Circulation in profound hypothermia

Circulation was maintained in dogs at 5°C using a noninvasive pulsatile pumping system (MVA) and studied using ^99mTechnetium-labeled microspheres. Cardiac output, blood pressure, and stroke volume decreased as temperature fell and peripheral resistance increased.Seven of eight dogs were successfully resuscitated after rewarming but cardiac output and blood pressure remained low and peripheral resistance remained high.The distribution of cardiac output increased to the heart (×3) and brain (×2) and decreased or remained the same in other organs at 5°C.Blood flow in the heart and brain remained high at 5°C, despite a low cardiac output. After rewarming, blood flow was normal in the heart but remained low in the brain, kidney, and gastrointestinal tract. Circulation in profound induced hypothermia may be similar to circulation in deep hibernation.     

Effects of indomethacin on blood flow in the normal pancreas in conscious dogs

In anesthetised animals basal pancreatic blood flow, both in the normal gland and in acute pancreatitis, and basal renal blood flow have been shown to be dependent on prostaglandins (PGs). However, in conscious dogs it has been demonstrated that the reliance of basal renal blood flow on PGs is only apparent, and probably due to the effect of anesthesia and surgery stimulating PG synthesis through enhanced stimulation of the sympathetic nervous system. This study was undertaken to investigate the changes in mean blood pressure, cardiac output, and pancreatic arterial blood flow, relative to the cardiac output, in the normal pancreas, with and without PG synthesis inhibition (indomethacin) in conscious dogs. Blood flows were measured with electromagnetic flow probes. The effects of indomethacin were measured over a 2-hr period and compared to a control group. The results show that the relative pancreatic blood flow is not affected by doses of indomethacin which decrease cardiac output (P less than 0.5). It is suggested that PGs may have no effect on blood flow in the normal pancreas in conscious animals.     

Effect of graded hemorrhage on renal cortical perfusion in dogs

Renal cortical tissue gas tensions, systemic oxygen supply and some features of energy metabolism and central hemodynamics were recorded in splenectomized dogs during graded hemorrhage and subsequent reinfusion of shed blood. Renal cortical partial pressure of oxygen and carbon dioxide responded rapidly to changes in blood volume and cardiac output. Lowest cortical partial pressure of oxygen values and highest cortical partial pressure of carbon dioxide levels were achieved at a maximal 50 percent blood loss. The decrease in arterial pressure, blood hemoglobin and hematocrit as well as the increase in blood lactate concentration lagged behind blood loss. Renal cortical partial pressure of oxygen, arterial pressure and cardiac output responded rapidly to reinfusions of withdrawn blood, while the cortical partial pressure of carbon dioxide, heart rate, arterial pH and blood lactate concentration returned to initial levels more slowly. Arterial blood gases remained normal throughout the observation period and did not provide an adequate index of tissue oxygenation. In contrast, the partial pressure of oxygen of the renal cortex proved an excellent and sensitive indicator of renal perfusion during hemorrhagic shock and its management.     

Pathophysiology of acute pancreatitis: Evaluation of the effects and mode of action of indomethacin in experimental pancreatitis in dogs

Prostaglandins are known to affect vascular flow and the inflammatory response. Since acute pancreatitis involves both of these phenomena, we undertook studies using anesthetized mongrel dogs to investigate changes in blood pressure, cardiac output and pancreatic arterial flow for 6 hr in both normal animals (10 dogs) and following induction of acute pancreatitis (15 dogs). Indomethacin (5 mg/kg), which inhibits synthesis of prostaglandins, was then injected intravenously, and the animals were subsequently monitored for 2 hr. Results showed: (1) A significant fall in pancreatic arterial flow, relative to cardiac output, over the first 6 hr of the disease in the acute pancreatitis animals (P < 0.001). (2) A further significant decrease in relative pancreatic arterial flow following indomethacin in these animals (P < 0.001). A similar reduction in pancreatic arterial flow was observed following indomethacin administration in the control animals (P < 0.001). Conclusions: (1) Relative pancreatic arterial flow falls during experimental acute pancreatitis. (2) Indomethacin reduces both basal and compromised pancreatic arterial flow in the anesthetized dog; this suggests that prostaglandins may participate in the maintainance of basal acid-compromised pancreatic blood flow in the anesthetized dog.     

