Pv). The range of mean volumes required to increase Pv to 20 and 30 mm Hg was 1.7 +/- 0.1 to 2.9 +/- 0.4 and 3.8 +/- 0.3 to 6.9 +/- 0.3 ml, respectively, in various groups of rats during a control period. Perfusion of the hindquarters with an SS containing 80 mM K+ reduced the volume required to increase Pv to 20 and 30 mm Hg to 47 +/- 2 and 42 +/- 2% of control, respectively, indicating venoconstriction. K+ (80 mM) SS also increased aterial perfusion pressure (Pa; measured from a sidearm off of the inflow catheter) to 141 +/- 9 mm Hg, indicating arterial vasoconstriction. Arterial and venous responses to 80 mM K+ were attenuated markedly by perfusion with SS containing zero Ca and 2 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid, indicating dependence on extracellular Ca. Phentolamine (10(-5) M) attenuated the arterial and venous response to 80 mM K+, indicating an alpha adrenergic contribution. Arterial responses to 80 mM K+ were attenuated markedly by the Ca entry blockers nifedipine (10(-6) and 10(-5) M) and verapamil (10(-6) and 10(-5) M). In contrast, venous responses were not affected by nifedipine and were reduced slightly only at the high concentration of verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[A model of the coronary vascular bed and its verification by a physiological experiment].

We analysed the relationship between artery pressure (AP) and coronary flow (F) in the canine coronary bed, using an electrical analog model of the coronary circulation. The model contained a capacitance of epicardial vessels, input and terminal resistances, diode, and the number of e.m.f., simulated the intramyocardial pressure and zero-flow pressure. These e.m.f. are assumed to be a linear functions of left ventricular and aortic pressure. The value of coronary blood flow was calculated from experimental curves of AP and LVP and setting parameters. Good agreement was obtained between theoretical and experimental curves of coronary blood flow.

Animals↗
PubMed2001

Intercellular communication in cultured human vascular smooth muscle cells.

Intercellular communication through gap junction channels plays a fundamental role in regulating vascular myocyte tone. We investigated gap junction channel expression and activity in myocytes from the physiologically distinct vasculature of the human internal mammary artery (IMA, conduit vessel) and saphenous vein (SV, capacitance vessel). Northern and Western blots documented the presence of connexin43 (Cx43) in frozen tissues and cultured cells from both vessels. Northern blots also confirmed the presence of Cx40 mRNA in cultured IMA and SV myocytes. Dual whole cell patch-clamp experiments revealed that macroscopic junctional conductance was voltage dependent and characteristic of that observed for Cx43. In the majority of records, in both vessels, single-channel activity was dominated by a main-state conductance of 120 pS, with subconducting events comprising less than 10% of the amplitude histograms. However, some records showed "atypical" unitary events that had a conductance similar to Cx40 (approximately 140-160 pS), but gating behavior like that of Cx43. As such, it is conceivable that the presence and coexpression of Cx40 and Cx43 in IMA and SV myocytes may result in heteromeric channel formation. Nonetheless, in terms of gating, Cx43-like behavior clearly dominates.

Aged↗
PubMedDate not supplied

Effects of prazosin and phenoxybenzamine on alpha- and beta-receptor-mediated responses in intestinal resistance and capacitance vessels.

Previous studies have suggested that prazosin is a selective post-synaptic alpha-receptor blocker. It has also been suggested that it may have greater blocking actions on arterioles than on venous beds. These aspects have been investigated in cats anesthetized with pentobarbital. Prazosin had no effect on conductance in the acutely denervated hindlimb bed but caused a slowly developing vasoconstriction in the acutely denervated intestinal bed. The vasoconstrictor responses to sympathetic nerve stimulation were reduced to a similar extent in both vascular beds. Since maximal doses of prazosin produce only partial block of the alpha-receptor responses, there may be more than one type of postsynaptic alpha-receptor, and it is suggested that the postsynaptic receptors are of both alpha 1- and alpha 2-types. In the intestinal bed, prazosin produced similar reductions in both resistance and capacitance responses to sympathetic nerve stimulation. In isolated guinea pig aorta and portal vein, prazosin blocked the responses to noradrenaline competitively, and the pA3 values for the aorta and portal vein were similar. Thus, no selectivity for resistance vessels compared to capacitance vessels could be demonstrated in the intestine, and this result is compared to our previous observations in the liver. Although prazosin only reduced the vasoconstrictor responses to sympathetic nerve stimulation in the intestine, phenoxybenzamine reversed the response to a beta-receptor-mediated vasodilatation, as reported some years ago. These observations support our earlier hypothesis that nerve stimulation does not normally activate beta-receptors, but after phenoxybenzamine, the increased release of noradrenaline combined with alpha-receptor blockade results in a beta-receptor-mediated vasodilatation in the intestinal bed.

Animals↗
PubMedDate not supplied

Ultrastructural localization of NADPH-diaphorase activity in the endothelial cells of human nasal respiratory mucosa.

The cavernous sinuses are the most peculiar feature of the nasal angioarchitecture, due to their ability to retain a large quantity of blood in reply to a variety of topical and systemic stimuli. Recently, nitric oxide (NO) has seemed to be crucially involved in the nasal vascular regulation. The distribution of NO-synthase (NOS), the enzyme that catalyzes the formation of NO, was studied in the endothelium of nasal blood vessels by the ultracytochemical detection of reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) enzymic activity. The endothelium of the cavernous sinuses appeared strongly positive, whereas the endothelium of arterioles was occasionally labeled. The endothelial cells of capillaries and venules were found to be NADPH-d negative. The strong enzymic activity observed in the cavernous sinuses suggests a major role of NO in the capacitance vessels compared to the resistance vessels. The hypothesis of a reciprocal inhibition between the NOS enzymic pathways present in the respiratory epithelium and in the endothelium of cavernous sinuses is put forward. The nasal disorders characterized by anomalous vasomotility and vascular permeability could be caused in part by the irregular control of these complex interactions.

Adolescent↗