scholarly journals Changes in Microvascular Reactivity and Systemic Vascular Resistance in Patients With Psoriasis

2020 ◽  
pp. 1-6
Keyword(s):  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Single Channel ◽  
Diastolic Pressure ◽  
Normal Skin ◽  
Psoriatic Skin ◽  
Medical Systems ◽  
Vascular Control ◽  
Cardiovascular Parameters

The aim: of this pilot study was to explore local blood flow in psoriatic plaques and normal skin before and after provocations known to alter cutaneous vascular resistance in order to test whether the increased flow was caused by a failure of normal vascular control processes in plaque skin and what association it has with cardiovascular parameters. Material and methods: 11 patients who had a diagnosis of psoriasis vulgaris were enrolled in the study. Cutaneous blood flow was recorded over plaque and clinically normal skin. 10 healthy sex and age matched subjects were selected as controls. Blood flow in psoriatic and normal skin was measured by a single- channel Laser Doppler blood flowmeter (Blood Flow meter, AD Instruments Ltd., Oxford, UK). Post-occlusive reactive hyperaemia was assessed on the plaque and non-plaque site. Cardiovascular parameters: heart rate, systolic and diastolic pressure, cardiac output, and vascular resistance were continuously monitored by a Finapres (FINAPRES Medical Systems, The Netherlands). Results: In patients, basal-LD flow was significantly higher in psoriatic skin compared to nonpsoriatic skin and significantly higher than in the controls. However, the post-occlusive hyperaemia test did not reveal significant differences between the patients and control subjects. Systemic vascular resistance was significantly lower in patients with psoriasis compared to healthy individuals. Conclusions: The results suggest that reduced microvascular resistance is associated with a significant increase in blood flow of psoriatic plaques and with lower systemic vascular resistance.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Progressive myocardial dysfunction associated with increased vascular resistance

1980 ◽  
Vol 239 (4) ◽  
pp. H477-H477 ◽  
Author(s):  
Joseph A. Franciosa ◽  
Richard Heckel ◽  
Catherine Limas ◽  
Jay N. Cohn
Keyword(s):  
Heart Failure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Peripheral Circulation ◽  
Left Ventricular ◽  
Stroke Work ◽  
Low Cardiac Output

To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 ± 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 ± 8.5 to 84.0 ± 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 ± 0.8 mmHg at control and rose to 11.8 ± 1.4 mmHg at 1 mo and 14.9 ± 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 ± 0.1 at control to 3.8 ± 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.

Circulatory changes following premature delivery in a baboon model of hyaline membrane disease

1991 ◽  
Vol 261 (4) ◽  
pp. H1148-H1154 ◽  
Author(s):  
J. P. Kinsella ◽  
D. R. Gerstmann ◽  
R. A. Delemos
Keyword(s):  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Oxygen Transport ◽  
Ductus Arteriosus ◽  
Hyaline Membrane Disease ◽  
Premature Delivery ◽  
Organ Blood Flow ◽  
Hemodynamic Changes ◽  
Hyaline Membrane

The premature baboon delivered by hysterotomy at 140 +/- 2 days (75%) gestation develops hyaline membrane disease (HMD) and left-to-right (L-R) shunting through the patent ductus arteriosus (PDA). To characterize hemodynamic changes that follow premature delivery, we measured systemic and organ blood flow, oxygen transport, and systemic vascular resistance over the first 96 h of life. We compared these measurements with those from more mature animals of the same species. Radiolabeled microspheres were used to measure organ blood flow (in ml.min-1.g-1) at 3 (n = 18), 23 (n = 17), and 96 h (n = 4) in the premature animals, and at 13 +/- 4 mo in the older animals (n = 5). Premature animals demonstrated over the first 96 h of life significant hemodynamic changes that included decreased systemic vascular resistance (P less than 0.001), increased systemic (P less than 0.05), intestinal (P less than 0.05), and hepatic blood flow (P less than 0.05), as well as resolution of L-R PDA shunting. These 96-h values were similar to those of the more mature infant baboons. Blood flow and oxygen transport to the kidneys and cerebrum did not significantly increase over the first 96 h in premature baboons and were significantly less than those of 13-mo-old animals (P less than 0.01, both). We speculate that low renal and cerebral blood flow in the 140-day premature baboon are manifestations of multisystem immaturity and, as such, may represent persistent physiological disturbances that are distinct from the severity of underlying lung disease in HMD.