The effect of hypertonic saline resuscitation on responses to severe hemorrhagic shock by the skeletal muscle, intestinal, and renal microcirculation systems: seeing is believing

BACKGROUND: Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion. METHODS: Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels. RESULTS: Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids. CONCLUSIONS: Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.     

The hemodynamic effects of intravenous infusions of serotonin in conscious dogs

The effects of exogenously infused serotonin on central and regional hemodynamics were investigated in 14 dogs. Using intravenous doses that mimic postprandial levels of serotonin, we were able to demonstrate no changes in cardiac output or mean arterial pressure. However, there were region-specific changes in blood flow. Blood flow to the fundus, antrum, brain, heart, and skeletal muscle were increased by both the low-dose (4 μ/kg-min) and the high-dose (10 μg/kg-min) infusions. In contrast, blood flow to the kidney, spleen, and liver decreased. Whole blood 5-HT levels were measured in mixed venous blood and systemic arterial blood. Based on the differences between serotonin levels in these two circulations, pulmonary inactivation of exogenously infused serotonin was calculated to be 44%. The half-life of exogenous serotonin was measured at 1.2 min. The data thus suggest that at doses which mimic those released from the intestinal enterochromaffin cells, serotonin may play a role in mediating postprandial hemodynamic responses.     

Adjuvant effects of beta-adrenergic drugs on indomethacin treatment of newborn canine endotoxic shock.

Newborns are susceptible to gram-negative sepsis/septic shock, but there is no established method of its treatment. This study was performed to evaluate the adjuvant effects of dopamine and dobutamine in the indomethacin treatment of newborn endotoxic shock. Endotoxic shock was induced in newborn dogs (2 to 10 days old; 300 to 800 g) by Escherichia coli lipopolysaccharide (LPS; 1.5 mg/kg, intravenously [IV]). Indomethacin (1.5 mg/kg, IV) was injected 5 minutes after LPS injection. Dopamine (5 micrograms/kg/min) or dobutamine (5 micrograms/mg/min) infusion started 5 minutes after LPS injection immediately following indomethacin injection. Hemodynamic parameters were monitored serially for 120 minutes. LPS induced bradycardia and hypotension, decreased the cardiac output and cardiac performance, and increased the total vascular resistance. When dopamine, dobutamine, or indomethacin were used alone, they attenuated the hemodynamic deterioration by LPS. Dopamine infusion following indomethacin administration improved the hemodynamics further, although dobutamine infusion did not. Therefore, we conclude that the adjuvant therapy of dopamine in the indomethacin treatment of newborn endotoxic shock is beneficial.     

Contribution of endogenous vasoactive compounds to renal vascular resistance in neonatal chronic partial ureteral obstruction

To evaluate the relative contribution of endogenous vasoactive compounds to maintenance of increased renal vascular resistance in neonatal obstructive nephropathy, cardiac output and renal blood flow were measured using radioactive microspheres in 25 +/- 3 day-old guinea pigs subjected to unilateral partial ureteral constriction within the first two days of life. Mass and renal blood flow of the obstructed kidney were significantly lower than those of the contralateral kidney. Following a control period, thromboxane synthesis was blocked by infusion of OKY-046, after which prostaglandin synthesis was inhibited by indomethacin. In a separate group of animals, angiotensin converting enzyme inhibitor, MK-422, was infused before or after administration of OKY-046. While neither OKY-046 nor indomethacin had a consistent effect on vascular resistance, infusion of MK-422 resulted in selective reduction of renal vascular resistance of the obstructed kidney compared to resistance in the intact kidney and other vascular beds. Removal of the contralateral kidney at the time of ureteral constriction in an additional group of animals resulted in hypertrophy and vasodilation of the obstructed kidney which was not altered by thromboxane or cyclooxygenase inhibition. We conclude that in the neonatal kidney subjected to ipsilateral chronic partial ureteral obstruction, vasoconstriction is mediated at least in part by angiotensin II, but not by thromboxane. Furthermore, vasodilation of the obstructed kidney resulting from contralateral nephrectomy is not dependent on prostaglandin synthesis. Renal vascular resistance of the kidney with prolonged partial ureteral constriction in early development thus appears to be inversely related to renal growth and is not significantly mediated by endogenous prostanoids.     

