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Mediastinal tube placement in children with pneumomediastinum: hemodynamic changes and description of technique.

OBJECTIVE: To describe the technique, hemodynamic response, and complication rate after the insertion of a percutaneous mediastinal tube for drainage of pneumomediastinum. DESIGN: A combined retrospective and prospective study in mechanically ventilated children with pneumomediastinum. SETTING: Multidisciplinary pediatric intensive care unit at a children's hospital. PATIENTS: The medical records and chest radiographs of 25 (15 retrospective and 10 prospective) patients who had placement of a mediastinal tube for drainage of pneumomediastinum from 1990 to 1995 were reviewed. Hemodynamic data were collected prospectively in the ten consecutive children from January 1994 to April 1995. INTERVENTION: Mediastinal tube placement: The subxyphoid area was cleansed with povidone-iodine and draped. An 18-gauge, thin-walled introducer needle was inserted 1 to 2 cm below the xyphoid process at an angle of 20 degrees from the anterior abdominal wall, directed at the substernal space. Either a 9-Fr or 11-Fr pericardiocentesis catheter was inserted over a wire and advanced to the third intercostal space. The catheter was secured and connected to 10 cm H2O suction, using a standard thoracostomy tube drainage device. MEASUREMENTS AND MAIN RESULTS: The size of the mediastinal air column on a lateral chest radiograph was measured before and after placement of the mediastinal tube. The mean change in the size of the mediastinal air column was -1.6 cm (median -1.5, p < .001). In the ten prospective patients, hemodynamic data were recorded immediately before and after placement of a mediastinal tube from previously placed arterial and central venous pressure catheters. The mean hemodynamic changes after the mediastinal tube placement were: heart rate -4 beats/min (median = -1, p = .14); systolic blood pressure 16 mm Hg (median = 10, p = .007); diastolic blood pressure 11 mm Hg (median = 11, p = .005); mean arterial pressure 12 mm Hg (median = 8, p = .005); and central venous pressure -2 mm Hg (median = -1, p = .04). In four patients with pulmonary artery thermodilution catheters, the mean increase in cardiac index immediately following placement of the mediastinal tube was 34%. No complications, including bleeding, cardiac puncture, or infection occurred. CONCLUSIONS: These findings suggest that hemodynamic compromise commonly accompanies pneumomediastinum in children. Decompression of the mediastinal space and drainage of the pneumomediastinum, using this simple bedside technique for continuous drainage, can be performed rapidly and safely in children, resulting in immediate hemodynamic improvement, and allowing for continuous drainage.

Adolescent↗

Prospective evaluation of short-term, high-volume isovolemic hemofiltration on the hemodynamic course and outcome in patients with intractable circulatory failure resulting from septic shock.

OBJECTIVE: To evaluate the effects of short-term, high-volume hemofiltration (STHVH) on hemodynamic and metabolic status and 28-day survival in patients with refractory septic shock. DESIGN: Prospective, interventional. SETTING: Intensive care unit (ICU), tertiary institution. PATIENTS: Twenty patients with intractable cardiocirculatory failure complicating septic shock, who had failed to respond to conventional therapy. INTERVENTIONS: STHVH, followed by conventional continuous venovenous hemofiltration. STHVH consisted of a 4-hr period during which 35 L of ultrafiltrate is removed and neutral fluid balance is maintained. Subsequent conventional continuous venovenous hemofiltration continued for at least 4 days. MEASUREMENTS AND MAIN RESULTS: Cardiac index, systemic vascular resistance, pulmonary vascular resistance, oxygen delivery, mixed venous oxygen saturation, arterial pH, and lactate were measured serially. Fluid and inotropic support were managed by protocol. Therapeutic endpoints were as follows during STHVH: a) by 2 hrs, a > or =50% increase in cardiac index; b) by 2 hrs, a > or =25% increase in mixed venous saturation; c) by 4 hrs, an increase in arterial pH to >7.3; d) by 4 hrs, a > or =50% reduction in epinephrine dose. Patients who attained all four goals (11 of 20) were considered hemodynamic "responders"; patients who did not (9 of 20) were considered hemodynamic "nonresponders." There were no differences in baseline hemodynamic, metabolic, and Acute Physiology and Chronic Health Evaluation and Simplified Acute Physiology Scores between responders and nonresponders. Survival to 28 days was better among responders (9 of 11 patients) than among nonresponders (0 of 9). Factors associated with survival were hemodynamic-metabolic response status, time interval from ICU admission to initiation of STHVH, and body weight. CONCLUSIONS: These data suggest that STHVH may be of major therapeutic value in the treatment of intractable cardiocirculatory failure complicating septic shock. Early initiation of therapy and adequate dose may improve hemodynamic and metabolic responses and 28-day survival.

