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PubMed1981

Cutaneous and skeletal muscle vascular responses to hypothermia.

Vascular resistance and capacitance were studied in innervated or denervated canine forelimbs. Hypothermia (38-28 degrees C) was induced systemically, by external cooling of blood which returned to the right heart, or locally, by cooling blood perfusing the forelimb. Systemic cooling to 33 and then to 28 degrees C elicited significant decreases in limb weight with substantial increases in both skin and skeletal muscle vascular resistances. Acute denervation of the forelimbs attenuated both the fall in limb weight and increase in skin vascular resistance associated with cooling. These data support the contention that cutaneous vasoconstriction during systemic cooling is mediated primarily by sympathetic nerves, whereas skeletal muscle vasoconstriction is mediated primarily by circulating hormones. Local cooling elicited skin and skeletal muscle vascular dilation at 33 degrees C in both innervated and denervated forelimbs whereas either no change or a slight increase in skin and skeletal muscle vascular resistance resulted upon local cooling to 28 degrees C, perhaps due to the inhibition of Na+ - K+ - ATPase activity and/or a rise in blood viscosity. The locally induced vasodilation was found to override the powerful vasoconstrictor response caused by systemic cooling. The vasodilation is considered active rather than passive, because the increase in forelimb weight and decreases in forelimb vascular resistances occurred in the denervated as well as innervated limbs.

Animals↗
PubMed1991

Effects of a new nitro compound on the systemic circulatory system in dogs.

The present study was undertaken to evaluate the effects of a newly synthesized nitro compound (E-4701) on the systemic circulatory system with special reference to venous return and vascular compliance. Dogs were anesthetized with sodium pentobarbital. After opening the chest, cannulae were inserted into the superior and inferior vena cavae and into the right atrial appendage. The venous flow from the caval veins was redirected to a blood reservoir with an outlet at a constant height. The blood was pumped into the right atrium at a constant flow rate. E-4701 had a hypotensive effect, and also caused a decrease in reservoir blood volume; i.e., a decrease in venous return. Venous return via the superior vena cava was increased, whereas return via the inferior vena cava was decreased. Similar effects on the systemic circulatory system were observed with nitroprusside. The lowest dose of nitroprusside that caused a significant reduction in blood pressure was the same dose as that which caused a decrease in reservoir blood volume. However, a low dose of E-4701 caused a significant reduction in reservoir blood volume without affecting the systemic blood pressure. Arterial and venous compliances were increased by both E-4701 and nitroprusside. Nitroglycerin and isosorbide dinitrate increased venous compliance, but did not affect arterial compliance. The results suggest that E-4701 caused an almost equipotent reduction in blood pressure and venous return by dilating the arterial and venous vascular beds. The capacitance vessels may be more sensitive to E-4701 than the resistance vessels.

Animals↗
PubMed1997

Mechanisms responsible for changes in abdominal vascular volume during sympathetic nerve stimulation in anaesthetized dogs.

This study was designed to determine the extent to which the decrease in volume of blood in the abdominal circulation in response to sympathetic stimulation was due to a passive effect of decreasing flow rather than active constriction of the capacitance vessels. In dogs anaesthetized with alpha-chloralose (100 mg kg-1 i.v.) the abdominal circulation was vascularly isolated and perfused either at constant flow or at constant pressure, and drained at constant pressure from the inferior vena cava. Changes in volume were determined by integration of the differences between inflow and outflow. Supramaximal stimulation of both splanchnic (sympathetic) nerves at 1 Hz decreased abdominal volume during constant pressure perfusion (active and passive components) by 3.04 +/- 0.58 ml kg-1 and at constant flow (active responses only) by 2.30 +/- 0.49 ml kg-1 (means +/- S.E.M.). The responses at 8 Hz were respectively 9.52 +/- 0.91 and 5.09 +/- 0.49 ml kg-1. The proportion of the responses calculated to be passive at 1 and 8 Hz was 23 +/- 6.3 and 45 +/- 5.1%, respectively. These responses were almost identical to those induced by changing inflow by increasing the pump speed. Following ligation of the splenic pedicle, the responses during both constant pressure and constant flow were reduced by similar amounts, indicating that only the active response was affected. After ligation of the splenic pedicle, the proportion of the response calculated to be passive at 1 and 8 Hz increased to 44 +/- 8.0 and 62 +/- 3.7% respectively. These results indicate the importance of passive volume change in affecting abdominal volume, particularly following ligation of the splenic circulation.

