PubMed HealthSearch

SEARCH · PubMed Health

Results for “TPR”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 37 records · Page 2Linked to original sources

Reflex and mechanical circulatory effects of graded Valsalva maneuvers in normal man.

In 17 normal subjects we studied the changes evoked by five levels of expiratory pressure (EP) ranging from 2.5 to 30 mmHg in a number of circulatory variables during the last 10 s of a 30-s Valsalva maneuver. Variables studied included mean arterial (MAP) and pulse (PP) pressures; right atrial (RAP) and peripheral vein (PVP) pressures; cardiac output (CO); total peripheral resistance (TPR) and heart rate (HR). EP-circulatory response curves were obtained in each subject a) before autonomic block; b) after cardiac effector block (atropine + propranolol); c) after "total" autonomic block (atropine + propranolol; guanethidine + phentolamine). Mechanical effects were determined from results during "total" autonomic block. They included EP-related rises in RAP and PVP each to about 0.7 mmHg/mmHg applied EP, and falls in CO, MAP, and PP to levels of approximately 50%, 70%, and 80% of resting respectively at EP 30 mmHg, but no changes in TPR and HR. Reflex effects included EP-related rises in HR and in TPR and in MAP, to levels of 160%, 160%, and 115% of resting respectively at EP 30 mmHg. The afferent input profile is probably complex, and the role of the different receptor groups may vary at the different levels of EP.

Atrial Function

Central hemodynamics in the developmental stage of spontaneous hypertension in the unanesthetized rat.

The hemodynamic alterations associated with the developmental phase of high blood pressure were investigated in the spontaneously hypertensive rat (SHR). All hemodynamic measurements were made in unanesthetized, unrestrained SHR and Wistar-Kyoto (WKY) rats instrumented with chronic electromagnetic flow probes on the ascending aorta and arterial pressure catheters. Rats were studied at 30-41 days, 80 days, and 120 days of age. Hemodynamics of SHRs and WKYs in the 30-41 day group were monitored daily. Spontaneously hypertensive rats demonstrated a higher cardiac index than WKYs (p less than 0.05) from 32 through 41 days of age. Total peripheral resistance (TPR) was not elevated in SHRs at this time. Heart rate and stroke index were elevated in SHRs (p less than 0.05) from 34 through 41 days, however, stroke volume was not. At 80 and 120 days SHRs had higher mean arterial pressure (MAP) and TPR than WKYs (p less than 0.05), although cardiac index was not significantly different. This hemodynamic pattern of a hyperkinetic circulation prior to the development of hypertension supports the theory of total body autoregulation. A transient increase in cardiac index precedes an increase in TPR, which then normalizes cardiac index while elevating MAP.

Aging

Hemodynamic responses to DOCA in young pigs.

Hemodynamic variables were measured in 20 young pigs; thirteen received subcutaneous implantations of desoxycorticosterone acetate (DOCA) impregnated in Silastic strips, seven received implants of Silastic strips alone and served as controls. No salt was added to the standard diet of either group. Mean arterial pressure (MAP) rose in a regular pattern in the DOCA-treated pigs, reaching on the average a level significantly greater than that of the control group 48 hours after the implantation. Pressure continued to rise, reaching a plateau 38% above that of the preimplant value 2 weeks later. In some pigs the MAP elevation was caused by an increase in cardiac output (CO); in others it was caused by an increase in total peripheral resistance (TPR). An increase in central venous pressure occurred in many DOCA-treated pigs regardless of whether the increase in MAP was caused by an increase in CO or in TPR. The results indicate that it is arterial pressure per se that is the regulated variable in this model of mineralocorticoid hypertension. The regulating system, whether it resides in the kidney or in the central nervous system, elevates pressure by effecting increases in either CO or TPR.

Animals

Ventilation:perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis.