Acid-Base Equilibrium↗

Doppler-based hemodynamic monitoring: a minimally invasive alternative.

Doppler-based hemodynamic assessment affords a magnitude of diagnostic applications including evaluation of blood flow from the left ventricle. Doppler echocardiography, in the form of transthoracic and transesophageal echocardiography, allows for intermittent evaluation of hemodynamic information including aortic blood flow, global and regional wall motion, and valvular integrity. In the hands of a skilled operator, transthoracic and transesophageal echocardiography provides reliable cardiac output determinations. However, these are not considered routine for hemodynamic monitoring in the critically ill. Neither of the echocardiographic approaches provides the continuously available data needed for ongoing evaluation of response to interventions. In contrast, esophageal Doppler monitoring, a minimally invasive hemodynamic assessment tool, provides the ability for ongoing real-time hemodynamic assessment of the critically ill or compromised patient. This simple-to-use technology requires that a probe, similar in size and shape to a gastric tube, be inserted into the esophagus to obtain measurement of blood flow in the descending aorta. Hemodynamic variables such as cardiac output, preload, afterload, and contractility are measured or derived from the esophageal Doppler monitoring waveform.

Algorithms↗

The effects of treatment with octreotide, diuretics, or both on portal hemodynamics in nonazotemic cirrhotic patients with ascites.

GOALS: To evaluate the effects of diuretic treatment, octreotide, or both on portal hemodynamics in nonazotemic cirrhotic patients with ascites. BACKGROUND: Diuretics and octreotide have been associated with a decrease in portal pressure in cirrhotic patients, suggested to be mediated by plasma volume depletion and splanchnic vasoconstriction, respectively. However, liver cirrhosis is characterized by activation of the renin-angiotensin-aldosterone axis, which increases hepatic vascular resistance and is augmented or suppressed by diuretics or octreotide, respectively. STUDY: Twenty nonazotemic cirrhotic patients with ascites were treated with furosemide and spironolactone. Of them, 10 (group 1) discontinued diuretic treatment for 7 days. Thereafter for 5 days, each patient received subcutaneous octreotide, 300 microg twice per day; ten of them (group 2) received the octreotide in addition to their usual diuretic treatment. Portal and systemic hemodynamics with Doppler ultrasound and endogenous vasoactive systems were evaluated while the patients received diuretics (both groups), after discontinuation of diuretics (group 1), and after octreotide administration (both groups). RESULTS: The withdrawal of diuretics did not alter portal hemodynamics, but it impaired systemic hemodynamics and suppressed the renin-aldosterone axis. The addition of octreotide to diuretic treatment but not octreotide alone improved portal and systemic hemodynamics. In both groups the initiation of octreotide administration suppressed the renin-aldosterone axis and plasma glucagon levels. CONCLUSIONS: In nonazotemic cirrhotic patients with ascites, the combination of diuretics and octreotide improves systemic hemodynamics and inhibits the diuretic-related component of the activated renin-aldosterone axis, which in turn augments the portal hypotensive effect of diuretic-induced plasma volume depletion.

