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PubMed1995

Hemodynamic alterations in the paravertebral venous plexus after spinal injury.

PURPOSE: To assess the prevalence of altered venous hemodynamics after spinal cord injury. MATERIALS AND METHODS: The authors performed venography in 200 ambulant patients and 107 patients with spinal injury. The hemodynamic characteristics of the paravertebral venous plexus were documented after pedal injection of contrast material. The hemodynamic and clinical data were correlated in patients with spinal cord injury. RESULTS: Abnormal venous return via the paravertebral venous plexus in the absence of iliac or inferior vena caval occlusion was shown in 73 (68%) of the 107 patients with spinal injury. This paravertebral venous flow route is not related to the time between injury and examination. It was demonstrable in the early as well as late post-traumatic period and was reproducible at subsequent examinations. The paravertebral venous flow route was more commonly seen in cervical than thoracolumbar injuries and was closely related to the severity of neurologic deficit (P = .0012). CONCLUSION: Abnormal vertebral venous hemodynamics occur in most patients with spinal cord injury and are more likely to occur in patients with complete neurologic deficit and cervical injury.

Case-Control Studies↗
PubMed1992

Different roles of IL-1 and TNF on hemodynamics and interorgan amino acid metabolism in awake dogs.

The present study examines the effects of interleukin 1 (IL-1) and tumor necrosis factor (TNF) on various hemodynamic parameters and interorgan fluxes of amino acids, glucose, and lactate in chronically catheterized awake dogs. The dogs received 5 micrograms.kg-1.h-1 of either human recombinant IL-1 beta or TNF intravenously for 2 h. Hemodynamic parameters and substrate fluxes across the gut and liver were determined during and 2 h after discontinuation of the cytokine infusions. Substrate fluxes were calculated by blood flows and arteriovenous differences. Both IL-1 and TNF enhanced the uptake of alanine, uptake of lactate, and output of glucose by the liver. These changes were associated with elevated arterial levels of alanine and lactate while arterial levels of glucose decreased. Uptake of glutamine by the liver was reduced by either IL-1 or TNF infusions. The effects of IL-1 and TNF on the hemodynamic parameters and on gut amino acid metabolism varied with the cytokine infused. IL-1 produced hyperdynamic state, increased splanchnic blood flow, and enhanced glutamine uptake by the gut. TNF infusion did not cause a hyperdynamic state, nor did it alter the gut handling of amino acids. We conclude that IL-1 and TNF exert distinct different effects on the systemic and hemodynamic parameters and on interorgan balances of amino acids, glucose, and lactate across the gut and the liver.

Amino Acids↗
PubMed1991

Adenosine and hemodynamic alterations in cirrhotic rats.

This study evaluated the hypothesis that adenosine may participate in the hemodynamic alterations observed in conscious unrestrained cirrhotic rats. In sham-operated rats, adenosine (20 micrograms.100 g body wt-1.min-1 iv) induced hyperdynamic circulation and significantly increased portal pressure, mimicking the hemodynamic changes observed in cirrhosis. Although adenosine significantly increased hyperdynamic circulation and portal pressure in cirrhotic rats, these changes were significantly less marked than in sham-operated rats. 8-Phenyltheophylline (20 micrograms.100 g body wt-1.min-1 iv), a specific and potent adenosine antagonist, significantly decreased portal tributary blood flow in sham-operated rats (-18.0 +/- 5.6%) but did not have a significant effect in cirrhotic rats. The limited effect of 8-phenyltheophylline was not due to an insufficient dose, since the dose administered antagonized the hemodynamic effect of exogenous adenosine up to 40 micrograms.100 g body wt-1.min-1. We conclude that in certain circumstances, although adenosine may aggravate the hyperdynamic circulation, in normal conditions, the hemodynamic alterations observed in cirrhotic rats are not mediated by adenosine.

Adenosine↗
PubMed2006

Developmental changes in hemodynamics of uterine artery, utero- and umbilicoplacental, and vitelline circulations in mouse throughout gestation.