Haemodynamic effects of vasopressin in man are related to posture

1986 ◽  
Vol 70 (2) ◽  
pp. 177-184 ◽  
Author(s):  
H. C. R. Simpson ◽  
J. E. Zubillaga ◽  
J. G. Collier ◽  
E. D. Bennett ◽  
V. T. Y. Ang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Low Dose ◽  
Forearm Blood Flow ◽  
Haemodynamic Effects ◽  
High Dose ◽  
Dose Infusion

1. Ten healthy volunteers received intravenous infusions of arginine vasopressin (AVP) at 0.1 m-unit min−1 kg−1 and 5% d-glucose on separate days. AVP caused a small fall in forearm blood flow and small rises in mean arterial pressure and systemic vascular resistance. Cardiac output was unaffected. 2. When subjects were tilted to 50° the fall in forearm blood flow was much greater, mean fall being 44.8% with AVP compared with 18.2% with d-glucose. Cardiac output also fell significantly more with AVP, and diastolic pressure, mean arterial pressure and systemic vascular resistance rose significantly more on tilting during AVP infusion than with d-glucose. 3. Six of the same volunteers were given sequential infusions of ‘low dose’ (0.0125 m-unit min−1 kg−1) and ‘high dose’ (0.3 m-unit min−1 kg−1) AVP on a third occasion. Tilting still produced a mean fall in forearm blood flow of 41.2% during low dose infusion, despite a mean plasma AVP level of only 1.9 pg/ml, which is well within the physiological range. When the AVP concentration was increased 24-fold to the high dose, forearm blood flow fell only a further 8.8%. The low dose infusion was also associated with a marked fall in cardiac output on tilting and a rise in systemic vascular resistance. 4. We conclude that AVP has profound haemodynamic effects in man at physiological concentrations. Although these effects are modest in the supine position, they become marked on tilting, suggesting a possible role for AVP in the postural control of blood pressure.

L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia

1996 ◽  
Vol 271 (4) ◽  
pp. H1296-H1301
Author(s):  
K. G. Allman ◽  
A. P. Stoddart ◽  
M. M. Kennedy ◽  
J. D. Young
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Nitric Oxide Production ◽  
Mesenteric Blood Flow ◽  
Oxide Production ◽  
Arterial Blood ◽  
Nitrate Concentrations

We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation

1995 ◽  
Vol 78 (5) ◽  
pp. 1642-1650 ◽  
Author(s):  
C. F. Pilati ◽  
M. B. Maron ◽  
F. J. Bosso
Keyword(s):  
Pulmonary Edema ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Edema Formation ◽  
Systemic Hemodynamic ◽  
Lv Dysfunction ◽  
The Right

This study was undertaken to determine whether endothelium-derived relaxing factor (EDRF) modulates the pulmonary and systemic hemodynamic responses to massive sympathetic nervous system (SNS) activation and, in so doing, also modulates the degree of SNS-induced left ventricular (LV) dysfunction and the likelihood for pulmonary edema formation. The SNS of 13 anesthetized untreated rabbits and 14 anesthetized rabbits pretreated with the EDRF inhibitor, N omega-nitro-L-arginine (L-NNA, 20 mg/kg), was massively activated with an intracisternal injection of veratrine. Pulmonary and systemic arterial pressures increased to the same extent in both groups, but LV end-diastolic pressure was significantly lower in untreated rabbits. During this time, cardiac output decreased by 37% in L-NNA pretreated rabbits compared with 8% in untreated animals. Peak systemic and pulmonary vascular resistances increased significantly in L-NNA rabbits, whereas only systemic vascular resistance increased significantly in untreated rabbits. However, this increase in systemic vascular resistance was threefold less than that observed for L-NNA-treated animals. Although the degree of LV dysfunction was greater in the L-NNA rabbits, pulmonary edema developed less frequently in this group. We suggest that when EDRF release is inhibited during massive SNS activity, pulmonary vascular resistance increases markedly, which causes the right ventricle to fail. We further suggest that the reduced right ventricular output maintains pulmonary microvascular pressure below levels required for edema development.

