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PubMed1984

Analysis of blood flow in pulmonary hypertension with the pulsed Doppler flowmeter combined with cross sectional echocardiography.

Blood flow patterns were analysed at nine points in the pulmonary area using the pulsed Doppler technique combined with cross-sectional echocardiography in 53 patients with heart disease and 10 healthy subjects. In subjects with a normal pulmonary artery pressure the blood flow pattern in systole showed a gradual acceleration and deceleration with a rounded summit in mid systole, designated the round type. In patients with pulmonary hypertension it showed a rapid acceleration and early deceleration with a sharp peak in early systole, designated the triangular type. The acceleration time index, defined as the ratio of the time interval from the beginning to the peak of ejection to the ejection time, showed a significant inverse correlation with mean pulmonary artery pressure. In pulmonary hypertension a prominent reverse flow occurred in the right posterior part of the pulmonary trunk during mid-systole and early diastole, indicating the presence of a vortex. Similar flow patterns were also seen in patients with idiopathic pulmonary artery dilatation. The factors responsible for the triangular type were principally the reduced capacitance and increased impedance of the pulmonary vascular tree. Those responsible for the reverse flow were the curved path of the blood flow and dilatation of the pulmonary artery.

Adult↗
PubMed2004

Active cutaneous vasodilation in resting humans during mild heat stress.

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40 degrees C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3 degrees C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVC(BT)) and sweat expulsion number increased at 38 and 40 degrees C compared with 34 degrees C (P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40 degrees C (P < 0.05, different from 34 degrees C). However, SSNA burst amplitude increased (P < 0.05), whereas SSNA burst duration decreased (P < 0.05), at the same time as we observed the increase in CVC(BT) and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.

Adult↗
PubMed1976

Physiological pump loading of isolated cardiac muscle.

Cat papillary muscles were subjected to a continuously changing load, resulting from an analysis of the left ventricle as a muscle pump system. The papillary muscle was assumed to be part of a circumferential bundle of muscle fibers of a simplified ejecting ventricle. The load included the pressure--stress relationship of this ventricle and the peripheral vascular load with its inertial, resistive and capacitive components. When this loading function was imposed on a shortening muscle through an electronic feedback circuit, the time course of force development and the velocity versus force plots closely resembled data obtained in the intact heart. Analysis of mechanical work (delta 1 X f) and power (V X f) and their respective time course permitted distinction between changes of contractile performance due to (1) positive or negative inotropic interventions, (2) altered hypothetical ventricular dimensions and changed preload, and (3) the long-term load-dependent memory of cardiac muscle.

Animals↗
PubMed1988

[Current aspects of nasal hyperreactivity].

The term hyper-reactivity defines an inadequate reaction of the nose to normal airborne stimuli that are harmless to most of the population. In such cases the nose always shows exactly the same symptoms, irrespective of whether the rhinitis is allergic (IgE- or cell-mediated) or nonspecific (vasomotor). These symptoms include sneezing, nasal obstruction, hypersecretion, and itching of the nose. The vascular supply of the nose consists of capacitance vessels (veins, venules, sinusoids), resistance vessels (arteries, arterioles), and exchange vessels (capillaries of fenestrated types). Drug and mediator effects may be directed to different nasal vessel systems. The autonomic innervation of the nose is complex. Some neuropeptides have been demonstrated, in addition to the classical neurotransmitters of the sympathetic and parasympathetic system. Neuropeptide Y (NPY) is found in adrenergic fibers, vasoactive intestinal peptide (VIP) in cholinergic neurones; substance P (SP), calcitonin-gene-related peptide (CGRP) and neurokinine (NKA) are found in sensory nerves. The possible significance of the different neurotransmitters and mediators in nasal hyperreactivity is discussed.

Humans↗
PubMed1976

Experience with pindolol, a betareceptor blocker, in the treatment of hypertension.

Ten patients, mean age 48 years, with essential hypertension of stage I and II according to the WHO classification, were studied at rest and during work before and after an average of two and 16 months of oral treatment with the beta-adrenergic blocking agent, pindolol. The pindolol treatment caused a significant decrease in the systemic systolic and diastolic blood pressure, both at rest and during work. Three mechanisms seem to be involved in the antihypertensive effect of pindolol: (1) a negative chronotropic effect on the heart, (2) a decrease in peripheral vascular resistance, and (3) an increase in venous capacitance affecting the venous return. However, the significance of these mechanisms seems to differ when the situations after two months of treatment are compared with those after 16 months of treatment. In the beginning, a decrease in cardiac output seems to be the main cause of the lowering of the blood pressure; later, a decrease in systemic vascular resistance might be of greater importance.

