Hormonal changes related to reduced renal blood flow and low urine output under prolonged increased intra-abdominal pressure in pigs.

OBJECTIVE: To investigate effects of prolonged increased intra-abdominal pressure (IAP) on diuresis, renal blood flow, and hormones that influence renal function, in particular endothelin. DESIGN: Experimental study. SETTING: Haukeland University Hospital, Norway. ANIMALS: 21 domestic pigs. METHODS: The TAP was maintained at normal (n = 7) or at 20 mmHg (n = 7) or 30 mmHg (n = 7) for three hours. MAIN OUTCOME MEASURES: Urine output, renal venous pressure, renal artery blood flow (transit-time flowmetry), renal cortex blood flow (microspheres), and renin, aldosterone, atrial natriuretic factor (ANF), adrenaline, noradrenaline, cortisol, and endothelin-1 (ET-1) in renal venous blood. RESULTS: An IAP of 20 mmHg was followed by no significant changes in the variables studied. An IAP of 30mmHg was associated with anuria, considerably reduced renal blood flow and increased renal vascular resistance. The renin activity and the blood concentrations of ET-1, aldosterone, noradrenaline, adrenaline, and cortisol increased during the three hours that IAP was at 30 mmHg. CONCLUSION: An IAP of 20 mmHg did not influence renal haemodynamics or diuresis. The low renal blood flow observed at an IAP of 30 mmHg probably results from reduced arteriovenous pressure difference and vasoconstriction. Increased concentrations of endothelin, angiotensin II, and noradrenaline may account for the vasoconstriction. The anuria can be explained by low renal blood flow and increased reabsorption of sodium in renal tubules caused by aldosterone.     

Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs

Background: The aim of the study was to investigate the effect of the angiotensin II receptor antagonist losartan on renal hemodynamics and diuresis in pigs with increased intraabdominal pressure (IAP). Methods: The IAP was maintained at 30 mmHg for 3 h by intraperitoneal instillation of Ringers solution. Ten animals were treated with losartan; another 10 animals served as controls. Renal blood flow, hormones in renal vein blood, and diuresis were measured. Results: In control animals, the renal vascular resistance increased renal blood flow remained constant, the blood concentration of aldosterone increased and the diuresis decreased during increased IAP. Losartan prevented the increase in vascular resistance and improved renal blood flow under increased IAP. It also prevented the rise in aldosterone concentration and increased the urine output to baseline level. Conclusion: Our results suggest that the renal vasoconstriction associated with increased IAP is due to increased production of angiotensin II. The oliguria associated with increased IAP is probably due, at least partly, to increased reabsorbtion of sodium and water in the renal tubuli caused by increased tissue concentration of aldosterone.     

Effects of prolonged increased intra-abdominal pressure on gastrointestinal blood flow in pigs

BACKGROUND: The aim of the study was to investigate the effects of prolonged intra-abdominal pressure on systemic hemodynamics and gastrointestinal blood circulation. METHODS: The intra-abdominal pressure in anesthetized pigs was elevated to 20 mmHg (7 animals), 30 mmHg (7 animals), and 40 mmHg (4 animals), respectively. These pressures were maintained for 3 h by intra-abdominal infusion of Ringer's solution. A control group of seven animals had normal intra-abdominal pressure (IAP). Transit time flowmetry and colored microspheres were used to measure blood flow. RESULTS: An IAP of 20 mmHg did not cause significant changes in systemic hemodynamics or tissue blood flow. An IAP of 30 mmHg caused reduced blood flow in the portal vein, gastric mucosa, small bowel mucosa, pancreas, spleen, and liver. Serum lactate increased in animals with an IAP of 30 mmHg, but microscopy did not disclose mucosal damage in the stomach or small bowel. An IAP of 40 mmHg was followed by severe circulatory changes. CONCLUSIONS: Prolonged IAP at 20 mmHg did not cause changes in general hemodynamics or gastrointestinal blood flow. Prolonged IAP at 30 mmHg caused reduced portal venous blood flow and reduced tissue flow in various abdominal organs, but no mucosal injury. A prolonged IAP of 40 mmHg represented a dangerous trauma to the animals.     

