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Shift workers from oil companies operating in the northern regions of Siberia were examined to develop signs of deterioration of the functional state of the body, such as a decrease in the ventilatory function of the lungs, a decrease in the adaptive reserve of the circulatory system, the prevalence of sympathetic tone in the autonomic nervous system, and thyroid imbalances, and all symptoms collectively reflect disorders in the physiological adaptation processes. The reported disorders are aggravated in the working shift period, but the disturbed functions fail to be recovered for the inter-shift rest period. A set of rehabilitation measures during the inter-shift period helps to reduce the signs of tension in the physiological adaptation, which is manifested in an improved functional state, a normalized adaptive potential, and a decrease in the sympathetic tone. [ABSTRACT FROM AUTHOR]

Administering relaxin to conscious rats and humans elicits systemic and renal vasodilation. The molecular mechanisms vary according to the duration of relaxin exposure-so-called 'rapid' (within minutes) or 'sustained' (hours to days) vasodilatory responses-both being endothelium-dependent. Rapid responses are mediated by G protein coupling to phosphoinositol-3 kinase/Akt (protein kinase B)-dependent phosphorylation and activation of nitric oxide synthase. Sustained responses are mediated by vascular endothelial and placental growth factors, as well as increases in arterial gelatinase activity. Thus, after hours or days of relaxin treatment, respectively, arterial MMP-9 or MMP-2 hydrolyze 'big' endothelin (ET) at a gly-leu bond to form ET, which in turn activates the endothelial ET receptor/nitric oxide vasodilatory pathway. Administration of relaxin to conscious rats also increases global systemic arterial compliance and passive compliance of select isolated blood vessels such as small renal arteries (SRA). The increase in SRA passive compliance is mediated by both geometric remodeling (outward) and compositional remodeling (decreased collagen). Relaxin-induced geometric remodeling has also been observed in brain parenchymal arteries, and this remodeling appears to be via the activation of peroxisome proliferator-activated receptor-γ. Given the vasodilatory and arterial remodeling properties of relaxin, the hormone may have therapeutic potential in the settings of abnormal pregnancies, heart failure, and pathologies associated with stiffening of arteries. [ABSTRACT FROM AUTHOR]

The systemic and peripheral hemodynamics was studied in male white rats under conditions of acute nitrite hypoxia (subcutaneous administration of sodium nitrite at doses of 1, 3, and 5 mg/100 g body mass). By the electrocardiographic, rheographic, and other methods there were recorded the heart rate (HR), minute circulation volume (MCV), cardiac output (CO), skeletal muscle circulation (SMC), brain circulation (BC), and systemic arterial pressure (AP). Nitrite was shown to produce a fast, dose-dependent AP fall accompanied by a decrease of MCV due to development of bradycardia and a fall of CO. At the phase of the steady hypotension, MCV increased due to a significant rise of CO on the background of the continuing bradycardia. The systemic circulatory effects of NaNO were found to be accompanied by a redistribution of peripheral circulation in the form of a dose-dependent increase of BC and a sharp fall of MCV. It was shown that 1-1.5 h after the nitrite injection the parameters of systemic and peripheral hemodynamics approached the initial levels. Possible triggering mechanisms of the initial stage of the rat cardiovascular adaptation to conditions of acute nitrite hypoxia are discussed. [ABSTRACT FROM AUTHOR]