Adrenergic beta-Antagonists↗
PubMed1980

Central haemodynamic and forearm vascular effects of morphine in patients after open heart surgery.

Central haemodynamic and forearm vascular changes following administration of morphine i.v. were studied in patients 24--30 h after open heart surgery. Right atrial pressure, heart rate, mean arterial pressure, cardiac output and stroke volume were measured before and after morphine 5 and 10 mg per 70 kg in 14 subjects. In a further group of eight subjects, forearm blood flow was measured after morphine 10 mg per 70 kg. Total systemic and forearm vascular resistance were derived from these measurements. In spite of wide individual variations, significant decreases in mean arterial pressure occurred in most of the patients and appeared to be dose related. Significant decreases in mean cardiac index were noted only after morphine 10 mg per 70 kg. Forearm blood flow increased consistently and significantly and there was a corresponding decrease in vascular resistance. The decrease in mean arterial pressure and the change in forearm vascular resistance indicated that vasodilatation was probably the principle cause of the decrease in arterial pressure, whereas the sustained decrease in cardiac output seemed to indicate an effect on venous capacitance. The predominant action of morphine appears to be peripheral, causing a decrease in vascular resistance and, possibly, an increase in venous capacitance.

Cardiac Surgical Procedures↗
PubMed1988

[The role of the kidney in the pathogenesis of hypertension].

Neither a temporary increase in salt intake nor the activation of endogenous vasoconstrictor hormones alone will cause a rise in blood pressure in healthy subjects. High blood pressure rather results from an augmented product of cardiac output and peripheral vascular resistance, which also requires defective baroreceptor function. Experimental and clinical evidence from renal transplantation suggests that high blood pressure may be transmitted by the kidney. Morphological or functional inability of the kidney to adequately eliminate excessive salt, as in renoparenchymal hypertension, or with enhanced renal adrenergic activity in the presence of high salt intake, may induce initially salt- and volume-dependent hypertension with increased cardiac output and normal peripheral vascular resistance. In the case of reduced nephron population, this first stage was shown to be followed by a normalization of cardiac output, but a simultaneous rise in peripheral vascular resistance, including decreased compliance of the venous capacitance vessels. What are the underlying mechanisms which convert volume-dependent hypertension into high resistance hypertension without necessarily reducing central blood volume? Increased central blood volume, which may stimulate the secretion of an endogenous Na-K-ATPase inhibitor or other endogenous factors, may cause decreased transmembranous sodium transport, resulting in elevated intracellular concentrations of sodium and calcium with enhanced responsiveness of the vascular smooth muscle cell to vasoconstrictor hormones. Since increased central blood volume also decreases baroreceptor sensitivity, the disturbed interplay of cardiac output and peripheral vascular resistance will result in high blood pressure.

Humans↗
PubMed1989

Effects of vasopressin on pulmonary and systemic vascular mechanics.

The direct effects of vasopressin on the resistance and capacitance properties of the pulmonary and systemic vasculature were studied in nine aneural dogs on systemic and pulmonary bypass. The systemic and pulmonary pressure-flow, the systemic and pulmonary arterial pressure-volume, and the systemic and pulmonary venous pressure-volume relationships were determined for five levels of infused vasopressin. Vasopressin levels of approximately 10, 30, 150, 300, and 500 pg/ml were achieved by intravenous infusions. Samples of venous blood were drawn before and after each set of pressure-flow and pressure-volume relationships for the determination of vasopressin level by radioimmunoassay. A linear relationship was found between vasopressin level and systemic vascular resistance. Systemic vascular resistance increased 0.072 +/- 0.011 mmHg.kg.min.ml-1 for a change in vasopressin level of 100 pg/ml. Vasopressin did not affect pulmonary vascular resistance or any vascular compliance. High doses of infused arginine vasopressin were necessary to elicit substantial vasoconstriction.

Animals↗
PubMed1994

Isolated circulatory response to intravenous administration of the ACE inhibitor enalaprilat.