Effects of the aldosterone receptor antagonist potassium canrenoate on renal blood flow and urinary output during prolonged increased intraabdominal pressure (IAP) in pigs

Background Increased intraabdominal pressure can be found after major abdominal trauma and necrotizing pancreatitis and is used during laparoscopic surgery. The purpose of this study was to investigate the effect of the aldosterone receptor antagonist (potassium canrenoate) on renal hemodynamics and urinary output in pigs during increased intraabdominal pressure (IAP).Methods The IAP was kept at 30 mmHg for 3 h by instillation of Ringers solution into the peritoneal cavity. Eight animals were treated with potassium canrenoate and eight animals served as controls. Renal blood flow, hormones in femoral artery blood, and the urinary output were measured.Results The administration of potassium canrenoate was followed by increased aldosterone concentrations in arterial blood, increased blood concentration of potassium, and increased concentration of sodium in the urine, indicating satisfactory inhibition of aldosterone. Potassium canrenoate did not cause changes in cardiac output and arterial pressure. It did not affect the renal vascular resistance that increased at an IAP of 30 mmHg, or the renal blood flow that remained constant during the experiments. The group treated with potassium canrenoate had higher mean urinary output than the controls, but the difference was not significant.Conclusion Increased IAP in pigs is associated with markedly reduced urinary output and increased serum concentrations of aldosterone. Although the urinary output did not increase significantly, the increased sodium concentration in the urine of canrenoate-treated animals suggests that the high blood level of aldosterone contributes to the oliguria under increased IAP.     

The endothelin receptor antagonist tezosentan improves renal microcirculation in a porcine model of endotoxemic shock

Background: Impaired renal microcirculation has been suggested as a factor contributing to the development of renal dysfunction in sepsis. This study was conducted to elucidate the role of endothelin‐1 (ET‐1)in mediating reductions in renal microcirculatory blood flow during endotoxemic shock. Methods: A prospective, randomized, and experimental study was performed with 16 anesthetized and mechanically ventilated pigs. After 2 h of lipopolysaccaride‐induced endotoxemia, eight animals received a bolus dose of the dual endothelin receptor antagonist tezosentan (1 mg/kg), followed by a continuous infusion of 1 mg/kg/h throughout the experiment. Eight animals served as the control group. Renal microcirculation, total renal blood flow, plasma creatinine levels, cardiac index, and mean arterial pressure were measured. Plasma samples were collected for the measurement of tumor necrosis factor α (TNF‐α), interleukin‐6 (IL‐6), interleukin‐10 (IL‐10), ET‐1, angiotensin II, and aldosterone. Results: Endotoxin infusion resulted in a state of circulatory shock with impairment of renal microcirculation. An increase in the plasma levels of TNF‐α, IL‐6, IL‐10, ET‐1, angiotensin II, and aldosterone was also observed. Tezosentan attenuated the decrease in renal microcirculation and renal blood flow, and attenuated the increase in plasma creatinine. Treatment with tezosentan did not significantly affect the plasma cytokine, angiotensin II, or aldosterone response to endotoxemia. Conclusion: These results indicate that treatment with the dual endothelin receptor tezosentan in endotoxemic shock attenuates the reduction of renal microcirculation and total renal blood flow independently of plasma changes in the renin–angiotensin–aldosterone system or early plasma cytokine response.     

Effects of chronic hypoxia on renal renin gene expression in rats.

BACKGROUND: The effects of hypoxia on renin secretion and renin gene expression have been controversial. In recent studies, we have demonstrated that acute hypoxia of 6 h duration caused a marked stimulation of renin secretion and renal renin gene expression. This hypoxia-induced stimulation of the renin-angiotensin system might contribute, for example, to the progression of chronic renal failure and to the development of hypertension in the sleep-apnoea syndrome. For this reason, we were interested in the more chronic effects of hypoxia on renal renin gene expression and its possible regulation. METHODS: Male rats were exposed to chronic normobaric hypoxia (10% O(2)) for 2 and 4 weeks. Additional groups of rats were treated with an endothelin ET(A) receptor antagonist, LU135252, or a NO donor, molsidomine, respectively. Systolic blood pressure and right ventricular pressures were measured. Renal renin, endothelin-1 and endothelin-3 gene expression were quantitated using RNAase protection assays. RESULTS: During chronic hypoxia, haematocrit increased to 72+/-2%, and right ventricular pressure increased by a mean of 26 mmHg. Renal renin gene expression was halved during 4 weeks of chronic hypoxia. This decrease was reversed by endothelin receptor blockade (105 or 140% of baseline values after treatment for weeks 3-4 or 1-4). Furthermore, there was a trend of increasing renal endothelin-1 gene expression (to 173% of baseline values) after 4 weeks of hypoxia. Systolic blood pressure increased moderately during 4 weeks of chronic hypoxia from 129+/-2 to 150+/-4 mmHg. This blood pressure increase was higher in rats treated for 4 weeks with an endothelin receptor antagonist (196+/-11 mmHg). CONCLUSIONS: Chronic hypoxia (in contrast to acute hypoxia) suppresses renal renin gene expression. This inhibition presumably is mediated by endothelins.     