Therapy of unresectable hepatic metastases may include tumor necrosis factor (TNF)-α treatment. Because of its serious systemic side effects, TNF-α is only used in isolated hepatic perfusion. This, however, is a technically demanding procedure with a substantial mortality rate. The infusion of TNF-α via the hepatic artery without hepatic isolation would be less invasive. Systemic side effects, however, have not been studied yet. Therefore, we evaluated in pigs the effects of TNF-α hepatic artery infusion (HAI) on systemic hemodynamics, inflammation, and organ injury. Animals were randomized in three groups. In group 1, HAI was performed with 0.9% NaCl ( n = 6). In group 2, 20 µg/kg TNF-α ( n = 6), and in group 3, 40 µg/kg TNF-α ( n = 6) were added. HAI was performed over 15 min, followed by 120 min of observation. Finally, 250 ml hydroxyethylstarch (HAES; 6%) was administered for resuscitation and hemodynamics were analyzed for another 30 min. Hepatic artery TNF-α infusion did not cause complications such as bleeding, cardiac depression, pulmonary dysfunction, or SIRS. TNF-α induced a 30% decrease of MAP and systemic vascular resistance, as well as a rise in heart rate and endexspiratory pCO2. TNF-α also moderately (10–20%) lowered the cardiac preload and induced a metabolic acidosis, which, however, could easily be controlled. TNF-α HAI did not induce liver toxicity, and all hemodynamic changes normalized either spontaneously within the 120-min observation period, or, at least, after HAES resuscitation. TNF-α-based HAI, which may represent a minimally invasive alternative to isolated hepatic perfusion, can be performed without early systemic hemodynamic complications. [ABSTRACT FROM AUTHOR]

Objective: The progression of liver cirrhosis eventually increases cardiac output, while blood pressure and systemic vascular resistance are reduced. A complex behavior of portal hemodynamic to hepatic artery and system circulation has not yet been presented. There is a lack in knowledge about the correlation of local and systemic circulation parameters to the degree of liver failure, with respect to presence of ascites and esophageal varices.Patients and Methods: The study sample was 76 patients hospitalized for established alcoholic liver cirrhosis. Patients were divided into groups according to Child-Pugh clinical score; grade A (n = 24), B (n = 18) and C (n = 18). Ascites was found in 28 patients and esophageal varices in 46. Portal vein flow velocity (PVFV), hepatic artery resistance index (HARI), heart and great vessels within mediastinal cavity were assessed with ultrasound devices equipped with spectral Doppler.Results: Significant differences in mean blood pressure, systemic vascular resistance index (SVRI) minute volume, cardiac index and PVFV were found in the group of patients with the most severe stage (C). In regard to presence of ascites statistically significant difference was observed in elevated mean blood pressure and SVRI. Correlation was found between conjugated HARI to blood pressure and to SVRI.Conclusions: In patients with liver cirrhosis there is an inversely reciprocal relationship of conjugated HARI with PVFV, correlating to disease grade. PVFV in cirrhosis decreases and HARI values were over 0.7. Study demonstrated that combining echocardiography with abdominal Doppler ultrasound served as valuable non-invasive diagnostic insight in liver and systemic circulation among different grade of cirrhosis. [ABSTRACT FROM AUTHOR]

Objective: To investigate whether neuromuscular block can affect bispectral index (BIS) or cerebral hemodynamics under moderate or deep sedation produced by propofol.Design and Setting: Prospective, controlled study in a university hospital affiliated intensive care unit.Patients: Seventeen surgical patients undergoing elective esophagectomy.Interventions: After stabilization with either light or deep sedation we investigated whether the BIS, electromyographic activity (EMG), or cerebral and systemic hemodynamic parameters were affected by administration of muscle relaxant.Measurements and Main Results: Neuromuscular block reduced the BIS during moderate sedation but not during deep sedation although the EMG at both levels of sedation was significantly reduced. No positive effects of neuromuscular block on cerebral hemodynamics were obtained with monitoring of regional cerebral oxygen saturation and middle cerebral artery blood velocity; however, significant effects on systemic hemodynamic parameters were observed only at moderate propofol sedation. The values of BIS and systemic hemodynamic variables with moderate sedation were also very similar to those with deep sedation and neuromuscular block although these values differed without neuromuscular block.Conclusions: Neuromuscular block altered the BIS score in moderately sedated patients but not in deeply sedated patients although cerebral hemodynamics was not affected by neuromuscular block during either moderate or deep sedation. Muscular relaxant also enhanced cardiovascular stability with moderate sedation. These results suggest that level of consciousness may be decreased by neuromuscular block during moderate sedation but not affected during deep sedation. [ABSTRACT FROM AUTHOR]