The isolated vascular effects of intravenous administration of the angiotensin converting enzyme (ACE) inhibitor enalaprilat were investigated. Thirty male patients undergoing cardiopulmonary bypass (CPB) were studied. According to a randomized sequence, 0.04 mg kg-1 enalaprilat (low-dose, n = 10), 0.08 mg kg-1 (high-dose, n = 10) enalaprilat or saline solution as placebo (control group, n = 10) was given as an i.v. bolus during CPB. Changes in mean arterial pressure (MAP) and venous reservoir (RV) of the extracorporeal circulation were studied as indices of arterial resistance and venous capacitance. Mean arterial blood pressure (MAP) and peripheral vascular resistance (SVR) were significantly more reduced in the high-dose enalaprilat group (MAP: -36 mm Hg after 9 min; SVR: -836 dyn s cm-5) than in the low-dose group (MAP: -13 mm Hg after 10 min). Volume of the reservoir (RV) decreased in both enalaprilat treated groups indicating additional (dose-dependent) venous pooling effects of the substance (low-dose: -300 ml; high-dose: -520 ml; control group: -100 ml). Skin capillary blood flow measured by laser Doppler flowmetry (LDF) increased after injection of 0.04 mg kg-1 enalaprilat, whereas it decreased significantly when MAP fell markedly in patients treated with high-dose enalaprilat. I.v. enalaprilat had dose-dependent vasodilating properties in the arterial and venous vessel system indicating reduction in pre- and afterload. Microcirculation in both enalaprilat treated groups improved as long as reduction in blood pressure was not limited.

Blood Pressure↗
PubMed1983

The effects of captopril on the acute vascular responses to frusemide in man.

To examine the importance of angiotensin II formation in the production of frusemide's acute peripheral venous and arterial responses, the effect of pretreatment with captopril was studied. Captopril abolished the acute increases in venous capacitance and blood pressure and attenuated the increases in forearm vascular resistance produced by intravenous frusemide. The study provides evidence that angiotensin II formation performs an essential role in the production of the acute vascular effects of frusemide in man.

Adolescent↗
PubMed1981

Effect of morphine on limb capacitance and resistance vessels.

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intraarterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.

Adult↗
PubMed1989

Skeletal muscle blood flow and venous capacitance in patients with severe sepsis and systemic hypoperfusion.

Alterations in peripheral vascular tone are presumed to contribute to circulatory failure during severe sepsis. Decreased venous tone with venous pooling may decrease effective circulatory blood volume, while decreased arterial tone with redistribution of systemic blood may compromise tissue nutrient flow. We compared forearm arterial and venous tone and forearm blood flow in ten patients with and ten patients without sepsis. The FVT, MVC, and FBF were measured by air plethysmography. In the septic patients, MCV was 1.4 +/- 0.1 ml compared with 3.1 +/- 0.2 ml in nonseptic patients (p less than 0.01). The FVT was 13.4 +/- 1.0 mm Hg/ml in septic patients versus 7.0 +/- 0.5 mm Hg/ml in nonseptic patients (p less than 0.01). The ratio of FBF to cardiac output was 0.28 +/- 0.07 percent in septic patients and 0.31 +/- 0.07 percent in nonseptic patients. These data suggest that increased peripheral venous capacitance and redistribution of skeletal muscle blood flow are not present in patients with sepsis.

Adult↗
PubMed2004

Agonist-induced internalization of leukotriene B(4) receptor 1 requires G-protein-coupled receptor kinase 2 but not arrestins.

The leukotriene B(4) (LTB(4)) receptor (BLT1) becomes desensitized upon repeated agonist stimulation. Little is known, however, about BLT1 internalization, which follows desensitization in most G-protein-coupled receptors (GPCR). In the current study, transiently expressed BLT1 readily internalized, after LTB(4) stimulation, in RBL-2H3 cells that express high levels of endogenous GPCR kinase 2 (GRK2) but did not in COS-7 or human embryonic kidney (HEK) 293 cells, which do not overexpress GRK. The internalization of BLT1 could be blocked in RBL-2H3 cells by coexpressing dominant-negative (DN) GRK2 K220R and could be promoted in HEK293 cells by coexpressing wild-type (WT) GRK2. Coexpression of WT or DN nonvisual arrestins had no effect on BLT1 internalization. Moreover, upon stimulation with LTB(4), BLT1 did not induce arrestin-green fluorescence protein redistribution in either cell type, even in the presence of overexpressed GRK2. Coimmunoprecipitation experiments confirmed that BLT1 could associate with GRK2 but not with arrestins. A C-tail-truncated mutant of BLT1 lost the capacity to internalize and associate with GRK2 upon exposure to LTB(4), suggesting that the C-tail was required for receptor internalization and association with GRK2. Taken together, our results indicate that the C terminus of BLT1 plays a pivotal role in receptor internalization and GRK2 association. Moreover, ligand-induced BLT1 internalization is dependent on GRK2 but independent of arrestins. This may allow differential, cell-type-specific signaling in response to LTB(4), depending on GRK expression levels.