Cardiovascular and respiratory parameters were obtained in 374 studies from 151 patients (64 septic or septic shock and 87 with nonseptic cardiogenic syndromes). Cardiac output and related measures, respiratory parameters, pulmonary blood volume (DV/m2), cardiac ejection fraction (EFx), left ventricular end-diastolic volume (LVEDV), peripheral resistance (TPR), pulmonary shunt (QS/QT), physiologic dead space (VD/VT) and mean ventilation perfusion ratios (VA/QT) were calculated. Both physiologic evaluation and multivariable statistical analyses of the data were performed. For a given level of (A-aO2 gradient/PaO2) septic patients have a higher QS/QT than cardiogenic patients. Hyperdynamic septic patients have a larger QS/QT, a greater VD/VT, and a lower VA/QT and TPR than cardiogenics. The decrease in VA/QT and the rise in VD/VT are strong functions of the increased EFx, which raises cardiac index (CI) and reduces LVEDV and the mean dispersion of pulmonary blood volume, thus causing hemodynamic redistribution of flow. QS/QT is mainly a direct function of the increase in CI which also tends to reverse the EFx-mediated rise in VD/VT. The role of the septic mediated decrease in TPR as a contributing pathologic feature and the use of volume infusion to raise LVEDV and VA/QT in high-CI septics with large QS/QT is discussed.

Blood Circulation

Circulatory adaptation after aortic valve replacement. A clinical study peroperatively and in the early postoperative period.

The myocardial function and the central and peripheral circulation were studied after aortic valve replacement. All patients showed a similar postoperative pattern of response. During the operation, after termination of bypass, the mean arterial blood pressure (Pa,m) was low. The total peripheral vascular resistance (TPR) and pulmonary vascular resistance (PVR) were normal. Immediately after the operation Pa,m, TPR and PVR were higher than peroperatively. The cardiac index (CI) and stroke index (SI) were low, and the heart rate (HR) was high. At this stage the oesophageal temperature was increasing, but there was no shivering. Then followed a period in which Pa,m and TPR decreased, while CI and SI remained essentially unchanged. The oesophageal temperature reached its highest value 5 hours postoperatively. Peripheral warming began in the 3rd hour postoperatively and was completed in the 6th hour, when the peripheral temperature was 35 degrees C. The progressive peripheral warming, with peripheral cutaneous vasodilatation and slight reduction of the heart rate, took place without signs of increasing CI or SI. The left and right ventricular function, expressed as the relation between LVSWI and Pla,m, and RVSWI and Pra,m, respectively, varied postoperatively and showed no signs of improvement at the time of peripheral warming. Cardiac output and myocardial function seemed to be little affected by the obvious changes appearing during the systemic and peripheral vasodilatation in connection with central and peripheral warming.

Aged

[Effect of the angiotensin antagonist saralasin on blood pressure and hemodynamics in patients with terminal renal insufficiency].

The angiotensin antagonist saralasin was infused both before and 10 hrs after dialysis in 10 hypertensive and 4 normotensive patients hemodialyzed for terminal renal failure. A significant increase in mean arterial pressure (MAP) and total peripheral resistance (TPR) without change in cardiac output measured by impedance cardiography were observed during the first few minutes of saralasin infusion. MAP and TPR decreased during the second half of the infusion in 4 hypertensive patients and remained at the preinfusion levels in 6 hypertensive and 4 normotensive patients. Plasma renin activity (PRA) was significantly higher in patients in whom MAP fell both before and after hemodialysis. There was a significant correlation between PRA before saralasin and the fall in MAP and TPR. The fall in MAP in 4 of 10 hypertensive patients demonstrates that inappropriately high renin and angiotensin levels are involved in the pathogenesis of hypertension in some patients with terminal renal failure. Volume factors are probably of primary importance in the other patients.

Adult

Circulatory changes during pregnancy in spontaneously and renal hypertensive rats.