In human pregnancy, abnormal placental hemodynamics likely contribute to the etiology of early-onset preeclampsia and fetal intrauterine growth restriction. The mouse is increasingly being deployed to study normal and abnormal mammalian placental development, yet the placental hemodynamics in normal pregnancy in mice is currently unknown. We used ultrasound biomicroscopy to noninvasively image and record Doppler blood velocity waveforms from the maternal and embryonic placental circulations in mice throughout gestation. In the uterine artery, peak systolic velocity (PSV) increased significantly from 23+/-2 (SE) to 59+/-3 cm/s, and end-diastolic velocity (EDV) increased from 7+/-1 to 28+/-2 cm/s in nonpregnant versus full-term females so that the uterine arterial resistance index (RI) decreased from 0.70+/-0.02 to 0.53+/-0.02. Velocities in the maternal arterial canal in the placenta were low and nearly steady and increased from 0.9+/-0.03 cm/s at embryonic day 10.5 (E10.5) to 2.4+/-0.07 cm/s at E18.5. PSV in the umbilical artery increased steadily from 0.8+/-0.1 cm/s at E8.5 to 15+/-0.6 cm/s at E18.5, whereas PSV in the vitelline artery increased from 0.6+/-0.1 cm/s at E8.5 to 4+/-0.2 cm/s at E13.5 and then remained stable to term. In the umbilical artery, the EDV detection rate was 0% at <or=E14.5 and 94% at E18.5, and the RI decreased from 1 to 0.82+/-0.01 during this interval. We conclude that ultrasound biomicroscopy can be used to monitor placental hemodynamics during pregnancy in mice. These results provide novel information concerning the development of the vitelline and placental circulations in mice and reveal strong similarities in placental hemodynamics between mice and humans.

Animals↗
PubMed2004

Protective effects of ascorbic acid on arterial hemodynamics during acute hyperglycemia.

Mortality increases when acute coronary syndromes are complicated by stress-induced hyperglycemia. Early pulse wave reflection can augment central aortic systolic blood pressure and increase left ventricular strain. Altered pulse wave reflection may contribute to the increase in cardiac risk during acute hyperglycemia. Chronic ascorbic acid (AA) supplementation has recently been shown to reduce pulse wave reflection in diabetes. We investigated the in vivo effects of acute hyperglycemia, with and without AA pretreatment, on pulse wave reflection and arterial hemodynamics. Healthy male volunteers were studied. Peripheral blood pressure (BP) was measured at the brachial artery, and the SphygmoCor pulse wave analysis system was used to derive central BP, the aortic augmentation index (AIx; measure of systemic arterial stiffness), and the time to pulse wave refection (Tr; measure of aortic distensibility) from noninvasively obtained radial artery pulse pressure (PP) waveforms. Hemodynamics were recorded at baseline and then every 30 min during a 120-min systemic hyperglycemic clamp (14 mmol/l). The subjects, studied on two separate occasions, were randomized in a double-blind, crossover manner to placebo or 2 g intravenous AA before the initiation of hyperglycemia. During hyperglycemia, AIx increased and Tr decreased. Hyperglycemia did not change peripheral PP but did magnify central aortic PP and diminished the normal physiological amplification of PP from the aorta to the periphery. Pulse wave reflection, as assessed from peripheral pulse wave analysis, is enhanced during acute hyperglycemia. Pretreatment with AA prevented the hyperglycemia-induced hemodynamic changes. By protecting hemodynamics during acute hyperglycemia, AA may have therapeutic use.

Acute Disease↗
PubMed2002

Influence of gender on the response to hemodynamic overload after myocardial infarction.