Abdomen↗
PubMed1985

Neurogenic hypertension: etiology and surgical treatment. II. Observations in an experimental nonhuman primate model.

In a companion paper (Ann Surg 1985; 201(3):391-398), clinical data which suggest that neurogenic hypertension may be caused by arterial compression of the left medulla oblongata was presented. A chronic pathophysiologic animal model of neurogenic hypertension using a substitute for arterial pulsation, the neurovascular compression simulator (NCS), was developed. This paper presents data that demonstrate how development of hypertension in a nonhuman primate baboon (5 subject animals, 5 control animals) can be caused by the NCS, and the blood pressure can subsequently return to normal following cessation of NCS activity. These experiments show that pulsatile compression of the left ventrolateral medulla oblongata results in cardiovascular changes consistent with the sequence found in human neurogenic hypertension. Arteriosclerosis and arterial ectasia in the human contribute to arterial elongation and looping at the base of the brain. An arterial loop, by causing pulsatile compression of neural structures, elicits an increase in blood pressure initiated by an increase in cardiac output. This may be due to interference with the autonomic control of the heart and/or by alteration of the relative capacitance of the vascular system.

Animals↗
PubMed1985

Sustained ventricular unloading action of the alpha-adrenergic antagonist nicergoline in the dog.

Preliminary studies indicate that nicergoline, a new alpha-antagonist, can lower HR at doses which decrease arterial BP. The present animal study was designed to quantitate the systemic and carotid (pulsed Doppler) hemodynamic and renin release consequences of nicergoline ventricular unloading, and to investigate the hemodynamic mechanisms of hypotension. In 11 anesthetized dogs, nicergoline infusion induced progressive, moderate, and prolonged hypotension associated with reduced vascular resistance and capacitance. Hypotension resulted from decreased HR and cardiac output, without an increase in plasma renin activity. The effects on carotid hemodynamics were less marked than those on the systemic circulation. Hypotension was caused primarily by vasoplegia, and was magnified subsequently by inhibition of the reflex rapid pressor control mechanisms. This suggests that repeated iv doses of nicergoline are preferable to prolonged infusion.

Animals↗
PubMed1991

Cardiac mass and aortic distensibility following calcium blockade in hypertension.

Calcium-entry blockade produced by verapamil was studied in 13 subjects with sustained essential hypertension. Noninvasive echo-Doppler methods were used to evaluate cardiac structure and function, maximum aortic acceleration (used as an indirect index of cardiac performance), and carotid-femoral pulse-wave velocity. Measurements were performed in baseline conditions, following 12 weeks of active treatment, and 4 weeks of placebo. Following verapamil, blood pressure (BP) significantly decreased (p less than 0.001) with a slight reduction in cardiac output (p less than 0.05) and a more substantial decrease in heart rate (p less than 0.002). No significant change occurred in maximum acceleration and in the curve relating percent fractional shortening to end-systolic stress, suggesting that verapamil decreased BP with minor changes in cardiac performance. Cardiac mass decreased by approximately 6.3% whereas pulse-wave velocity did not change, suggesting that the small decrease in cardiac mass could be related to the lack of improvement in the capacitative component of vascular impedance, as judged from the determination of pulse-wave velocity. The study provides evidence that calcium blockade due to verapamil results in a dissociation between the antihypertensive effect and the absence of significant changes in cardiac and arterial structure and function.

Adult↗
PubMed1990

Rat venular pressure-diameter relationships are regulated by sympathetic activity.

The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.

Animals↗
PubMed1997

Doppler flow velocity waveforms of human fetal ductus arteriosus and branch pulmonary artery.

Doppler waveforms of the human fetal ductus arteriosus and the branch pulmonary artery are distinct in their shape and might reflect fetal cardiovascular hemodynamics and vessel wall characteristics. The waveform of ductus arteriosus had two peaks, a higher one in systole and a lower one in diastole. Both peaks had slow acceleration and deceleration and looked like two narrow base isosceles triangles. This unique waveform might be due to vessel wall characteristics and an instantaneous pressure gradient between the main pulmonary artery and descending aorta. The waveform of the branch pulmonary artery showed very steep acceleration with the onset of ejection followed by steep decline, then low velocity flow during diastole. The characteristic shape of the branch pulmonary artery might be related to high vascular resistance, decreased capacitance and the earlier reflection wave of pulmonary vessels.

Blood Flow Velocity↗
PubMed1989

[Hemorheology, hemodynamics and microcirculation. 1].