Adult↗

Potential role for prostaglandin F2 alpha, D2, E2 and thromboxane A2 in mediating the metabolic and hemodynamic actions of sympathetic nerves in perfused rat liver.

In isolated rat liver perfused at constant pressure perivascular nerve stimulation caused an increase of glucose and lactate output and a reduction of perfusion flow. The metabolic and hemodynamic nerve effects could be inhibited by inhibitors of prostanoid synthesis, which led to the suggestion that the effects of nerve stimulation were, at least partially, mediated by prostanoids [Iwai, M. & Jungermann, K. (1987) FEBS Lett. 221, 155-160]. This suggestion is corroborated by the present study. 1. Prostaglandin D2, E2 and F2 alpha as well as the thromboxane A2 analogue U46619 enhanced glucose and lactate release and lowered perfusion flow similar to nerve stimulation. 2. The extents, the kinetics and the concentration dependencies of the metabolic and hemodynamic actions of the various prostanoids were different. Prostaglandin F2 alpha and D2 caused relatively stronger changes of metabolism, while prostaglandin E2 and U46619 had stronger effects on hemodynamics. Prostaglandin F2 alpha elicited greater maximal alterations than D2 with similar half-maximally effective concentrations. Prostaglandin F2 alpha mimicked the nerve actions on both metabolism and hemodynamics best with respect to the relative extents and the kinetics of the alterations. 3. The hemodynamic effects of prostaglandin F2 alpha could be prevented completely by the calcium antagonist nifedipine without impairing the metabolic actions of the prostanoid. Apparently, prostaglandin F2 alpha influenced metabolism directly rather than indirectly via hemodynamic changes. The present results, together with the previously described effects of prostanoid synthesis inhibitors, suggest that prostanoids, probably prostaglandin F2 alpha and/or D2, could be involved in the actions of sympathetic hepatic nerves on liver carbohydrate metabolism. Since prostanoids are synthesized only in non-parenchymal cells, nervous control of metabolism appears to depend on complex intra-organ cell-cell interactions between the nerve, non-parenchymal and parenchymal cells.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Postural stability of hemodynamic responses during mental challenge.

Laboratory stress testing is typically conducted while subjects are seated, whereas real-life stressors may often be encountered while standing. The present study of 20 healthy young men evaluated blood pressure and underlying hemodynamic adjustments to a standardized mental arithmetic task performed twice while seated and twice while standing. Blood pressure increased during mental arithmetic in both postures, but the underlying hemodynamic determinants of the pressor responses were different for the two postures. Augmented cardiac output was responsible for increasing blood pressure during seated task performance, whereas increased vascular resistance was the mechanism for the pressor response to the task performed while standing. Blood pressure and hemodynamic responses were reproducible subject characteristics for a given posture; test-retest correlations were significant for all cardiovascular measures. However, seated blood pressures responses were not significantly correlated with standing blood pressure responses. In contrast, significant between-posture correlations were found for cardiac output and vascular resistance responses. This preliminary evidence of postural stability of the hemodynamic determinants of blood pressure responses during stress is consistent with growing evidence that hemodynamic response tendencies are robust characteristics of reactivity. Ambulatory monitoring of hemodynamic response patterns during real-life stress may reveal more idiosyncratic profiles of stress reactivity than are displayed by blood pressure responses alone.

Adult↗

Real-time observation of glomerular hemodynamic changes in diabetic rats: effects of insulin and ARB.