After myocardial infarction (MI), the left ventricle (LV) undergoes ventricular remodeling characterized by progressive global dilation, infarct expansion, and compensatory hypertrophy of the noninfarcted myocardium. Little attention has been given to the response of remodeling myocardium to additional hemodynamic overload. Studies have indicated that gender may influence remodeling and the response to both MI and hemodynamic overload. We therefore determined 1) structural and function consequences of superimposing hemodynamic overload (systemic hypertension) on remodeling myocardium after a MI and 2) the potential influence of gender on this remodeling response. Male and female Dahl salt-sensitive and salt-resistant rats underwent coronary ligation, resulting in similar degrees of MI. One week post-MI, all rats were placed on a high-salt diet. Four groups were then studied 4 wk after initiation of high-salt feeding: MI female, MI female + hypertension, MI male, and MI male + hypertension. Hypertension-induced pressure overload resulted in additional comparable degrees of myocardial hypertrophy in both females and males. In females, hypertension post-MI resulted in concentric hypertrophy with no additional cavity dilation and no measurable scar thinning. In contrast, in males, hypertension post-MI resulted in eccentric hypertrophy, further LV cavity dilation, and scar thinning. Physiologically, concentric hypertrophy in post-MI hypertensive females resulted in elevated contractile function, whereas eccentrically hypertrophied males had no such increase. Female gender influences favorably the remodeling and physiological response to hemodynamic overload after large MI.

Animals↗
PubMed2004

Hyperoxia causes oxygen free radical-mediated membrane injury and alters myocardial function and hemodynamics in the newborn.

Newborn children can be exposed to high oxygen levels (hyperoxia) for hours to days during their medical and/or surgical management, and they also can have poor myocardial function and hemodynamics. Whether hyperoxia alone can compromise myocardial function and hemodynamics in the newborn and whether this is associated with oxygen free radical release that overwhelms naturally occurring antioxidant enzymes leading to myocardial membrane injury was the focus of this study. Yorkshire piglets were anesthetized with pentobarbital sodium (65 mg/kg), intubated, and ventilated to normoxia. Once normal blood gases were confirmed, animals were randomly allocated to either 5 h of normoxia [arterial Po(2) (Pa(O(2))) = 83 +/- 5 mmHg, n = 4] or hyperoxia (Pa(O(2)) = 422 +/- 33 mmHg, n = 6), and myocardial functional and hemodynamic assessments were made hourly. Left ventricular (LV) biopsies were taken for measurements of antioxidant enzyme activities [superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)] and malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) as an indicator of oxygen free radical-mediated membrane injury. Hyperoxic piglets suffered significant reductions in contractility (P < 0.05), systolic blood pressure (P < 0.03), and mean arterial blood pressure (P < 0.05). Significant increases were seen in heart rate (P < 0.05), whereas a significant 11% (P < 0.05) and 61% (P < 0.001) reduction was seen in LV SOD and GPx activities, respectively, after 5 h of hyperoxia. Finally, MDA and 4-HNE levels were significantly elevated by 45% and 38% (P < 0.001 and P = 0.02), respectively, in piglets exposed to hyperoxia. Thus, in the newborn, hyperoxia triggers oxygen free radical-mediated membrane injury together with an inability of the newborn heart to upregulate its antioxidant enzyme defenses while impairing myocardial function and hemodynamics.

Aldehydes↗
PubMed2004

Exercise-induced and nitroglycerin-induced myocardial preconditioning improves hemodynamics in patients with angina.

In humans, regional myocardial dysfunction during ischemia may be improved by ischemic and pharmacological preconditioning. We assessed the possibility that exercise- and nitroglycerin-induced myocardial preconditioning may improve global cardiac performance during subsequent efforts in patients with angina. Ten patients suffering from chronic stable angina and ten healthy volunteers were studied. Through impedance cardiography we assessed hemodynamics during a maximal exercise test, which was used as a baseline (Bas test) and considered as a preconditioning exercise. The Bas test was followed by a sequence of maximal efforts performed during the first (FWOP; 30 min after the Bas test) and second (SWOP; 48 h after the Bas test) windows of protection conferred by ischemic preconditioning. Hemodynamics was further evaluated during maximal exercise performed 48 h later with pharmacologically induced SWOP (PI-SWOP) obtained by transdermal administration of 10 mg of nitroglycerin. In the angina patients, FWOP, SWOP, and PI-SWOP delayed the time to ischemia and allowed them to achieve higher workloads compared with the Bas test. Furthermore, heart rate and cardiac output at peak exercise were enhanced during all the preconditioning phases with respect to the Bas test. However, only SWOP and PI-SWOP increased myocardial contractility and stroke volume. No changes in hemodynamics were detectable in the control subjects. This study demonstrates that in patients with stable angina, although hemodynamics during exercise can be positively improved during both FWOP and SWOP, differences exist between these two phases. Furthermore, the mimicking of exercise-induced SWOP by PI-SWOP with transdermal nitroglycerin may represent an important clinical aspect.