Hemodynamic effects of periodic obstructive apneas in sedated pigs with congestive heart failure

2000 ◽  
Vol 88 (3) ◽  
pp. 1051-1060 ◽  
Author(s):  
Ling Chen ◽  
Quihu Shi ◽  
Steven M. Scharf
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Air Breathing ◽  
Obstructive Sleep

Because of similar physiological changes such as increased left ventricular (LV) afterload and sympathetic tone, an exaggerated depression in cardiac output (CO) could be expected in patients with coexisting obstructive sleep apnea and congestive heart failure (CHF). To determine cardiovascular effects and mechanisms of periodic obstructive apnea in the presence of CHF, 11 sedated and chronically instrumented pigs with CHF (rapid pacing) were tested with upper airway occlusion under room air breathing (RA), O2 breathing (O2), and room air breathing after hexamethonium (Hex). All conditions led to large negative swings in intrathoracic pressure (−30 to −39 Torr) and hypercapnia ([Formula: see text] ∼60 Torr), and RA and Hex also caused hypoxia (to ∼42 Torr). Relative to baseline, RA increased mean arterial pressure (from 97.5 ± 5.0 to 107.3 ± 5.7 Torr, P < 0.01), systemic vascular resistance, LV end-diastolic pressure, and LV end-systolic length while it decreased CO (from 2.17 ± 0.27 to 1.52 ± 0.31 l/min, P < 0.01), stroke volume (SV; from 23.5 ± 2.4 to 16.0 ± 4.0 ml, P < 0.01), and LV end-diastolic length (LVEDL). O2 and Hex decreased mean arterial pressure [from 102.3 ± 4.1 to 16.0 ± 4.0 Torr ( P < 0.01) with O2 and from 86.0 ± 8.5 to 78.1 ± 8.7 Torr ( P < 0.05) with Hex] and blunted the reduction in CO [from 2.09 ± 0.15 to 1.78 ± 0.18 l/ml for O2 and from 2.91 ± 0.43 to 2.50 ± 0.35 l/ml for Hex (both P< 0.05)] and SV. However, the reduction in LVEDL and LV end-diastolic pressure was the same as with RA. There was no change in systemic vascular resistance and LVEDL during O2 and Hex relative to baseline. In the CHF pigs during apnea, there was an exaggerated reduction in CO and SV relative to our previously published data from normal sedated pigs under similar conditions. The primary difference between CHF (present study) and the normal animals is that, in addition to increased LV afterload, there was a decrease in LV preload in CHF contributing to SV depression not seen in normal animals. The decrease in LV preload during apneas in CHF may be related to effects of ventricular interdependence.

scholarly journals 94 SYSTOLIC LEFT VENTRICULAR AND AORTIC BLOOD FLOW RE-Q4 SPONSE TO INCREASING SYSTEMIC VASCULAR RESISTANCE

1985 ◽  
Vol 19 (4) ◽  
pp. 126A-126A
Author(s):  
Christine M Donnelly ◽  
Linda J Addonizio ◽  
Fredrick Z Bierman ◽  
Lynne L Johnson
Keyword(s):  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Aortic Blood Flow ◽  
Aortic Blood

Diaphragmatic perfusion heterogeneity during exercise with inspiratory resistive breathing

1990 ◽  
Vol 68 (5) ◽  
pp. 2177-2181 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Exercise Capacity ◽  
Vascular Resistance ◽  
Maximal Exercise ◽  
Perfusion Pressure ◽  
Work Of Breathing ◽  
Regional Distribution ◽  
Resistive Breathing ◽  
Exercise Induced

Regional distribution of diaphragmatic blood flow (Q; 15-microns-diam radionuclide-labeled microspheres) was studied in normal (n = 7) and laryngeal hemiplegic (LH; n = 7) ponies to determine whether the added stress of inspiratory resistive breathing during maximal exercise may cause 1) redistribution of diaphragmatic Q and 2) crural diaphragmatic Q to exceed that in maximally exercising normal ponies. LH-induced augmentation of already high exertional work of breathing resulted in diminished locomotor exercise capacity so that maximal exercise in LH ponies occurred at 25 km/h compared with 32 km/h for normal ponies. The costal and crural regions received similar Q in both groups at rest. However, exercise-induced increments in perfusion were significantly greater in the costal region of the diaphragm. At 25 km/h, costal diaphragmatic perfusion was 154 and 143% of the crural diaphragmatic Q in normal and LH ponies. At 32 km/h, Q in costal diaphragm of normal ponies was 136% of that in the crural region. Costal and crural diaphragmatic Q in LH ponies exercised at 25 km/h exceeded that for normal ponies but was similar to the latter during exercise at 32 km/h. Perfusion pressure for the three conditions was also similar. It is concluded that diaphragmatic perfusion heterogeneity in exercising ponies was preserved during the added stress of inspiratory resistive breathing. It was also demonstrated that vascular resistance in the crural and costal regions of the diaphragm in maximally exercised LH ponies remained similar to that in maximally exercising normal ponies.

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