BACKGROUND: The progression of diabetic nephropathy is closely related to disturbances in glomerular hemodynamics, such as glomerular hypertension and/or hyperperfusion. The aim of this study was to observe and to analyze glomerular hemodynamics in rats with diabetes mellitus (DM) in vivo using confocal laser scan microscopy (CLSM). We also examined the effects of candesartan cilexetil (TCV-116), a selective angiotensin II type 1 receptor blocker (ARB), on glomerular hemodynamics in DM. METHODS: Munich-Wistar rats were divided into six groups: (1) four-day control; (2) four-day DM; (3) 28-day control; (4) 28-day DM; (5) DM treated with insulin; (6) DM treated with TCV-116. The kidney-to-body weight ratio, glomerular volume, and proteinuria were estimated. Glomerular hemodynamic changes were observed using CLSM and renal expression of endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) was evaluated by immunofluorescence. RESULTS: The kidney-to-body weight ratio, glomerular volume, the diameters of afferent arterioles (AA) and efferent arterioles (EA), erythrocyte velocities within glomeruli, and volume flow in glomerular capillary loops in four-day DM were significantly higher than in control rats, and increases were even more pronounced in the 28-day DM. TCV-116 treatment ameliorated all these findings and significantly decreased proteinuria, but there was no effect on the blood glucose level. On the other hand, insulin treatment was followed by normalization of all these changes induced in DM. Enhanced renal expression of eNOS in DM was suppressed when treated with either TCV-116 or insulin, while expression of nNOS was unaltered among the four groups. CONCLUSION: This imaging procedure allowed us to evaluate glomerular microcirculation in vivo, including the diameters of AA and EA, erythrocyte velocity, and volume flow. DM significantly induced glomerular hemodynamic alteration and renal hypertrophy. DM treated with either insulin or ARB ameliorated these changes. This study shows that progress in imaging technology promises to make major contributions to revealing the involvement of hemodynamic changes in glomerular diseases, aiding prognosis and the monitoring of therapeutic effects, as well.

Angiotensin II Type 1 Receptor Blockers↗

Doppler echocardiographic assessment of the hemodynamic benefits of rate adaptive AV delay during exercise in paced patients with complete heart block.

To determine if rate adaptation of the atrioventricular (AV) delay (i.e., linearly decreasing the AV interval for increasing sinus rate) improves exercise left ventricular systolic hemodynamics, we performed paired maximal semi-upright bicycle exercise tests (EXTs) on 14 chronotropically competent patients with dual chamber pacemakers. Nine patients with complete AV block (CAVB) and total ventricular pacing dependence during exercise comprised the experimental group. Pacemakers in these patients were programmed randomly to rate adaptive AV delay (AVDR) for one EXT and fixed AV delay (AVDF) for the other EXT. AVDF was 156 msec; AVDR decreased linearly from 156-63 msec from rates of 78-142 beats/min. The other five patients had intact AV conduction and comprised the control group who were exercised in identical fashion while their pacemakers were inhibited throughout exercise to assure reproducibility of hemodynamic measurements between EXTs. Cardiac hemodynamics were calculated using measured Doppler echocardiographic systolic aortic valve flows recorded suprasternally with an independent 2-MHz Doppler transducer during a graded ramp exercise protocol. For analysis, exercise was divided into four phases to compare Doppler measurements at submaximal and maximal levels of exercise: rest, early exercise (1st stage), late exercise (stage preceding peak), and peak. Patients achieved statistically similar heart rates between EXTs at each phase of exercise. Although at lower levels of exercise cardiac hemodynamics did not differ, experimental patients (with CAVB) showed a statistically significant benefit to cardiac output at peak exercise with heart rates of 129 +/- 13 beats/min (AVDR: 9.4 +/- 2.8 L/min; AVDF: 8.2 +/- 2.6 L/min, P = 0.002), stroke volume (AVDR: 74.1 +/- 25.6 mL; AVDF: 64.3 +/- 24.4 mL, P = 0.0003), and aortic ejection time (AVDR: 253.3 +/- 35.7 msec; AVDF: 226.7 +/- 35.0 msec, P = 0.002). Duration of exercise, peak rate pressure product, peak aortic flow velocities, and acceleration times did not differ. In contrast, control group patients (intact AV conduction throughout exercise) showed no statistical differences between any hemodynamic parameters measured at any phase of exercise from the first to second exercise test. These data demonstrate that systolic cardiac hemodynamics measured echocardiographically at the high heart rates achieved with peak exercise are improved with AVDR compared to AVDF in chronotropically competent patients with complete AV block. This is due primarily to improved stroke volume and a longer systolic ejection time with AV delay rate adaptation.