Angina Pectoris↗
PubMed1987

Hemodynamic alterations in chronically conscious unrestrained diabetic rats.

Important cardiovascular dysfunctions have been described in streptozotocin (STZ)-diabetic rats. To determine the influence of these changes on the hemodynamic state and whether insulin treatment can avoid them, different hemodynamic parameters, obtained by the thermodilution method, were studied in STZ-induced (65 mg/kg) diabetic male Wistar rats, as well as in age-control, weight-control, and insulin-treated diabetic ones. All rats were examined in the conscious, unrestrained state 12 wk after induction of diabetes or acidified saline (pH 4.5) injection. At 12 wk of diabetic state most important findings were normotension, high blood volume, bradycardia, increase in stroke volume, cardiac output, and cardiosomatic ratio, and decrease in total peripheral resistance and cardiac contractility and relaxation (dP/dtmax and dP/dtmin of left ventricular pressure curves). The insulin-treated diabetic rats did not show any hemodynamic differences when compared with the control animals. These results suggest that important hemodynamic alterations are present in the chronic diabetic state, possibly conditioning congestive heart failure. These alterations can be prevented by insulin treatment.

Animals↗
PubMed1992

Hemodynamic and proteolytic effects of intravenous injection of purified human plasma kallikrein.

To investigate the precise hemodynamic effects of purified human plasma kallikrein, small doses (0.3 U/kg) of this proteolytic enzyme were infused over 10 s in five pigs. Hemodynamic performance was evaluated by means of a Swan-Ganz catheter, and parameters of the plasma kallikrein-kinin, coagulation, and fibrinolytic systems were determined by means of chromogenic peptide substrate assays. The infusions of plasma kallikrein were followed by rapid decreases in mean arterial pressure (to 43 +/- 2% of baseline values) and increases in cardiac output (to 145 +/- 6% of baseline values), accounting for marked decreases in systemic vascular resistance, to 28 +/- 1% of initial values. Heart rate, mean pulmonary arterial, central venous, and pulmonary capillary wedge pressures did not change after the injection. Pulmonary vascular resistance decreased to 69 +/- 3% of baseline values. The hemodynamic changes gradually normalized during the following 10 min. Functional levels of prekallikrein, kallikrein, kallikrein inhibition, prothrombin, antithrombin III, plasmin, and antiplasmin were not affected by the injection or the resulting hemodynamic changes; the hematocrit and the number of circulating leukocytes or platelets were also unaffected.

Animals↗
PubMed1994

Effects of intra-atrial injection of colored microspheres on systemic hemodynamics and regional blood flow in rats.

The hemodynamic effects of various numbers of colored nonradioactive microspheres (CMS) and those of accumulation of CMS caused by multiple sequential injection were evaluated in 51 Sprague-Dawley male rats. CMS (15 microns) were injected into the left atrium. Regional blood flow and cardiac output were evaluated using the reference blood sample technique. Ficoll-70 was given after each blood sample withdrawal as a fluid replacement. A bolus injection of < or = 1,000,000 CMS caused no significant hemodynamic disturbances. Amounts of 500,000 CMS can be repeatedly injected up to four times (cumulative dose of 2,000,000 CMS) without producing any adverse hemodynamic effects. The values of cardiac output obtained with the CMS technique were correlated well (r = 0.971, P < 0.0001) with those obtained with electromagnetic flow probes. An excellent reproducibility of organ blood flow was observed after four sequential injections of 500,000 CMS. This study establishes the limits of CMS that can be injected into the rat without inducing hemodynamic changes and also suggests that the CMS technique can be employed to evaluate cardiac output and regional blood flow precisely and repeatedly.