Effects of increased intra-abdominal pressure in severe obesity

This article gives an overview, citing animal and clinical studies, of the effects of increased intra-abdominal pressure (IAP) in severe obesity. Animal studies demonstrate that increased IAP increases pleural pressure, cardiac filling pressures, femoral venous pressure, renal venous pressure, systemic blood pressure, and vascular resistance, renin and aldosterone levels, and intracranial pressure. Thus, the comorbidities presumed secondary to increased IAP in obese patients include congestive heart failure, hypoventilation, venous stasis ulcers, gastroesophageal reflux, urinary stress incontinence, incisional hernia, pseudotumor cerebri, proteinuria, and systemic hypertension.     

The effects of intra-abdominal pressure on regional renal blood flow during peritoneal dialysis

This experimental studies were designed to investigate the effects of intra-abdominal pressure (IAP) on renal regional blood flow and renal function during peritoneal dialysis (PD) for acute renal failure (ARF). The mongrel dogs were divided into four groups. Group I (n = 10): IAP of atmospheric pressure without PD (control group); Group II (n = 10): Intermittent PD with IAP of 10 mmHg; Group III (n = 10): Intermittent PD with IAP of 20 mmHg; Group IV (n = 10): Continuous PD with IAP of 3-5 mmHg. The following results were obtained. Significant decrease (p less than 0.01-0.05) of renal cortical blood flow (RCBF), total renal blood flow (TRBF), ratio of RCBF to renal medullar blood flow, renal perfusion pressure (RPP), cardiac index and urinary output, and increased renal vascular resistance and inferior vena caval pressure were observed in group III, but in group IV, values of these parameters returned to control level. The limit of influence to renal function was confirmed to be as follows. (1) IAP of 30 mmHg or more, (2) RPP of less than 65 mmHg, (3) TRBF of less than 2.2 ml/g/min, (4) and RCBF of less than 78 ml/100 g/min. These studies suggest that RPP are simple and excellent index to reflex renal hemodynamics, and the continuous PD are better procedure than the intermittent PD from a view of renal regional blood flow.     

Comparative analysis about hemodynamic and renal blood flow effects during open versus laparoscopic nephrectomy. An experimental study

BackgroundThe increase of intraabdominal pressure to 10 mmHg provokes a decrease of renal blood flow (RBF). Pneumoperitoneum during laparoscopic techniques with intra-abdominal pressure (IAP) to 15 mmHg, results in a decrease in RBF, urine output and glomerular filtration rate (GFR).PurposeAnalyze the changes in RBF, urine output an GFR in a porcine experimental model during open vs laparoscopic nephrectomy.Materials and methods30 pigs (medium weigh= 22.6+3.2 Kg) were divided into two groups: Laparoscopic nephrectomy was performed using 15 pigs and open nephrectomy in 15 pigs, following a living donor nephrectomy autotransplantation model. Study parameters were urine volume and GFR baseline values, 30 and 60 minutes during nephrectomy. RBF was measured using an electromagnetic flow catheter around the main renal artery during the initial 60 minutes of nephrectomy.ResultsThe laparoscopic technique was associated with a significant reduction of RBF (80+2.7 vs 262+3 ml/min) (p < 0.005), diuresis (42%) and GFR (38%), vs the open group.ConclusionsLaparoscopic nephrectomy involves a significant reduction of RBF, GFR and diuresis, which is potentially transcendent in living donor nephrectomy and kidney transplantation.     