The effect of hypotensive anesthesia on renal hemodynamics

Deliberate hypotensive anesthesia (MBP = 36 mm Hg) using Halothane, hyperventilation, and positive pressure respiration (peak inspiratory pressure = 15 cm H₂O) was used in 7 dogs for a 2-hr period. Xenon-133 washout was employed by injection of 800–1500 μCi through a catheter placed under fluoroscopic control in the right renal artery. Washout curves were obtained before hypotensive anesthesia, during and after a return of normal hemodynamics using a collimater placed over the right flank. The curves were analyzed and total renal blood flow plus four components of renal blood flow were developed: I cortex; II juxtamedulla; III inner medulla; and IV hilar fat. Using an indocyanine green indicator dilution curve, cardiac output was measured. Urinary output was collected and blood gases monitored.Total renal blood flow decreased significantly during hypotensive anesthesia only to return toward normal within 30 min of discontinuing deliberate hypotension (328 control → 159 during hypotensive anesthesia → 227 ml/100 g/min after hypotensive anesthesia). This decrease in renal blood flow was associated with a fall in cardiac output which also returned toward normal promptly after discontinuing inhalation anesthesia (3.2 → 1.7 → 3.0 liter/min). The ratio of renal blood flow/cardiac output did not change with hypotensive anesthesia indicating an absence of renal vasoconstriction, and renal vascular resistance actually fell from .427 to .306 mm Hg/ml/100 g/min. During the recovery phase, because the blood pressure and cardiac output returned to the control level before renal blood flow, the ratio of renal blood flow/cardiac output fell from 7.1 to 4.9% and the renal vascular resistance rose from .306 to .611 mm Hg/ ml/100 g/min. It was apparent that during recovery renal vasoconstriction developed.The fall in renal blood flow with hypotensive anesthesia was associated with a significant fall in Component I (cortical) flow (414 → 257 → 330 ml/100 g/min) but no significant change in Component II (outer medullary) flow (72 → 74 → 98 ml/ 100 g/min) or the percent distribution of radioactivity between cortex and medulla. This indicates a selective decrease in cortical flow and an absence of marked intrarenal shunting which is seen with hypovolemic hypotension. Urine output fell during hypotension (65 → 20 → 80 ml/hr) but did not cease entirely in any animal. The explanation for the known renal safety of hypotensive anesthesia rests primarily with the absence on intrarenal shunting and associated vasoconstriction during hypotension.     

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.     

The effects of severe progressive hemodilution on regional blood flow and oxygen consumption.

Electrolyte solutions are effective in the immediate treatment of hemorrhagic shock, but the acceptable limits of hemodilution are not well defined. In this study oxygen consumption was measured in various tissues at rest and in maximally exercising skeletal muscle during progressive hemodilution. Twenty splenectomized, anesthetized dogs were studied (weight 22.6 +/- 2.0 kilograms). Measurements were made of cardiac output, capillary muscle blood flow in the hind limb, and renal and superior mesenteric arterial blood flow. Arteriovenous oxygen differences in the hind limb, kidney, gut, and in the whole body were calculated from the oxygen content of arterial and appropriate venous samples.     

The effect of alpha(2) agonist-induced sedation and its reversal with an alpha(2) antagonist on organ blood flow in sheep