The microcirculation constitutes an ubiquitous vascular network presenting a mesh pattern, and comprising different types of vessels, arterioles, small veins, capillaries, arteriovenous shunts or similar structures, and lymphatics. Many dimensions have to be recognized, or simply mentioned, if one is to understand the hemodynamic and hemorheological particulars of this territory, which differ, in many aspects, from those specific to the macrocirculation (number and length of the vessels, diameter and cross section, intercapillary distance, geometric characteristics, intravascular pressure, pressure gradient, pressure-volume relationship, flow rate, mean velocity of plasma and RBC, velocity profile, local hematocrit, in situ viscosity, kinematic viscosity, wall shearing conditions, local oxygen transport, aggregation and deformability of RBC, leukocyte properties, etc.). The flow rate in capillary tubes and capillary vessels of the living organism varies with many factors, such as proximal hemodynamics, hemorheological characteristics of blood (fibrinogen, macro- and micro-hematocrit), some known effects (Farheus, Farheus Lindqvist), local diameter, the plasma layer which plays the role of the limiting layer, the endothelial film, the wall effect, and so forth. Models of the circulation have been propounded, none of which takes into account the whole of these phenomena due to their great complexity. Hemodynamic and hemorheological interactions provide for a better understanding of certain concepts, such as vascular resistance, hindrance, capacitance, local flow rates, real capillary opening and closing, development of two-directional functional shunts, autoregulation, pressure-volume relationship, critical closing pressure, circulatory current slowing effect, sequelae of intravascular aggregation of formed blood elements.

Hemodynamics↗
PubMed1980

Blood pressure and vasomotor responses to sympathetic stimuli in patients with chronic myocardial infarction.

The responses of resistance and capacitance vessels of skin and muscle, and of blood pressure to reflex influences mediated by the sympathetic system were investigated in a group of 63 male patients in a chronic phase of myocardial infarction. In the group of patients with MI, as compared to the controls: (1) the reactive increase of systolic BP and heart rate was significantly smaller but longer lasting after cessation of the stimuli; (2) the vasoconstrictory reactions in skin were significantly prolonged in resistance as well as in capacitance segments of vascular bed; and (3) the resting blood flow in muscle was significantly lower and the vasodilatation during an emotional reaction was less pronounced and shorter. Possible underlying mechanisms of this vasomotor pattern are discussed.

Adult↗
PubMed2006

Mechanism of non-capacitative Ca2+ influx in response to bradykinin in vascular endothelial cells.

Bradykinin is a potent vasoactive nonapeptide. It elicits a rise in cytosolic Ca(2+) (Ca(2+))(i) in endothelial cells, resulting in Ca(2+)-dependent synthesis and release of endothelial vasodilators. In the present study, we investigated the mechanism of bradykinin-induced Ca(2+) influx in primary cultured rat aortic endothelial cells and in a mouse heart microvessel endothelial cell line (H5V). Bradykinin-induced Ca(2+) influx was resolved into capacitative Ca(2+) entry (CCE) and non-CCE. The non-CCE component was inhibited by a B2 receptor antagonist (HOE140; 1 microM) and a phospholipase C (PLC) inhibitor (U73122; 10 microM). The action of bradykinin could be mimicked by 1-oleoyl-2-acetyl-glycerol, an analogue of diacylglycerol (DAG), and by RHC80267, a DAG-lipase inhibitor. Immunoblots showed that TRPC6 was one of the main TRPC channels expressed in endothelial cells. Transfection of H5V cells with two siRNA constructs against TRPC6 both markedly reduced the TRPC6 protein level and, at the same time, decreased the percentage of cells displaying bradykinin-induced non-CCE. siRNA transfection also reduced the magnitude of non-CCE among the cells responding to bradykinin. Taken together, our data suggest that bradykinin-induced non-CCE is mediated via the B2-PLC pathway, and that DAG may be involved in this process. Further, TRPC6 is one of the important channels participating in bradykinin-induced non-CCE in endothelial cells.

Animals↗
PubMed1998

Distribution of coronary arterial capacitance in a canine model.