Octreotide is effective during 48 h in the treatment of acute variceal bleeding, probably by reducing variceal blood flow and pressure. Its basal and postprandial effects on splanchnic and systemic hemodynamics, and hormonal changes over this time interval have not yet been studied. Twenty-four patients with cirrhosis and portal hypertension were randomized to receive a liquid meal and either octreotide (Oct, 100 μg bolus intravenous, followed after 2 h by a continuous infusion of 25 μg/hr for 20 hr) or placebo (Plac) given at three consecutive days. Splanchnic (Doppler ultrasound) and systemic hemodynamics (noninvasive cardiac monitoring) were assessed on four consecutive days (one control day and three treatment days) during 2 hr. The postprandial increase in mean blood velocity of the superior mesenteric artery (SMA- Vmean, +44%), portal blood velocity (PV- Vmean, +44%) and total hepatic blood flow (HBF, +40%) observed in the placebo group during the control day was abolished during the first day of treatment (SMA-Vmean, +3%, P < 0.01; PV-Vmean, +6%, P < 0.05; HBF, −25%, P < 0.01) and still reduced after 48 hr in the octreotide group (SMA-Vmean, +28%, P < 0.05; PV-Vmean, +22%, P > 0.05; HBF, −8%, P < 0.05). The postprandial increase in cardiac index (CI, +10%) and decrease in systemic vascular resistance index (SVRI, −6%) were blunted after the initial injection of octreotide only (CI, −8%, P < 0.05; SVRI, +18%, P < 0.01). Endothelin-1-levels, which were increased at baseline (Plac 25 ± 17, Oct 16 ± 13 ng/liter, P > 0.05) decreased significantly after 48 hr of treatment with octreotide (Plac 27 ± 20, Oct 8 ± 4 ng/liter, P < 0.05). Octreotide is effective during 48 hr in the prevention of postprandial hyperemia in cirrhotics, even if its efficacy is decreasing over time. Moreover it may have positive effects on systemic vasodilation in cirrhotics. These findings suggest a potential role of this drug in the chronic treatment of portal hypertension. [ABSTRACT FROM AUTHOR]

Correlation between blood pressure and parameters of systemic hemodynamics was studied on cats using electrical stimulation of the ventral medulla oblongata. Changes in blood pressure induced by presoor activation were related to venous hemodynamics in the anterior rather than posterior vena cava. Venous blood flow is assumed to be involved in hemodynamic changes caused by stimulation of pressor centers but not depressor centers in the ventral medulla oblongata. [ABSTRACT FROM AUTHOR]

Calcitonin gene-related peptide (CGRP) produces vasodilation, hypotension, and tachycardia. We compared the hemodynamic effects of CGRP-induced hypotension with the effects of prostaglandin E (PGE), which is currently used as a hypotensive agent during anesthesia. Eighteen mongrel dogs were anesthetized with pentobarbital (25 mg·kg), and 0.87% halothane in oxygen (1MAC). Measurements of hemodynamic variables were made before, during, and after induced hypotension. The mean arterial pressure (MAP) was lowered to 60 mmHg by the infusion of either CGRP ( n=10) or PGE ( n=8). This decrease in MAP was appoximately 50% of the baseline value. The CGRP- and PGE-induced hypotension resulted in 61% and 51% maximum reductions ( P<0.01, respectively) in systemic vascular resistance associated with a significant increase in stroke volume index; the two treatments, however produced inconsistent changes in cardiac index (CI). With CGRP, a maximum increase of 144% ( P< 0.01) in CI was observed during induced hypotension. In contrast, PGE-induced hypotension caused no significant changes in CI throughout the observation period. Left ventricular maximum dP/dt decreased ( P<0.01) during the hypotensive period with PGE, whereas it remained un-changes during CGRP-induced hypotension. The different results for changes in CI and cardiac contractility during the CGRP- and PGE-induced hypotension were probably due to differences in ventricular filling pressure. Hypotension induced by PGE was associated with a significant decrease in heart rate (HR), whereas CGRP did not affect HR. This study shows that both CGRP and PGE are effective in decreasing afterload and in inducing hypotension; the results suggest that CGRP is a useful vasodilator for inducing hypotension during halothane anesthesia. [ABSTRACT FROM AUTHOR]