We investigated changes in cardiac output and organ blood flow induced by medetomidine in sheep and determined changes in cardiac output and organ blood flow after reversal of medetomidine-induced sedation by atipamezole. Eight sheep were chronically instrumented. Medetomidine was infused IV to target plasma levels of 0, 0.8, 1.6, 3.2, 6.4, and 12.8 ng/mL for 25 min each, followed by a 5-min infusion of atipamezole. Hemodynamic values and organ blood flow (using colored microspheres) were measured just before medetomidine infusion (baseline), at the end of each medetomidine infusion step, and 30 min after the administration of atipamezole. Medetomidine (12. 8 ng/mL) decreased cardiac output from 6.3 +/- 1.0 to 3.2 +/- 0.7 L/min (P < 0.0001) and increased systemic vascular resistance from 1310 +/- 207 to 3467 +/- 1299 dynes. s(-1). cm(-5) (P < 0.0001). Blood flow decreased in the cerebral cortex from 1.29 +/- 0.40 to 0. 66 +/- 0.12 mL. g(-1). min(-1) (P < 0.0001), left ventricle from 2. 11 +/- 0.61 to 1.40 +/- 0.40 mL. g(-1). min(-1) (P < 0.0001), kidney from 8.28 +/- 3.17 to 6.07 +/- 2.65 mL. g(-1). min(-1) (P < 0.0001), skin from 0.09 +/- 0.04 to 0.05 +/- 0.02 mL. g(-1). min(-1) (P < 0. 0001), intestine from 0.56 +/- 0.13 to 0.27 +/- 0.07 mL. g(-1). min(-1) (P < 0.0001), and skeletal muscle from 0.28 +/- 0.15 to 0.04 +/- 0.01 mL. g(-1). min(-1) (P < 0.0001). Blood flow in the liver (hepatic artery) increased from 0.05 +/- 0.03 to 0.24 +/- 0.16 mL. g(-1). min(-1) (P < 0.0001). After atipamezole infusion, cardiac output and systemic vascular resistance returned to baseline, but the cerebral cortex, left ventricle, and renal blood flows remained below baseline at 0.89 +/- 0.22, 1.37 +/- 0.50, and 6.25 +/- 2.76 mL. g(-1). min(-1), respectively; skeletal muscle blood flow increased above baseline to 0.44 +/- 0.27 mL. g(-1). min(-1), spleen blood flow decreased below baseline to 1.65 +/- 0.61 mL. g(-1). min(-1) (P < 0.0001), and liver, intestine, and lung blood flows returned to baseline values. In conclusion, medetomidine decreased and redistributed organ blood flow in sheep. Atipamezole reversed the medetomidine-induced hemodynamic changes, but redistributed blood flow from the brain, heart, and kidney to the skeletal muscle.     

Effects of celiac plexus block on splanchnic circulation--II: Changes in the systemic hemodynamics and the blood flow of the liver and kidney in dogs

Effects of celiac plexus block (CPB) on systemic and splanchnic circulation, especially of liver and kidney, were investigated in twenty nine mongrel dogs. CPB was performed by an anterior approach through a catheter placed in a paraaortic compartment using 7 mg.kg-1 of 2% mepivacaine. Tissue blood flow measurement was performed by a hydrogen clearance method in eleven dogs, and vascular blood flow was measured in eighteen dogs by an electromagnetic flow meter. Swan-Ganz catheter was inserted to measure mean arterial pressure (ABP), heart rate (HR), central venous pressure (CVP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). Then stroke volume (SV), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated. Following CPB, ABP, HR, CVP and C.O. were significantly decreased at 7 to 9%. PAP decreased at 5%. PCWP, SV, SVR and PVR were unchanged. The hepatic arterial blood flow increased significantly, and portal venous blood flow decreased after CPB transiently, and then recovered to control value or to a higher level at 60min after CPB. The tissue blood flow of the liver tended to increase, but the change was not significant. In the kidney, both arterial and tissue blood flows increased significantly after CPB. The results suggest that following CPB, hepatic and renal tissue blood flows increased because of the increments of their arterial blood flows, unless a profound systemic hemodynamic depression occurred.     

Influence of desflurane,isoflurane and halothane on regional tissue perfusion in dogs