The capacitative properties of the major left coronary arteries, left main (LM), left anterior descending (LAD), and left circumflex (LCX), were studied in 19 open-chest isolated dog hearts. Capacitance was determined by using ramp perfusion and a left ventricular-to-coronary shunt diastolic decay method; both methods gave similar results, indicating a minimal systolic capacitative component. Increased pericardial pressure (PCP), 25 mmHg, was used to experimentally alter transmural wall pressure. The response to increased PCP was different in the LAD vs. LCX; increasing PCP decreased capacitance in the LCX but increased capacitance in the LAD. This may have been due to the different intramural vs. epicardial volume distribution of these vessels and a decrease in intramural tension during increased PCP. Increased PCP decreased LCX capacitance by approximately 13%, but no changes in conductance or zero flow pressure intercept occurred in any of the three vessels, i. e., evidence against the waterfall theory of vascular collapse at these levels of PCP. Coronary arterial capacitance was also linearly related to perfusion pressure.

Animals↗
PubMed1989

Observations on the intracoronary administration of milrinone and dobutamine to patients with congestive heart failure.

A direct intracoronary infusion technique was used to characterize the mechanisms of action of milrinone, a new phosphodiesterase inhibitor. Because of the small quantity of drug infused, it is possible to achieve a therapeutic concentration of drug in the heart with little or no systemic accumulation. Because loading conditions are largely unaffected during intracoronary drug infusion, it is possible to use left ventricular +dP/dt as a convenient measure of changes in contractility. Intracoronary milrinone infusion caused a dose-related increase in +dP/dt associated with a substantial improvement in left ventricular pump function. In addition, there is a small decrease in heart rate, which appeared to be secondary to reflex withdrawal of sympathetic tone, since it was associated with a decrease in plasma norepinephrine. Measurement of forearm vascular resistance and forearm venous capacitance by plethysmography indicated that although there was no significant decrease in forearm vascular resistance during intracoronary drug infusion, there was a small increase in venous capacitance. Subsequent intravenous administration of milrinone caused a substantial further improvement in left ventricular pump function, associated with a substantial decrease in left- and right-sided cardiac filling pressures and forearm vascular resistance, and an increase in forearm venous capacitance. These findings suggest that reflex sympathetic withdrawal may contribute to the venous dilation that occurs with milrinone, but that the major effects of milrinone on vascular tone are due to a direct vascular action of the drug. Intracoronary infusion of dobutamine has also demonstrated a substantial decrease in the inotropic response to beta-adrenergic stimulation in patients with congestive heart failure, presumably because of down-regulation of beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Circulation↗
PubMed2001

Crucial role of type 1, but not type 3, inositol 1,4,5-trisphosphate (IP(3)) receptors in IP(3)-induced Ca(2+) release, capacitative Ca(2+) entry, and proliferation of A7r5 vascular smooth muscle cells.

Stimulation of G protein- or tyrosine kinase-coupled receptors regulates cell proliferation through intracellular Ca(2+) ([Ca(2+)](i)) signaling. In A7r5 cells, we confirmed that inositol 1,4,5-trisphosphate (IP(3)) mediates vasopressin (VP)-evoked Ca(2+) release from intracellular stores and showed that types 1 (IP(3)R(1)) and 3 (IP(3)R(3)) IP(3) receptors were expressed. Using antisera selective for IP(3)R(1) or IP(3)R(3) and another that interacted equally well with both subtypes, together with membranes from SF:9 cells expressing only single IP(3)R subtypes to calibrate immunoblotting, we established that A7r5 cells express 81% IP(3)R(1) and 19% IP(3)R(3). To elucidate the contributions of IP(3)R(1) and IP(3)R(3) to Ca(2+) signaling and proliferation, stable clones expressing promoter-inducible antisense cDNA fragments (-90 to +9) corresponding to the two IP(3)R subtypes were selected. Mild inhibition of IP(3)R(1) (71+/-8% of control level) slightly attenuated the IP(3)-evoked Ca(2+) release (IICR) induced by VP but significantly decreased the subsequent capacitative Ca(2+) entry (CCE) and proliferation. Moderate inhibition (34+/-6%) strongly decreased both IICR and CCE and further blocked proliferation. Complete inhibition almost abolished IICR and CCE and arrested proliferation entirely. Complete inhibition of IP(3)R(3) expression slightly attenuated IICR without affecting CCE or proliferation. In cells microinjected with a low dose of heparin, VP-induced CCE was more susceptible than IICR to mild inhibition of both IP(3)R(1) and IP(3)R(3). A high dose of heparin had a similar effect to complete inhibition of IP(3)R(1) expression: it blocked VP-evoked IICR entirely and CCE by 90%. We conclude that IP(3)R(1), but not IP(3)R(3), is crucial for IICR, CCE, and proliferation of vascular smooth muscle cells.