Adult↗

Effects of electrical stimulation postcardiomyoplasty in a model of chronic heart failure: hemodynamic results after daily 12-hour cessation versus a nonstop regimen.

The hemodynamic effects of cardiomyoplasty (CMP) have been investigated in many centers, but the question of whether it is necessary to stimulate the latissimus dorsi muscle (LDM) 24 hours a day has not been answered. The main goal of our investigation was to determine whether hemodynamic results after CMP were impaired when continuous electrical stimulation (ES) was off for 12 hours a day. A model of chronic heart failure was created in 12 sheep by performing an arteriovenous anastamosis and administering doxorubicin. Two weeks after the anastomosis, CMP was performed in eight sheep (experimental series); ES training was begun at 2 weeks after CMP. After completion of the initial ES conditioning (8 weeks after CMP), one group of sheep continued to receive ES 24 hours daily. Another group of sheep had only 12 hours of ES daily. Hemodynamic parameters were investigated 2 weeks later with the stimulator turned on and then off. With doxorubicin administration, arteriovenous anastamosis created a stable model of biventricular heart failure (right atrial pressure 20 +/- 3 mmHg vs 6 +/- 2 mmHg at baseline; pulmonary capillary wedge pressure 18 +/- 3 mmHg vs 9 +/- 2 mmHg; left ventricular end-diastolic area 15.2 +/- 1.2 cm2 vs 6.4 +/- 0.7 cm2; left ventricular ejection fraction 0.38 +/- 0.6 vs 0.65 +/- 0.7). Cardiomyoplasty improved hemodynamic status in all eight experimental sheep. However, when the investigation was performed with the stimulator off, this improvement was statistically insignificant. With stimulation on, there was decreased right atrial pressure, pulmonary capillary wedge pressure, left ventricular end-diastolic volume, and increased left ventricular ejection fraction. With the stimulator turned off for 12 hours daily, hemodynamic measurements did not differ from data with continuous ES for 24 hours daily. Because hemodynamic results do not seem to be impaired, we recommend daily, periodic cessation of stimulation to prevent damage to the LDM after CMP.

Animals↗

Continuous hemodynamic monitoring in heart failure.

Chronic congestive heart failure is associated with high morbidity and mortality, frequent hospital admissions, and high treatment costs. As the prevalence and incidence of the disease are increasing, there is a clear need to improve the management of heart failure patients. Continuous hemodynamic monitoring with an implanted device is technically feasible and safe. It provides reliable information on central hemodynamic parameters and allows for analysis of long-term hemodynamic trends. It has been suggested that continuous hemodynamic monitoring might improve the management of patients with chronic heart failure. This article describes the technical details of the monitoring system and presents possible clinical applications, with a focus on beta-blocker therapy, diuretics, and volume management. A case is reported, illustrating how hemodynamic long-term trends might add valuable information during up-titration of beta-blockers. Future implications of hemodynamic monitoring are discussed.

Adrenergic beta-Antagonists↗

Hemodynamic assessment of transluminal angioplasty for lower extremity ischemia.

Seventy-two patients underwent hemodynamic testing before and after treatment for occlusive disease of their lower extremities. Percutaneous transluminal angioplasty (PTA) was used to treat lesions in 26 iliac segments and produced 23 initially improved ankle or upper thigh indices, two hemodynamic failures, and one technical failure; PTA for 54 femoropopliteal lesions produced initial hemodynamic improvement in 41 cases, three hemodynamic failures, and ten technical failures. Hemodynamic follow-up of the iliac segments showed improvement in 25 (92%) as measured by the systolic pressure index of the ankle; follow-up of the femoropopliteal segments showed continued patency of 41 (65.9%). The authors analyze these hemodynamic data.