Effects of renal arterial endothelin-1 and endogenous endothelins on regional kidney blood flow and renal antihypertensive mechanisms in anesthetized rabbits

To determine how endothelins affect regional kidney blood flow and responses to increased renal artery pressure (RAP), an extracorporeal circuit was established to control RAP independent of the mean systemic arterial pressure (MAP). RAP was first set at approximately 65 mm Hg, and endothelin-1 (1 ng/kg/min for 30 min then 0.4 ng/kg/min) or vehicle was infused into the renal artery, or the ET(A)/ET(B) antagonist TAK-044 (3 mg/kg plus 3 mg/kg/h) or vehicle was administered intravenously. RAP was then progressively increased in steps from approximately 65 to approximately 160 mm Hg. When RAP was approximately 65 mm Hg, endothelin-1 increased renal vascular resistance (RVR, 72%), and reduced cortical (CBF, 26%) but not medullary blood flow (MBF). TAK-044 reduced MAP (12%) and RVR (15%) and increased CBF (21%) but not MBF. When RAP was increased, renal blood flow (RBF), glomerular filtration rate, and urine and sodium excretion increased, while MAP fell. These responses were unaffected by endothelin-1. TAK-044 potentiated the increases in RBF and reductions in MAP in response to increased RAP, but did not affect urine and sodium excretion. Plasma renin activity was reduced by endothelin-1 and increased by TAK-044. Thus, both exogenous and endogenous endothelins reduce CBF but not MBF, and reduce plasma renin activity, but neither affect pressure natriuresis.     

Respiratory changes during prolonged increased intra-abdominal pressure in pigs

BACKGROUND: Increased intra-abdominal pressure (IAP) elevates thoracic pressure and airway pressures and reduces lung compliance in humans and laboratory animals. We studied respiratory alterations and arterial blood gas changes in pigs with IAP maintained at 20 mmHg or 30 mmHg for 3 h. METHODS: Domestic pigs of both sexes weighing 30.0 +/- 5.1 kg (mean +/- SD) (n = 21) were divided into three groups. The animals were anesthetized and kept at 20 mmHg IAP (n = 7) or 30 mmHg IAP (n = 7) for 3 h. The third group (n = 7) served as control without an elevated IAP. We recorded respiratory alterations and changes in acid-based parameters at baseline and after 90 min and 180 min of increased IAP. RESULTS: No significant hypoxia or hypercarbia was found in animals with an IAP of 20 mmHg IAP. At an IAP of 30 mmHg, pO2 decreased to an average 19.6 kPa and pCO2 increased to about 6 kPa, and the animals were slightly acidotic. Airway pressure increased significantly and lung compliance decreased in both groups of elevated IAP. CONCLUSION: In our porcine model, an IAP of 20 mmHg or higher for 3 h is harmful for the respiratory function of the animals due to deterioration of respiratory parameters, increased airway pressure and decreased lung compliance.     

Losartan increases renal blood flow during isoflurane anesthesia in sheep

BACKGROUND: Inhaled anesthetics cause a transient reversible depression of renal function by direct renal effects or indirectly by changes in neurohumoral systems or cardiovascular performance. When the sympathetic nervous activity is decreased during anesthesia, other vasoactive systems like vasopressin (AVP) and particularly the renin angiotensin system (RAS) are of importance for blood pressure maintenance. Little is known about how the renal circulation is affected by angiotensin receptor blockade during isoflurane anesthesia. METHODS: The study was performed on isoflurane anesthetized sheep equipped with flow probes (placed around a femoral and a renal artery) and a pulmonary artery catheter. During stable conditions the sheep were given one or more of the following substances: isotonic saline (NaCl); losartan (LOS) 10 mg x kg(-1); prazosin (PRAZ) 0.2 mg x kg(-1) and a vasopressin V1-receptor antagonist (AVP-a) 10 microg x kg(-1). RESULTS: LOS and AVP-a did not affect mean arterial pressure (MAP), whereas PRAZ lowered MAP significantly (from 98+/-12 to 65+/-7 mmHg). Renal blood flow (RBF) increased after LOS treatment (148+/-34 to 222+/-33 ml x min(-1)). The other substances were without effect on RBF. Femoral blood flow remained unchanged after all treatments. CONCLUSION: We conclude that the sympathoadrenal system is still the major determinant for blood pressure maintenance during isoflurane anesthesia in sheep. The apparently increased activity of the renin angiotensin system in this situation causes a reduction in renal blood flow, which is counteracted by angiotensin II AT1-receptor blockade.     

Enhanced external counterpulsation: a new technique to augment renal function in liver cirrhosis.