Animals↗
PubMed1980

Magnesium ions control prostaglandin reactivity of venous smooth muscle from spontaneously hypertensive rats.

Prostaglandins (PGs) may play an important role in the pathogenesis of hypertension via their effects on vascular smooth muscle tone. It has been suggested that the capacitance (venous) vessels in the peripheral circulation exhibit an increased tone in the development of hypertension. Recent findings from our laboratory indicate that magnesium ions ([Mg2+]o) play a role in the control of vascular tone, vascular reactivity and Ca2+ content and its distribution in blood vessels. The present study indicates that reactivity of isolated portal venous smooth muscle, obtained from spontaneously hypertensive rats, is markedly reduced in the absence of [Mg2+]o. In addition, our findings indicate that portal venous smooth muscle from age-matched inbred Wistar-Kyoto, but not from normal age-matched Wistar controls, also exhibits decreased responsiveness to PGs in the absence of [Mg2+]o. These new data suggest that Mg2+ may be an important and overlooked factor in the etiology of hypertensive vascular disease.

Animals↗
PubMed1983

alpha 2-Adrenoceptors in rat resistance vessels.

In pithed rats increases in blood pressure were induced by i.v. injections of the alpha 1-agonist methoxamine and the alpha 2-agonists clonidine, oxymetazoline and B-HT 920. The pressor responses were further analyzed by repeated measurements of cardiac output with the thermodilution technique and by calculation of total peripheral vascular resistance. During the pressor phase both vascular resistance and cardiac output were found to be elevated. This indicates that increases in both haemodynamic variables contributed to the pressure rise. Under the assumption that elevated vascular resistance reflected constriction of arterioles and elevated cardiac output constriction of capacitance vessels via increased venous return to the heart, and considering that the magnitude of the increase of both haemodynamic parameters was similar for all three agonists, the results suggest the existence of both alpha 1- and alpha 2-adrenoceptors in resistance as well as in capacitance vessels of rats. For alpha 2-adrenoceptors in resistance vessels this conclusion was supported by the finding that the calcium antagonists verapamil and/or tiapamil virtually abolished the increases of blood pressure and vascular resistance in response to clonidine, oxymetazoline or B-HT 920, but not to methoxamine. The calcium antagonists did not affect the increases in cardiac output, irrespective of which type of alpha-agonist was administered. While the present results support the existence of alpha 2-adrenoceptors in resistance vessels of the rat, they do not allow a firm conclusion as to their occurrence in rat capacitance vessels.

Adrenergic alpha-Agonists↗
PubMed1987

Hemodynamic mechanisms in CPR: a theoretical rationale for resuscitative thoracotomy in non-traumatic cardiac arrest.

Experimental work over the past decade has revealed three distinct mechanisms for generating artificial circulation during cardiac arrest and resuscitation. To isolate these mechanisms and study them in pure form, and in particular to characterize circulation during open vs. closed chest cardiopulmonary resuscitation (CPR), we developed an electrical model of the human circulatory system. Heart and blood vessels were modeled as resistive-capacitive networks, pressures in the chest, abdomen, and vascular compartments as voltages, blood flow as electric current, blood inertia as inductance, and the cardiac and venous valves as diodes. External pressurization of thoracic and abdominal vessels, as would occur in CPR, was simulated by application of half-sinusoidal voltage pulses. Simulations included two modes of creating artificial circulation: the cardiac pump mechanism, in which the atria and ventricles of the model were pressurized simultaneously, as occurs during open chest cardiac massage, and the thoracic pump mechanism, in which all intrathoracic elements of the model were pressurized simultaneously, as is likely to occur in closed chest CPR. The two mechanisms were compared for the same peak applied pressure (80 mmHg). Pure cardiac pump CPR generated near normal systemic perfusion pressures throughout the compression cycle. Pure thoracic pump CPR generated much lower systemic perfusion pressure only during the diastolic phase of the compression cycle. Simulation of cardiac compression at rates from 40 to 100/min produced total flows of 2500-3300, myocardial flows of 150-250 and cranial flows of 600-800 ml/min, depending on the compression rate. In contrast, thoracic pump CPR produced a total flow of approx. 1200, myocardial flow of 70, and cranial flow of 450 ml/min, independently of the compression rate. Direct cardiac compression is an inherently superior hemodynamic mechanism, because it can generate greater perfusion pressure throughout the compression cycle. If one presumes that improved blood flow during CPR is the key to more successful resuscitation, then it is reasonable to conclude that direct heart massage is the most effective available way to achieve this end.

Computer Simulation↗