Aged↗

Hemodynamically significant atherosclerotic renal artery stenosis: MR angiographic features.

PURPOSE: To identify magnetic resonance (MR) angiographic features of hemodynamically significant renal artery stenosis. MATERIALS AND METHODS: Forty-seven patients underwent MR angiography of the renal arteries, including T1-weighted spin-echo and three-dimensional gadolinium-enhanced spoiled gradient-echo and three-dimensional phase-contrast pulse sequences, followed by renal revascularization. Thirty-five patients (52 arteries) were identified who benefited from renal revascularization, which indicated that they had hemodynamically significant renal artery stenoses. Kidney length, cortical thickness, parenchymal enhancement, and poststenotic dilatation were measured. Arteries were also examined for signal drop-out (dephasing) on phase-contrast angiograms; dephasing was considered severe if the stenotic artery appeared occluded on phase-contrast angiograms. RESULTS: Poststenotic dilatation of greater than 20% was present in 36 (59%) of 52 hemodynamically significant renal artery stenoses, and severe dephasing was present in 45 (87%) of 52. In patients with unilateral hemodynamically significant stenosis or occlusion, mean ischemic kidney length was reduced to 9.3 cm compared with 10.7 cm for the contralateral normal kidney (P = .009), mean parenchymal thickness was reduced (1.2 vs 1.7 cm; P < .001), and mean parenchymal enhancement was 15% less on the ischemic side (P = .05). Severe dephasing on phase-contrast angiograms was present in nine (75%) of 12 unilateral hemodynamically significant stenoses but in only one contralateral normal renal artery (P < .001). CONCLUSION: MR angiography depicts features of renal artery stenosis that are markers of hemodynamic significance.

Adult↗

Hemodynamic changes in pseudopregnancy in chronically instrumented conscious rats.

It is unclear whether the trophoblast is needed for the normal early-pregnancy hemodynamic adaptation. In this study we tested the hypothesis that the presence of trophoblast is not essential for the initial hemodynamic adaptation in pregnancy. To this end, we measured systemic hemodynamics in conscious pseudopregnant rats and compared the results with those obtained in a concomitantly studied control group of virgin rats as well as with a previously studied group of pregnant rats. The rats were studied daily from day 4 postmating until day 10 and on days 12, 14, 18, and 20. In pseudopregnant rats, cardiac output (CO) increased from day 5 onward, to 14 +/- 3% above the initial value by day 8. This rise in CO was entirely accomplished by a rise in stroke volume (21 +/- 4% by day 8). Mean arterial pressure did not change appreciably. Therefore, total peripheral resistance also decreased by 21 +/- 4% by day 8. Meanwhile, peak flow, aortic flow acceleration, and stroke work, indicators of myocardial performance, had increased, and the hematocrit had decreased (15 +/- 1% by day 8). Between day 10 and day 20 the hemodynamic parameters gradually returned to baseline. We conclude that systemic hemodynamic changes do take place in pseudopregnancy. They consist of a rise in CO by a rise in stroke volume, an increase in myocardial performance, and hemodilution. The observed changes closely resemble those in early normal pregnancy. Therefore, we accept our hypothesis that trophoblast is not essential for the initial hemodynamic changes in rat pregnancy.

Animals↗

Effect of heating on the hemodynamic responses to vasoactive agents.