BACKGROUND: Advanced liver cirrhosis is characterized by cardiovascular changes, such as low arterial blood pressure, peripheral vasodilation and renal vasoconstriction. As a consequence, renal hypoperfusion, impaired diuresis and natriuresis and eventual hepatorenal syndrome may ensue. Previous studies using head-out water immersion to increase central blood volume have demonstrated the functional nature of the renal abnormalities. Enhanced external counterpulsation (EECP) is a new non-invasive cardiac assist device to augment diastolic blood pressure by electrocardiogram-triggered diastolic inflation and deflation of cuffs wrapped around the lower extremities. We investigated whether EECP would improve renal dysfunction of liver cirrhosis. METHODS: Twelve healthy controls and 19 patients with liver cirrhosis were observed during 2 h of baseline followed by 2 h of EECP. The following parameters of renal and cardiovascular function were measured: renal plasma flow by para-aminohippurate clearance, glomerular filtration rate (GFR) by inulin clearance, urine flow rate, urinary excretion rates of sodium and chloride, mean arterial blood pressure (MAP), renal vascular resistance (RVR) and plasma concentrations of renin, atrial natriuretic peptide (ANP), endothelin-1, antidiuretic hormone, epinephrine and N-epinephrine. RESULTS: EECP was well tolerated by healthy controls and cirrhotic patients alike. EECP increased MAP (cirrhotic patients: from 74+/-18 to 88+/-20 mmHg, P<0.01; controls: from 89+/-8 to 94+/-5 mmHg, P = NS) and ANP (cirrhotic patients: from 23+/-18 to 30+/-20 ng/l, P<0.05; controls: from 11+/-4 to 16+/-5 ng/l, P<0.01). The plasma renin concentration decreased (cirrhotic patients: from 98+/-98 to 58+/-57 ng/l, P<0.01; controls: from 4.6+/-1.6 to 3.4+/-1.1 ng/l, P<0.01). This was associated with improvement of the urinary flow rate (cirrhotic patients: from 3.6+/-1.8 to 4.6+/-0.7 ml/min, P<0.05; controls: from 1.8+/-1.5 to 2.8+/-1.9 ml/min, P<0.05), as well as of the sodium and chloride excretion rates in both groups. However, in contrast to healthy controls, GFR and renal plasma flow in cirrhotic patients failed to rise significantly. Renal vascular resistance fell numerically in healthy controls (68+/-5 vs 55+/-4 mmHg . min/l; P = NS). In contrast, RVR showed a significant increase by approximately 20% in cirrhosis (67+/-4 vs 80+/-8 mmHg . min/l; P<0.05). Endothelin-1 levels fell in controls (0.38+/-0.42 vs 0.31+/-0.35; P<0.05), whereas they remained statistically unchanged in cirrhotic patients. Epinephrine, N-epinephrine and vasopressin were not altered by EECP in either group. CONCLUSIONS: EECP is an effective procedure to augment renal excretory function in healthy volunteers as well as in patients with cirrhosis. In healthy volunteers, GFR and renal plasma flow increased during EECP. In contrast, these parameters remained unchanged in the patients and their renal vascular resistance increased during EECP. Therefore, EECP improves diuresis, but does not influence the vasoconstrictive dysregulation of the kidneys in liver cirrhosis.     

Elevated intra-abdominal pressure and renal function.

The effect of increased intra-abdominal pressure on cardiac output and renal function was investigated using anesthetized dogs into whom inflatable intraperitoneal bags were placed. Hemodynamic and renal function measurements were made at intra-abdominal pressures of 0, 20, and 40 mmHg. Renal blood flo and glomerular filtration rate decreased to les than 25% of normal when the intra-abdominal pressure was elevated to 20 mmHg. At 40 mmHg intra-abdominal pressure, three dogs became anuric, and the renal blood flow and glomerular filtration rate of the remaining dogs was 7% of normal, while cardiac output was reduced to 37% of normal. Expansion of the blood volume using Dextran-40 easily corrected the deficit in cardiac output, but renal blood flow and glomerular filtration rate remained less than 25% of normal. Renal vascular resistance increased 555% when the intra-abdominal pressure was elevated from 0 to 20 mmHg, an increase fifteen-fold that of systemic vascular resistance. This suggests that the impairment in renal function produced by increased intra-abdominal pressure is a local phenomenon caused by direct renal compression and is not related to cardiac output.     

Effects of increased intra-abdominal pressure and volume expansion on renal function in the rat.