1. Mean arterial pressure, heart rate, cardiac output (dye-dilution technique), stroke volume, total peripheral resistance (TPR), utero-placental blood supply (microsphere technique) and foetal weights were determined 2 days before expected birth in normotensive control (NC) rats, spontaneously hypertensive (SH) rats, rats with short-standing renal hypertension induced early in pregnancy and rats with established renal hypertension induced 4 weeks before pregnancy. Non-pregnant rats in comparable states served as controls. 2. In normal pregnancy cardiac output increased by 33% and blood pressure and TPR decreased by 17 and 38% respectively. The same principal changes were noted in SH rats and those with short-standing renal hypertension, but no changes were found in rats with established renal hypertension during pregnancy. 3. Myometrial and placental blood supply was lower in all hypertensive groups compared with NC rats, the reduction being 46 and 36% in SH rats and in rats with established renal hypertension as much as 74 and 68% respectively. 4. In SH rats foetal weights were reduced compared with NC rats, but despite the 68% reduction of placental blood flow in rats with established renal hypertension foetal weights were here unchanged.

Animals

Characterization of the coronary vasodilator and hemodynamic actions of monensin, a carboxylic ionophore.

The effects of monensin on coronary blood flow (CBF) and other hemodynamic parameters were studied in anesthetized dogs. A dose-response relationship was established, and it was found that the lowest doses of monensin (5-25 micrograms/kg) produced a dose-dependent increase (3-5x) in CBF with a concomitant decrease in total peripheral resistance (TPR). Pretreatment with diphenhydramine, atropine, indomethacin, or propranolol resulted in no reduction in peak increase in CBF or in the duration of response to monensin. However, the response was partially blocked by aminophylline. Large doses (100 and 200 micrograms/kg) produced a dose-dependent increase in cardiac output, aortic pressure, and LV dP/dt max. The duration of these effects was dose-dependent, ranging from 60 to 120 min or longer. Heart rate remained unchanged with all doses of monensin. Pretreatment with propranolol, H87/07 (a cardioselective beta-blocker), and D-600 given alone or in combination significantly reduced, but did not completely abolish, the monensin-induced increase in LV dP/dt max and aortic pressure responses. The increase in CBF in the left anterior descending coronary artery was not significantly affected by these drug pretreatments. Thus, our studies indicate that monensin has two distinct pharmacological effects--in the lower dose range (less than 25 micrograms/kg) it produces a direct relaxation of the blood vessels resulting in an increase in CBF and a decrease in TPR; at high doses (greater than 25 micrograms/kg) it increases myocardial contractility and aortic blood pressure.

Animals

The influence of thoracic epidural analgesia on the circulation at rest and during physical exercise in man.

The effects of thoracic epidural analgesia (TEA) on the circulation at rest, during, and after physical exercise were investigated in 10 volunteers. At rest, TEA did not affect oxygen consumption (VO2) or cardiac output (Q), but heart rate (HR) was, increased by 7 beats/min, and stroke volume decreased correspondingly by 13 ml. Systolic arterial blood pressure was slightly reduced, but no other changes in systemic or pulmonary circulatory parameters were produced. TEA did not change VO2 during exercise, a 2.11/min reduction of Q being accompanied by a 4.2% increase of oxygen utilization coefficient. HR showed a relative reduction of about 10%. At moderate work loads during TEA, systemic arterial blood pressures were significantly lower than during control exercise. The resulting rate pressure product (RPP) was markedly reduced, while total peripheral resistance (TPR) remained unchanged. During recovery after the termination of exercise during TEA, VO2, Q, HR, RPP and TPR fell more rapidly towards values obtained at rest. From a clinical point of view the results support the safeness of TEA and also support its use in surgical patients with heart disease.

Adult

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats.

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.

Animals

An evaluation of large arteries compliance in man.

Cardiac output, blood pressure, and the characteristics of diastolic pressure decay were studied in 12 normal subjects and 23 sustained hypertensive patients of the same age. In normal subjects and in hypertensives, analysis of the diastolic decay showed that i) the form of the decay approximated a simple monoexponential curve during the last two-thirds of the diastolic segment, and ii) the time constant (t) of the curve was positively correlated with the total peripheral resistance (TPR), with an intercept of nearly zero. The validity of the relationship t = K x TPR was demonstrated both in groups of patients and also in individuals. Using a simple model for the vascular system, the K value was identified as the large arteries compliance and could thus be calculated in each individual. The values of arterial compliance was 1.26 +/- 0.04 ml.mmHg-1.m-2 in normal subjects and was significantly reduced in hypertensive patients (0.88 +/- 0.02 ml.mmHg=1.m-2,. P less than 0.001).