During hyperthermia, vasoconstrictor tone in the viscera is lost despite high levels of sympathetic neural outflow and plasma catecholamines, suggesting that vascular responsiveness to adrenergic receptor stimulation is reduced. The purpose of this study was to determine whether adrenoceptor-mediated control of vascular resistance is altered at high body core temperatures. The hemodynamic responses to adrenoceptor agonists were examined in chloralose-anesthetized rats heated to colonic temperatures (Tco) of 37, 39, and 41.5 degrees C. Elevating Tco to 39 degrees C did not alter the hemodynamic responses to any of these agents. Further heating to 41.5 degrees C markedly attenuated the hemodynamic responses to alpha- and beta-adrenoceptor agonists. Similarly, the regional and systemic hemodynamic responses to ANG II and endothelin were also reduced at 41.5 degrees C. In contrast, the hemodynamic responses to endothelium-dependent and -independent vasodilator agents were unchanged or slightly reduced at 41.5 degrees C. The blunted hemodynamic responses observed at 41.5 degrees C indicate that vascular reactivity to vasoconstrictor agents is reduced with hyperthermia and suggest that this nonspecific change in vascular responsiveness may contribute the circulatory collapse associated with high body temperatures.

Acetylcholine↗

Glomerular hemodynamic alterations during renal nerve stimulation in rats on high- and low-salt diets.

Renal adrenergic nerve activity exerts a major influence on glomerular hemodynamics and tubular fluid reabsorption. Modulation of the functional expression of adrenergic activity in the kidney can be mediated, in part, by the renin-angiotensin system and by prostanoid activity. Alterations in dietary salt intake have been previously shown to modify the activity of various vasoactive systems, including angiotensin and prostaglandin activity and thereby have a potential of modifying the glomerular hemodynamic response to a given renal adrenergic stimulus. Munich-Wistar rats were fed either a high-, low-, or normal salt diet for 2 wk before the day of the study. Measurements of glomerular hemodynamics were performed in both unstimulated with basal renal nerve traffic eliminated and during exogenous renal nerve stimulation (RNS) (3 Hz). RNS decreased glomerular capillary hydrostatic pressure and single-nephron plasma flow to a similar extent in all three dietary conditions via increases in afferent arteriolar resistance. The data demonstrated that dietary preconditioning does not alter the glomerular hemodynamic response to an exogenous, fixed RNS. Glomerular prostaglandin E2 production and plasma renin activity were significantly greater in rats fed a low-salt diet compared with either normal- or high-salt diet. The constancy of glomerular hemodynamic responses to RNS in spite of wide variations in dietary salt intake indicates that functional renal hemodynamic differences observed as a result of NaCl intake must be primarily the consequence of differences in renal nerve traffic and not hormonal alterations.

Absorption↗

Relative roles of nitric oxide, prostanoids and angiotensin II in the regulation of canine glomerular hemodynamics. A micropuncture study.