BACKGROUND: The effects of increased intra-abdominal pressure (IAP) and volume expansion on renal function in the rat were studied to gain more knowledge of the oliguria seen during laparoscopic procedures and to reduce the detrimental renal effects of IAP. METHODS: IAP was elevated to 5 or 10 mmHg by insufflation of CO(2) and maintained for 2 h in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. An angiotensin II receptor I antagonist, candesartan, was given as a bolus injection and a 5% volume expansion was achieved by i.v. saline infusion. An angiotensin-converting enzyme (ACE) inhibitor was also given. Renal parameters were the glomerular filtration rate (GFR), urine production, the urinary concentrations of sodium and potassium and the osmolality in the urine. The arterial acid-base balance and blood pressure were also monitored. RESULTS: The GFR deteriorated by 70% during pneumoperitoneum (PP) of 10 mmHg. There was a dramatic drop in sodium excretion (88-97%). With candesartan and elevated IAP, there was a drop in mean arterial pressure (from 90 to 55 mmHg) and the negative renal effects were very pronounced. Renal function was better preserved during elevated IAP in combination with volume expansion. CONCLUSIONS: Capnoperitoneum suppresses renal function, especially in combination with angiotensin II receptor 1 blockade and ACE inhibition. Volume expansion reduces the deleterious effects of PP on renal function during elevated IAP. The results suggest that patients should not be given pharmaceuticals blocking the renin-angiotensin-aldosterone system prior to procedures that may increase IAP. It may be beneficial, however, to reduce angiotensin II tension by volume expansion.     

The Preventive Effect of Dopamine Infusion in Rats with Abdominal Compartment Syndrome

ABSTRACT

Background: The most significant perfusion disorder of the intra-abdominal viscera occurs in the abdominal compartment syndrome (ACS). Free oxygen radicals diffuse into the body during the reperfusion phase of ACS. Our aim was to determine the effects of dopamine infusion (3 μg/kg/min) on renal perfusion, cytokine levels, free oxygen radicals, and renal histopathological changes in the presence of ACS in a prospective randomized manner. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into four groups (n = 6). Group 1 was used as control. In group 2, air was inflated until the intra-abdominal pressure (IAP) reached 20 mmHg. In group 3, dopamine was infused for 60 min meanwhile IAP was kept at 20 mmHg. In group 4, dopamine was infused for 60 min before IAP rise. After this phase, renal artery (RA) perfusion was measured continuously. Myeloperoxidase activity (MPO), glutathione (GSH), and lipid peroxidation (MDA) levels were measured in tissue samples and histopathological scoring was performed. Results: Dopamine treatment before and during ACS significantly decreased MPO and MDA levels and also increased renal blood flow and GSH levels. However, histopathological damage was improved simultaneously. Conclusion: Dopamine infusion before and during ACS, increases renal perfusion and decreases free oxygen radicals. According to our findings, dopamine infusion may be proposed for the treatment of ACS and perfusion disorders in critically ill patients.     

Effects of increased renal parenchymal pressure on renal function

OBJECTIVE: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). The cause of acute renal failure in AACS is thought to be multifactorial, including increased renal venous pressure, renal parenchymal pressure (RPP), and decreased cardiac output. Previous studies have established the role of renal venous pressure as an important mediator of this renal derangement. In this study, we evaluate the role of renal parenchymal compression on renal function. METHODS: Two groups of swine (20-26 kg) were studied after left nephrectomy and placement of a renal artery flow probe and ureteral cannula. Two hours were allowed for equilibration, and an inulin infusion was begun to calculate inulin clearance as a measurement of glomerular filtration. In group 1 animals (n = 6), RPP was elevated by 30 mm Hg for 2 hours with renal parenchymal compression. RPP then returned to baseline for 1 hour. In group 2 (n = 6), the RPP was not elevated. The cardiac index, preload, and mean arterial pressure remained stable. Blood samples for plasma renin activity and plasma aldosterone were taken at baseline and at hourly intervals. RESULTS: Elevation of RPP in the experimental group showed no significant decrease in renal blood flow index or glomerular filtration when compared with control animals. There were no significant elevations of plasma aldosterone or plasma renin activity in the experimental animals when compared with control. CONCLUSION: Elevated renal compression alone did not create the pathophysiologic derangements seen in AACS. However, prior data from this laboratory found that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma aldosterone, and urinary protein leak. These changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS. These data strengthen the proposal that renal vein compression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.     