Animals↗
PubMed2005

Modulation of intracellular Ca2+ release and capacitative Ca2+ entry by CaMKII inhibitors in bovine vascular endothelial cells.

The effects of inhibitors of CaMKII on intracellular Ca2+ signaling were examined in single calf pulmonary artery endothelial (CPAE) cells using indo-1 microfluorometry to measure cytoplasmic Ca2+ concentration ([Ca2+]i). The three CaMKII inhibitors, KN-93, KN-62, and autocamtide-2-related inhibitory peptide (AIP), all reduced the plateau phase of the [Ca2+]i transient evoked by stimulation with extracellular ATP. Exposure to KN-93 or AIP alone in the presence of 2 mM extracellular Ca2+ resulted in a dose-dependent increase of [Ca2+]i consisting of a rapid and transient Ca2+ spike followed by a small sustained plateau phase of elevated [Ca2+]i. Exposure to KN-93 in the absence of extracellular Ca2+ caused a transient rise of [Ca2+]i, suggesting that exposure to CaMKII inhibitors directly triggered release of Ca2+ from intracellular endoplasmic reticulum (ER) Ca2+ stores. Repetitive stimulation with KN-93 and ATP, respectively, revealed that both components released Ca2+ largely from the same store. Pretreatment of CPAE cells with the membrane-permeable inositol 1,4,5-trisphosphate (IP3) receptor blocker 2-aminoethoxydiphenyl borate caused a significant inhibition of the KN-93-induced Ca2+ response, suggesting that exposure to KN-93 affects Ca2+ release from an IP3-sensitive store. Depletion of Ca2+ stores by exposure to ATP or to the ER Ca2+ pump inhibitor thapsigargin triggered robust capacitative Ca2+ entry (CCE) signals in CPAE cells that could be blocked effectively with KN-93. The data suggest that in CPAE cells, CaMKII modulates Ca2+ handling at different levels. The use of CaMKII inhibitors revealed that in CPAE cells, the most profound effects of CaMKII are inhibition of release of Ca2+ from intracellular stores and activation of CCE.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

The influence of isoflurane on the vascular reflex response to lung inflation in dogs.

Positive pressure ventilation can affect hemodynamic stability by neuroreflex-mediated activity. Inhalational anesthesia is known to attenuate the arterial baroreflex function; however, little information is known about the effect of volatile anesthetics on the lung inflation reflex. The influence of isoflurane on static lung inflation reflex-induced changes in venous capacitance and systemic resistance was investigated in dogs. After controlling carotid sinus pressure at 50 mmHg and initiating total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10 and 20 mmHg. The systemic vascular resistance index (SVRI) decreased by 0.04 +/- 0.03 and 0.13 +/- 0.03 mmHg.kg.min.ml-1 during tracheal inflation pressures of 10 and 20 mmHg, respectively. There as an accompanying change in systemic vascular capacitance index (SVCI) by 1.0 +/- 0.65 and 3.3 +/- 0.82 ml.kg-1 during tracheal inflation pressures of 10 and 20 mmHg. The addition of isoflurane decreased the reflex vascular response to lung inflation in a dose-dependent manner. A concentration of 1 MAC isoflurane administered via the cardiopulmonary bypass machine attenuated the change in SVRI to tracheal inflation pressures of 10 and 20 mmHg by 75% and 67%, respectively. Isoflurane at 1 MAC also reduced the reflex capacitance response to tracheal pressures of 10 and 20 mmHg by 36% each. Lung inflation-induced changes in SVRI and SVCI were abolished at isoflurane concentrations of 2 MAC. We conclude that under the conditions of this study, 1 MAC isoflurane was shown to attenuate lung reflex-induced changes in SVRI and SVCI and that at higher isoflurane concentrations (2 MAC) these reflex-induced changes were not seen.

Animals↗
PubMed1986

[Effect of beta-adrenoreceptor blockade on the filtration-absorption function of the vascular bed of the skeletal musculature of the cat].

Perfusion of the cat hindlimb with alternating stabilization of pressure and blood flow in response to electrical stimulation of sympathetic fibers prior to and after blockade of beta-adrenoreceptors decreased considerably changes of the capillary filtration coefficient and the capillary hydrostatic pressure, improving changes of the filtration-absorption balance induced with the stimulation. beta-Adrenoreceptors of vascular bed are shown to take part in neurogenic regulation of both the exchange and the capacitance functions of the vascular bed, as well as its resistance function. Activation of sympathetic fibers seems to enhance permeability of the vascular wall.

Animals↗