Animals↗
PubMed1999

Hypertrophic response to hemodynamic overload: role of load vs. renin-angiotensin system activation.

Myocardial hypertrophy is one of the basic mechanisms by which the heart compensates for hemodynamic overload. The mechanisms by which hemodynamic overload is transduced by the cardiac muscle cell and translated into cardiac hypertrophy are not completely understood. Candidates include activation of the renin-angiotensin system (RAS) and angiotensin II receptor (AT1) stimulation. In this study, we tested the hypothesis that load, independent of the RAS, is sufficient to stimulate cardiac growth. Four groups of cats were studied: 14 normal controls, 20 pulmonary artery-banded (PAB) cats, 7 PAB cats in whom the AT1 was concomitantly and continuously blocked with losartan, and 8 PAB cats in whom the angiotensin-converting enzyme (ACE) was concomitantly and continuously blocked with captopril. Losartan cats had at least a one-log order increase in the ED50 of the blood pressure response to angiotensin II infusion. Right ventricular (RV) hypertrophy was assessed using the RV mass-to-body weight ratio and ventricular cardiocyte size. RV hemodynamic overload was assessed by measuring RV systolic and diastolic pressures. Neither the extent of RV pressure overload nor RV hypertrophy that resulted from PAB was affected by AT1 blockade with losartan or ACE inhibition with captopril. RV systolic pressure was increased from 21 +/- 3 mmHg in normals to 68 +/- 4 mmHg in PAB, 65 +/- 5 mmHg in PAB plus losartan and 62 +/- 3 mmHg in PAB plus captopril. RV-to-body weight ratio increased from 0.52 +/- 0.04 g/kg in normals to 1.11 +/- 0.06 g/kg in PAB, 1.06 +/- 0.06 g/kg in PAB plus losartan and 1.06 +/- 0.06 g/kg in PAB plus captopril. Thus 1) pharmacological modulation of the RAS with losartan and captopril did not change the extent of the hemodynamic overload or the hypertrophic response induced by PAB; 2) neither RAS activation nor angiotensin II receptor stimulation is an obligatory and necessary component of the signaling pathway that acts as an intermediary coupling load to the hypertrophic response; and 3) load, independent of the RAS, is capable of stimulating cardiac growth.

Angiotensin II↗
PubMed2005

Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

Adrenergic beta-Antagonists↗
PubMed1989

Hemodynamic effects of activation of renal and mesenteric sensory nerves in rats.

Afferent nerves from the kidney and mesentery reflexly influence the cardiovascular system when activated. To examine the specificity of these reflexes, comparisons were made of the regional hemodynamic responses elicited by intra-arterial infusion of various agents into the renal (ir) and mesenteric (im) circulation. Experiments were performed in conscious rats, chronically instrumented with Doppler flow probes. Local ir as well as im infusions of bradykinin caused a hemodynamic reflex pattern characterized by a dose-dependent increase in arterial pressure, heart rate, and resistance in the renal and mesenteric vascular beds, whereas hindquarter resistance did not change. Similar hemodynamic reflex patterns were evoked by ir and im infusions of adenosine and 5-hydroxytryptamine. Thus neither application of different chemicals nor their route of infusion resulted in qualitatively different hemodynamic reflex patterns. This suggests that afferent nerve fibers from the kidney and mesentery share a common physiological function.

Adenosine↗
PubMed1989

Effects of converting-enzyme inhibitor on hemodynamic actions of ANP in renal hypertensive rats.