Laparoscopic cholecystectomy: haemodynamic and neuroendocrine responses after pneumoperitoneum and changes in position

We have assessed the potential for myocardial ischaemia during laparoscopic cholecystectomy in 16 otherwise healthy patients. Continuous ambulatory ECG monitoring was commenced 12 h before operation and continued for 24 h after operation. The neuroendocrine stress response was assessed by measuring plasma concentrations of adrenaline and noradrenaline, human growth hormone, cortisol, renin and aldosterone, and prolactin, at specified times during surgery. Acute ST segment changes in the ECG occurred in only two patients. These episodes were independent of creation of pneumoperitoneum and changes in position. Acute intraoperative increases in MAP were noted during insufflation of carbon dioxide and reverse Trendelenburg positioning (P < 0.05). A four-fold increase in plasma concentrations of renin and aldosterone was noted after pneumoperitoneum and reverse Trendelenburg positioning (P > 0.05). There was a linear correlation between changes in plasma renin and aldosterone concentrations and MAP (r = 0.97 and r = 0.85, respectively). Prolactin concentrations increased four-fold after induction of anaesthesia. Cortisol, HGH, adrenaline and noradrenaline concentrations increased after deflation of the pneumoperitoneum. The time profile-concentration changes of increased MAP and renin-aldosterone suggests a cause-effect relationship. Increased intra-abdominal pressure and reverse Trendelenburg positioning may reduce cardiac output and renal blood flow. The early increase in prolactin concentration was probably secondary to the effect of the opioid fentanyl.      

Atrial pressure and hormonal and renal responses to acute cardiac tamponade

The effect of acute cardiac tamponade on atrial pressures, plasma atrial natriuretic factor concentration and renin activity, and renal water and electrolyte excretion was studied in pigs loaded intravenously with hydroxyethyl starch and maintained on a continuous intravenous infusion of isotonic saline solution. Saline solution was infused into the pericardial space in 6 anesthetized pigs until a predetermined decrease of 20% in mean arterial pressure was achieved. Another 6 sham-treated pigs served as controls. Tamponade increased atrial intracavitary pressures but decreased atrial transmural (distending) pressures. These changes in atrial pressures were reversed after release of tamponade. Changes in plasma atrial natriuretic factor concentration correlated positively with changes in atrial transmural pressures. Tamponade increased plasma renin activity and decreased urine flow and renal sodium and potassium excretion, and release of tamponade reversed these changes. Thus, the tamponade-induced reduction in atrial distention is associated with hormonal changes, which may contribute to the reductions in diuresis and natriuresis observed in this connection.     

Studies on the mechanism of action of angiotensin converting enzyme inhibitors on the dog kidney]

The effects of angiotensin-converting enzyme (ACE) inhibitors, rampipril, captopril and enalapril, on the renal circulation and function were examined in normotensive dogs, in relation to the renin-angiotensin-aldosterone (R-A-A) and kallikrein-kinin (K-K) systems and prostaglandins (PGs). These inhibitors markedly decreased renal vascular resistance (RVR) in parallel with a reduction in systemic blood pressure, and increased renal blood flow (RBF). Captopril exerted its effects rapidly, but its disappearance was also rapid. The onset of ramipril's effects was slightly delayed, but its antihypertensive and RVR-decreasing effects were fairly prolonged. Ramipril showed more potent and longer-lasting RBF-increasing effect and induced marked Na diuresis. Enalapril had no diuretic effect, and captopril's effect was only temporary. Plasma renin activity was increased similarly by the three inhibitors, but only ramipril significantly decreased plasma aldosterone concentration. This aldosterone secretion inhibition by ramipril may be partly involved in the diuretic effect. Involvement of the K-K system and PGs in ramipril's effects on the dog kidney was examined. When systemic PG biosynthesis was inhibited by indomethacin pretreatment, ramipril-induced increases in RBF and urine volume were inhibited about 50%. Inhibition of the K-K system by aprotinin pretreatment resulted in marked inhibition of urine volume increase, but scarcely affected RBF increase. These results indicate that ramipril produces the most potent effect on the renal circulation and function of the dog among the three ACE inhibitors and that its diuretic action is mostly due to kinins and kinin-induced PGs in the kidney and the RBF increase, due to the R-A-A system and PGs.