Glomerular hemodynamics are controlled by a variety of physical, nervous and hormonal factors including the potent vasoconstrictors, angiotensin (ANG) II and endothelin-1 (ET-1), and the vasodilator prostanoids (prostaglandin = PG) and nitric oxide (NO). Since no micropuncture data on the canine kidney exist with respect to the relative roles of the endogenous vasoactive hormones/autacoids NO, PG and ANG II in modulating glomerular hemodynamics, in the present study using the micropuncture technique in anesthetized dogs on a normal salt intake, we investigated the relative effects of these hormones/autacoids by means of the L-arginine analog, N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), a competitive NO synthase (NOS) inhibitor, the cyclooxygenase inhibitor indomethacin (INDO), and the AT(1) receptor blocker EXP 3174. An intrarenal arterial (i.r.a.) bolus (within 5 min) of 2.5 mg of L-NAME led to a significant decrease in total renal blood flow (RBF) and single nephron glomerular blood flow (SNGBF) from 4.46 +/- 0.51 to 3.52 +/- 0.41 ml/min/g kidney weight and from 0.393 +/- 0.041 to 0.341 +/- 0.037 microl/min (p < 0.01), respectively, without a change in glomerular filtration rate (GFR). The increase in arteriolar resistance was more pronounced at the efferent (+31%) than at the afferent (+13%) arteriole, and K(f) decreased from 4.5 +/- 0.5 to 3.7 +/- 0.4 nl/min/mm Hg (p < 0.01). INDO (5 mg/kg i.v. bolus followed by 0.17 mg/kg/min i.v.) had no effect on glomerular hemodynamics. EXP 3174 (30 microg/kg/min i.r.a.) increased RBF and SNGBF from 4.35 +/- 0.45 to 4.99 +/- 0.50 ml/min/g kidney weight and from 0.403 +/- 0.028 to 0.478 +/- 0.039 microl/min (p < 0.01), respectively, without an effect on GFR. It reduced the efferent arteriolar resistance by 25% as compared to 13% at the afferent arteriolar level. EXP 3174 increased K(f) from 5.1 +/- 0.4 to 8.1 +/- 0.6 mm Hg (p < 0.01) in the presence of a decrease in effective filtration pressure from 13.2 +/- 1.7 to 8.3 +/- 1.0 mm Hg (p < 0.01). The glomerular hemodynamic effects of L-NAME were unaltered by pretreatment with INDO or EXP 3174, whereas its tubular effects were restored in the presence of EXP 3174. Thus, from these first micropuncture data in the anesthetized dog on a normal sodium intake we conclude that (1) acute intrarenal inhibition of NOS by L-NAME decreases RBF and SNGBF due to vasoconstriction of the afferent and, more pronounced, efferent arterioles. Since L-NAME simultaneously decreases K(f), GFR remains unaltered. (2) These renal hemodynamic effects of NOS inhibition were not mediated by prostanoids or intrarenal ANG II. Thus, the tonic activity of intrarenal NOS plays an important role in maintaining glomerular hemodynamics in the canine kidney.

Angiotensin II↗

Canine renal and systemic hemodynamic measurements after 4 weeks of a magnesium deficient diet.

To probe renal hemodynamic measurements in relation to simultaneous systemic hemodynamic measurements in normal, adult, conscious dogs on a magnesium-deficient diet, 6 experimental animals were given 4 weeks of a magnesium-deficient diet compared to 9 animals whose dietary magnesium was normal. Systemic hemodynamics were estimated using a thermodilution catheter, and renal hemodynamics were estimated by standard renal clearance techniques. Electrolytes and hormones were also surveyed in these same animals at the time of hemodynamic measurements. Heart rate was significantly higher in magnesium-deficient dogs, but there were no other systemic hemodynamic differences between the two groups of dogs. Renal blood flow, effective renal plasma flow, and urinary osmolality were significantly higher in the magnesium-deficient animals. Whole-blood ionized calcium and potassium, serum magnesium, and fractional excretion of magnesium were lower in the magnesium-deficient dogs. We conclude that the renal circulation is more sensitive than the systemic circulation to disturbances in magnesium balance. Disturbances of other electrolytes accompanying magnesium deficiency were also confirmed.

Animals↗

Systemic factors and renal hemodynamic effects of high-protein meal versus low-protein meal in conscious dogs.

The effects of a high-protein (HP) and low-protein (LP) meal on glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and renal vascular resistance (RVR) were examined in conscious dogs. Ingestion of the HP and LP meal produced a temporary increase in systemic hemodynamic parameters due in part to a 'cephalic phase' of sympathetic excitement. However only the HP significantly altered renal hemodynamics, i.e. GFR, ERPF and RVR. Plasma renin activity (PRA), serum aldosterone and plasma atrial natriuretic peptide (ANP) concentrations were not significantly altered by either a HP or LP meal. Of all the serum electrolytes measured, serum Ca2+ concentrations were significantly lower after a HP meal. It would appear that protein-meal-induced changes in renal hemodynamics are independent of changes in systemic hemodynamics. The exact mechanism of action of a HP meal on renal hemodynamics is not clear, but it appears that one mechanism by which a HP meal may alter renal hemodynamics is by altered calcium homeostasis.

Animals↗