Calcitonin gene-related peptide (CGRP) is known to produce vasodilation, hypotension, and tachycardia. To investigate the interaction between CGRP and anesthetics, the hemodynamic response to infusions of CGRP was studied in dogs anesthetized with halothane or pentobarbital. In halothane-anesthetized dogs given 0.4 μg·kg of CGRP, mean arterial pressure (MAP) did not change significantly. However, there was a significant reduction in systemic vascular resistance (SVR) associated with significant increases in cardiac index (CI) and stroke volume index (SVI). Higher doses (4 and 40 μg·kg) of CGRP produced dose-dependent decreases in MAP accompanied by a reduction in SVR. Further, both CI and SVI significantly increased at 4 μg·kg CGRP but remained unchanged at the 40 μg·kg infusion rate. Heart rate (HR) was not increased at all doses but was decreased at 40 μg·kg. In pentobarbital-anesthetized dogs, CGRP at doses of 4 μg·kg produced a qualitatively similar cardiovascular responses as that observed in halothane-anesthetized dogs, but with one exception: HR was significantly increased. The results show that the hemodynamic profiles induced by CGRP during halothane or pentobarbital anesthesia are a decrease in MAP accompanied by a reduction in SVR and no consistent alterations in CI. However, CGRP effects on HR showed in a different way. The results also show that HR response differs depending on the anesthetics used: HR increases during pentobarbital anesthesia, while it does not increase during halothane anesthesia. [ABSTRACT FROM AUTHOR]

The cardiovascular responses to an infusion of KRN2391, a potassium channel opener, was studied in halothane-anesthetized dogs. Intravenous administration of KRN2391 at 1.0 and 5.0 μg·kg·min for 60 min produced dose-dependent decreases in mean arterial pressure (MAP) and systemic vascular resistance (SVR) associated with dose-dependent increases in the cardiac index (CI) and stroke volume index (SVI) but was not accompanied by an increase in heart rate (HR). The maximum decrease in MAP during the infusion of KRN2391 at 1.0 and 5.0 μg·kg·min was −13±7% (P<0.01) and −37±10% (P<0.01), respectively. The maximum reduction in SVR after 1.0 and 5.0 μg·kg·min was −20±11% (P<0.01) and −60±16% ( P<0.01), respectively. A KRN2391 infusion of 1.0 and 5.0 μg·kg·min increased Cl a maximum of 11±13% ( P<0.05) and 65±33% (P<0.01), respectively. KRN2391 1.0 μg·kg·min showed a tendency to increase SVI but this change was not significant, KRN2391 5.0 μg·kg·min, however, produced a significant increase in SVI. The present results demonstrate that the decrease in MAP and the increases in CI and SVI caused by KRN2391 are due to a reduction in the afterload. Therefore, we conclude that these cardiovascular profiles of KRN2391 may be benificial in perioperative uses including the control of systemic blood pressure and the treatment of hypertension during halothane anesthesia in clinical practice. [ABSTRACT FROM AUTHOR]

The effects of five sclerosants used for treating esophageal varices on blood coagulation and fibrinolysis, systemic hemodynamics, and vascular endothelial cells were studied in mongrel dogs. With each sclerosant, hemolysis and a decrease in the platelet count were observed. Changes in the blood coagulation system occurred immediately after sclerosant administration. Prolongation of the PT and APTT and decreases in fibrinogen and ga-PI were seen in the thrombin (TH), sodium tetradecyl sulfate (STS), and ethanolamine oleate (EO) groups. Polidocanol (PO) and absolute ethanol (ET) had less pronounced effects on these systems. A transient decrease in the cardiac index (CI), pulmonary artery pressure (PAP) and pulmonary artery resistance (PAR) was observed with the administration of the sclerosants, especially in the TH and STS groups. Excessive vascular endothelial damage was observed in the ET group, marked damage was seen in the EO and STS groups and slight damage was recorded in the PO and TH groups. [ABSTRACT FROM AUTHOR]