Adult

Twenty-four-hour pattern of circulation by radiotelemetry in the unrestrained dog.

Eight dogs with indwelling transducers for continuous radiotelemetry of the hemodynamic function were acclimatized in an unisolated room under 12:12 LD photoperiods, in phase with the solar day cycle, and constant temperature (20 +/- 1 degrees C). Light was turned on at 0600 and off at 1800. Mean aortic blood flow (ABF), mean aortic blood pressure (ABP), heart rate (HR), respiratory rate (RR), and cardiac work (CW) were maximal at about 1800 and minimal at time 0600. Total peripheral resistance (TPR) was highest and stroke volume (SV) lowest at about 1200. The 24-h mean was for HR 77 beats/min, SV 28 ml/beat, RR 11 breaths/min, ABF 177 ml/min per kg body wt, ABP 102 Torr, TPR 3,960 dyn . s . cm-5, and CW 218 Torr . 1/min. The range of amplitude fluctuations for daytime means was about 6% for ABP and SV and 11-17% for all others. It is suggested that the homeostatic balance and timing of circulation is circadian time dependent.

Animals

Liquid ventilation: cardiovascular adjustments with secondary hyperlactatemia and acidosis.

Cardiovascular adjustments during liquid ventilation were investigated in seven cats. Cardiac output (CO) and regional blood flow were measured with radioactive microspheres during both spontaneous air breathing (control) and ventilation with fluorocarbon liquid, FC-80. CO was found to decrease 48% (P less than 0.05) during liquid breathing as compared to control. This decrease largely reflected a reduced stroke volume. Despite the decreased CO, mean arterial pressure remained unchanged, indicating a 48% increase (P less than 0.002) in total peripheral resistance (TPR). Secondary to the reduced CO and increased TPR, extensive redistribution of blood flow occurred during liquid ventilation. The arterial lactate concentration and lactate-to-pyruvate ratio (L/P) were significantly increased (P less than 0.02). Furthermore, the increase in L/P correlated with the decrease in CO (r = 0.70; P less than 0.01). In turn, the significant decrease in pH during liquid breathing was found to correlate with the increase in L/P (r = 0.85; P less than 0.001). These data clearly demonstrate signficant alterations in cardiovascular dynamics during liquid ventilation with secondary hyperlactatemia and acidosis.

Animals

Systemic hemodynamics in nephrotoxic acute renal failure.

Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated (microsphere method) in awake rats, 3, 6, and 24 h after induction of acute renal failure by mercuric chloride (HgCl2; 4.7 mg/kg body weight). 3 h after injection of HgCl2, CO and RBF decreased to 77 and 72% of respective control values of 32.0 +/- 2.4 and 4.65 +/- 0.44 ml/min/100 g. Renal vascular resistance (RVR) and total peripheral resistance (TPR) were significantly increased compared to control at this time. Similar results were observed 6 h after administration of HgCl2. Volume expansion with plasma (2% of body weight) restored CO, RBF, TPR, and RVR to normal 3 h after injection of HgCl2. Despite significantly elevated blood urea nitrogen 24h after injection of HgCl2 (103.7 mg%), all hemodynamic parameters were within control range. Plasma volume was normal 3 h after HgCl2 but was significantly elevated compared to control 24 h after HgCl2 (4.73 vs. 3.92 ml/100 g, p less than 0.01). These findings indicate that factors other than preferential renal vasoconstriction may be involved in the transient renal ischemia of HgCl2-induced acute renal failure.

Acute Kidney Injury

Peripheral handling of angiotensin II and blood pressure control in hypertensive patients with unilateral and bilateral renal disease.