In the present study, we have evaluated whether the hemodynamic effects of atrial natriuretic peptide (ANP) infusion in two-kidney, one-clip (2K, 1C) hypertensive rats are mediated by inhibition of the renin-angiotensin system (RAS). Hemodynamic determinations were performed by thermodilution in conscious, chronically instrumented animals. ANP (1.5 micrograms.kg-1.min-1) and converting-enzyme (CE) inhibitor captopril (1 mg/kg plus 1 mg.kg-1.h-1), produced a similar fall of blood pressure through different hemodynamic mechanisms. ANP induced hypotension by decreasing cardiac index (CI; from 337.3 +/- 24.9 to 255.1 +/- 21.3 ml.min-1.kg-1, P less than 0.001), whereas a fall in total peripheral resistance (TPR) was observed during CE inhibition (from 0.568 +/- 0.02 to 0.488 +/- 0.02 mmHg.min.ml-1.kg, P less than 0.05). In addition, the ANP-induced decrease in CI was not significantly modified by previous CE inhibition. Furthermore, the decrease in TPR induced by CE inhibition did not change when CE inhibitor was administered during ANP treatment. The results of the present study indicate that the acute hemodynamic responses to ANP in 2K, 1C hypertensive rats are not mediated through antagonism of the vasoconstrictor actions of the RAS.

Angiotensin II↗
PubMed1993

Relationship between dietary sodium intake, hemodynamics, and cardiac mass in SHR and WKY rats.

To study the effects of sodium intake on circulatory homeostasis and cardiac structure, changes in cardiac mass, systemic hemodynamics, and organ blood flows were determined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats after 10 wk of controlled dietary intake of low sodium (0.01%), standard sodium (0.44%), and high sodium (2 levels: 1.44 and 4%). Systemic and regional hemodynamics were measured in conscious rats using the radioactive microsphere reference method. The various dietary sodium manipulations did not cause any changes in systemic and regional hemodynamics in the WKY rats. In contrast, the high-sodium diets increased arterial pressure and total peripheral resistance progressively in the SHR rats while decreasing cardiac index, heart rate, and organ blood flows to heart, kidneys, and splanchnic area. The higher sodium intake (4%) increased total and left ventricular mass index in both the SHR and the WKY rats even though hemodynamics of the WKY rats remained unchanged. These data indicate that the high-sodium diet, in addition to producing general vasoconstriction and exacerbation of hypertension, increased cardiac mass further in SHR rats; it also increased cardiac mass in the WKY rats independent of arterial pressure changes, suggesting that high sodium intake may be an independent pathogenetic factor for the development of cardiac hypertrophy.

Aging↗
PubMed2001

Hemodynamic response patterns to acute behavioral stressors resemble those to cocaine.

Hemodynamic responses to cocaine vary greatly between animals, and the variability is related to the incidence of cocaine-induced cardiomyopathies and hypertension. The variability in cardiac output and systemic vascular resistance responses to cocaine in individuals is correlated with the responses to acute startle (air jet). This experiment was designed to determine whether responses to cocaine and to air jet are related to those evoked by a conditioned stimulus (tone preceding foot shock) and to an unconditioned stimulus (cold water). We verified the relationship in hemodynamic response patterns between cocaine and cold stress using selective receptor antagonists. Rats were instrumented with a pulsed Doppler flow probe on the ascending aorta for determination of cardiac output and with an arterial cannula for recording arterial pressure and heart rate. After recovery, some rats were tested multiple times with four different stimuli: air jet (6 trials), 15-s tone preceding 1-s foot shock (12 trials), cold water exposure (1 cm deep for 1 min, 4-12 trials), and cocaine (5 mg/kg iv, 4-6 trials) while hemodynamic parameters were recorded. Each stimulus was capable of eliciting a pressor response that was associated with variable changes in cardiac output. The cardiac output response to cocaine was correlated with the initial responses to each stressor in individual rats. Responses evoked by cold stress were most similar to those elicited by cocaine. Furthermore, nicardipine (25 microg/kg iv) or atropine methylbromide (0.5 mg/kg iv) pretreatment prevented the cardiac output differences to acute cold stress, as noted after cocaine administration. On the other hand, propranolol (1 mg/kg iv) exacerbated both the decrease in cardiac output and the stress-induced increase in systemic vascular resistance as previously reported with cocaine. Therefore, the initial response to cold water exposure is a reliable method of evoking characteristic hemodynamic response patterns that, as seen with cocaine, may provide a suitable model for identifying the causes for predilection to stress-induced cardiovascular disease.

Acute Disease↗
PubMed1984

Ca-dependent hemodynamic and natriuretic effects of atrial extract in isolated rat kidney.

The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.

Animals↗