Portal pressure and systemic hemodynamics were evaluated for 30 minutes after intravenous injection of 400 mg of cimetidine in patients with and without liver cirrhosis when they were operated upon for varying surgical diseases. A transient fall of arterial pressure was seen in both groups of patients, but the change was statistically significant only in those with cirrhosis. Cimetidine did not substantially alter pulse rate, CVP, and portal pressure in both groups. The present results seem to indicate that rapid administration of cimetidine does not induce a fall of portal venous pressure in both cirrhotic and non-cirrhotic patients. [ABSTRACT FROM AUTHOR]

The features of systemic hemodynamics were analyzed in 19 non-cirrhotic patients with prominent esophageal varices. The patients were divided into two groups; Group I comprised 8 patients with an occluded extra-hepatic portal vein and Group II comprised 11 patients with a patent extra-hepatic portal vein whose histopathological diagnosis was idiopathic portal hypertension or hepatic fibrosis. An increase in the cardiac index and a decrease in the total peripheral resistance were significant in both groups when compared with 12 control patients (p<0.01). There was a significant correlation between the cardiac index and plasma volume in the 14 non-cirrhotic patients with portal hypertension (r=0.537, p<0.05), but no significant relationships were identified between the cardiac index and liver functional values. These results reveal that the systemic hemodynamics in non-cirrhotic portal hypertension are significantly hyperdynamic, as in cirrhotic portal hypertension. They also suggest that the expanded plasma volume secondary to the enlargement of the portal bed might be closely related to the mechanism of hyperdynamic systemic circulation in non-cirrhotic portal hypertension. [ABSTRACT FROM AUTHOR]

The randomized single-blind study was designed to compare the effects of captopril (Cap) and nadolol (Nad) on renal hemodynamics in 60 patients with essential hypertension. They were divided into two groups at random. Cap was given in dosage of 37. 5-75 mg/d per os and Nad 40-80 mg/d. The results show that both drugs increase the blood volume distributed to the kidneys from cardiac output (renal blood flow/cardiac output), Cap increasing 10% ( P<0. 05) and Nad 8% ( P<0. 05). Renal vascular resistance (RVR) is lowered by the two drugs, 13% ( P<0. 05) by Cap and 11% ( P<0. 05) by Nad. These suggest that both drugs facilitate the maintenance of renal blood circulation in patients with essential hypertension, being beneficial for longterm treatment of hypertension. [ABSTRACT FROM AUTHOR]

Recently, we showed that L-propionylcarnitine did not affect recovery of regional contractile function of porcine myocardium subjected to 1 h of low-flow ischemia followed by 2 hr of reperfusion. In that study, ischemia may have been too severe and/or the duration of reperfusion too short to detect a beneficial effect of the compound. Therefore, in the present study we investigated the effects of saline (control group; n = 14) or pretreatment with L-propionylcarnitine (3 days of 50 mg/kg p.o. b.i.d. + 50 mg/kg i.v. prior to the experiment; n = 13) on recovery of regional contractile function of the myocardium in open-chest anesthetized pigs, subjected to two cycles of 10 min of left anterior descending coronary artery (LADCA) occlusion, each followed by 30 min of reperfusion. In the control animals, at the end of the second reperfusion period, systemic vascular resistance had increased by 18%, which, however, was not observed in the L-propionylcarnitine-treated pigs. In the control group, during the first occlusion, systolic segment length shortening (SSLS) of the LADCA-perfused area decreased from 18.5 ± 5.5% to - 3.7 = 3.2%. After 30 min of reperfusion, SSLS of the LADCA-perfused area had only partially recovered to 6.2 ±5.9%. During the second occlusion-reperfusion cycle similar values for SSLS were observed. In the treated animals., SSLS of the LADCA-perfused area was slightly improved after the second occlusion-reperfusion cycle (p = 0.056). This effect did not result in an overall improvement in cardiac pump function. We conclude that in a model of myocardial stunning, L-propionylcarnitine prevents systemic vasoconstriction in response to ischemia and reperfusion and, possibly as a result of this effect, slightly ameliorates post-ischemic hypofunction. (Mol Cell Biochem 116: 147-153, 1992) [ABSTRACT FROM AUTHOR]