PRA, AII CR, AII E and cardiac output have been measured in 9 normals and in 22 hypertensives: 8 with URD, 12 with BRD and 2 with MHY. PRA, as well as AII E, shows the highest values in BRD and MHY patients. AII CR is directly correlated with blood pressure levels in URD and BRD patients (p less than 0.05 and p less than 0.001, respectively). A significant positive correlation is found between AII E and TPR (within each group of patients and among all subjects) and between PRA and TPR within the hypertensive patients. These data suggest that peripheral handling of AII is involved in the control of blood pressure in the patients studied.

Angiotensin II

Effect of halothane and pentobarbital anesthesia on the dispersion of indicator particles passing through the central circulation of the dog.

To investigate the effect of different anesthetics on the flow properties of the central circulation, curves were obtained by the multiple indocyanine-green indicator-dilution technic from 7 dogs anesthetized with halothane or pentobarbital. The width of the curve provided a measure of the dispersion of indicator particles during passage through the central circulation. The vascular resistance of the animals was altered by the administration of methoxamine and sodium nitroprusside. The authors found that dispersion in the central circulation is linearly related to the total peripheral resistance (TPR). For any value of TPR, the amount of dispersion of indicator particles passing through the central circulation was greater with halothane plus pentobarbital anesthesia than with pentobarbital only. The study indicates that the type of anesthesia influences the dispersion of indicator particles passing through the central circulation. A better under standing of this process will be helpful in interpreting the results of indicator-dilution cardiac-output determinations performed in persons under general anesthesia.

Anesthesia

Comparative vasodilator effects of nitroprusside, phentolamine, and nitroglycerin on hemodynamics, regional myocardial function and epicardial electrogram in dogs with acute myocardial ischemia.

The effects of nitroprusside (NP), phentolamine (PH), and nitroglycerin (NTG) were studied on systemic hemodynamics, regional contraction and epicardial ST segment in the border and non-ischemic zones of the left ventricle of anesthetized open chest dogs. The anterior descending coronary artery (LAD) was completely occluded. NP (5 microgram/Kg/min) or PH (100 microgram/Kg/min) was drip-infused, or a bolus injection of NTG (20 microgram/Kg) was administered intravenously. The 3 vasodilator agents produced somewhat similar reductions in systemic arterial pressure. However, NP caused a greater reduction in total peripheral resistance (TPR) than in left ventricular end-diastolic pressure (LVEDP), and caused a decline, in the ischemic marginal zone, in both ST segment eievation and paradoxical systolic lengthening. PH decreased TRP without reducing LVEDP and elevated the ST segment. NTG markedly reduced LVEDP and TPR slightly. NTG improved the elevated ST segment and paradoxical systolic expansion of the segmental myocardium in the border zone. Cardiac output rose with NP and PH, whereas injected NTG caused a reduction in cardiac output. These findings suggest that NP favourably affects the ischemic myocardium mainly by reducing the afterload and that the NTG-induced improvement of myocardial ischemia can be attributed mainly to preload reduction, while PH enhances cardiac function with slight or no improvement of myocardial ischemia in the border zone.

Acute Disease

Comparison of Cardiopulmonary Parameters in awake and anesthetized chickens.

Steady state cardiovascular and respiratory parameters in adult male chickens while they were awake and after anesthetization with a mixture of chloral hydrate, magnesium sulfate, and pentobarbital were compared. Blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), peripheral resistance (TPR), tidal volume (VT), respiratory rate (RR), minute ventilation (V), end-experatory carbon dioxide partial pressure (PACO2), and arterial blood gases and pH were measured simultaneously on birds spontaneously breathing air. Anesthetization resulted in increased HR and RR and decreased BP, CO, TPR, VT, PACO2, and blood gas tension. The data indicate a depression of cardiovascular function but no change in total ventilation although the relative contributions of VT and RR were changed. Anesthetization increased variability in SV although the other parameters were maintained in a steady-state condition over a 2-h period.

Anesthesia