The actions of desflurane, isoflurane and halothane on regional tissue perfusion were studied using radioactive microspheres in dogs chronically instrumented for measurement of arterial and left ventricular pressure, global (left ventricular dP/dtmax) and regional (percent segment shortening) contractile function, and diastolic coronary blood flow velocity. Systemic and coronary haemodynamics and regional tissue perfusion were measured in the conscious state and during anaesthesia with equihypotensive concentrations of desflurane, isoflurane, and halothane. All three volatile anaesthetics (P < 0.05) increased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dtmax Myocardial perfusion was unchanged in subendocardial midmyocardial, and subepicardial regions by the administration of either dose of desflurane. No redistribution of intramyocardial blood flow (endo/epi ratio) was observed during desflurane anaesthesia. Although regional myocardial perfusion was reduced (P < 0.05) in a dose-related fashion by halothane and by isoflurane at high concentrations, redistribution of intramyocardial blood flow was not observed during halothane or isoflurane anaesthesia. All three volatile anaesthetics reduced blood flow to the renal cortex, but only desflurane produced a decrease in renal cortical vascular resistance. Hepatic blood flow decreased in response to halothane but not desflurane or isoflurane. Concomitant decreases in hepatic resistance were observed during administration of desflurane and isoflurane. Dose-related decreases in intestinal and skeletal muscle blood flow were observed during halothane and isoflurane but not desflurane anaesthesia. The results suggest that desflurane maintains myocardial, hepatic, intestinal, and skeletal muscle blood flow while halothane and isoflurane decrease regional tissue perfusion in these vascular beds to varying degrees during systemic hypotension in the chronically instrumented dog.     

HAEMODYNAMIC EFFECTS OF TUBOCURARINE, GALLAMINE AND SUXAMETHONIUM IN DOGS

In anaesthetized open-chest dogs, neuromuscular blocking dosesof tubocurarine reduced phasic aortic flow, aortic blood pressure,stroke volume, heart rate, cardiac output and peripheral resistance.These haemodynamic effects could be attributed to blockade ofsympathetic ganglia and to histamine release. Paralyzing dosesof gallamine slightly increased phasic aortic flow, stroke volumeand cardiac output; such changes could be related to cardiovagalblock. Blood pressure and peripheral resistance were slightlyreduced. Contrary to known effects in anaesthetized patients,gallamine or atropine did not produce important tachycardiain anaesthetized dogs. Suxamethonium caused a small reductionin peripheral resistance; phasic aortic flow, stroke volumeand cardiac output were slightly increased. These minor circulatorydisturbances may be attributable to muscarinic effects of thedrug.     

Influence of long-term anesthesia on regional blood flow distribution and hemodynamics in the dog.

The effects of 8 h sodium pentobarbital anesthesia on the cardiovascular function and blood flow distribution have been studied on dogs under controlled ventilation. A myocardial depressant action was registered in heart rate, cardiac output and left ventricular work, compensated by an increased peripheral resistance. Blood flow distribution judged by 15 mum carbonized microspheres revealed reduction of the fraction of the blood distributed to the brain. Simultaneously infused microspheres of 15 and 50 mum showed arteriovenous shunting of the smaller spheres compared to the larger through the heart, kidneys, stomach, small and large intestine and the brain. Correspondingly increased fractions of the smaller microspheres were found in the lungs and the liver. The preportal arteriovenous shunting to the liver was larger after 8 h of pentobarbital anesthesia than after 20 min or in conscious dogs.     

Prostaglandin synthesis inhibition prevents placental dysfunction after fetal cardiac bypass.

Surgical therapy of certain congenital heart lesions in utero may have advantages over postnatal repair or palliation. For fetal heart operations to be done, it will be necessary to devise a method of fetal cardiac bypass. Previous studies in which standard cardiopulmonary bypass techniques were used have reported fetal death resulting from increased placental vascular resistance, which causes decreased placental blood flow and depressed respiratory gas exchange. The mechanism responsible for this increase in placental vascular resistance has remained unknown. In a series of 10 fetal cardiac bypass experiments we examined the role of prostaglandins as the mediators of this response. Observations were made during a 1-hour prebypass period, a 30-minute bypass period, and a 2-hour postbypass period. The cardiac bypass circuit consisted of a centrifugal pump, and bypass flows were adjusted to equal a normal fetal cardiac output of 400 ml/min/kg. In six of the experiments indomethacin (3 mg/100 ml) was added to the pump priming to block prostaglandin synthesis. By means of the microsphere technique, fetal cardiac output, placental blood flow, individual organ blood flow, and placental vascular resistance were determined at five times during the experiments: presternotomy, poststernotomy, during cardiac bypass, at 5 minutes after cessation of bypass, and 30 minutes after cessation of bypass. Fetal arterial blood gas measurements were made every 15 to 30 minutes. When indomethacin was used to inhibit prostaglandin synthesis, placental vascular resistance did not increase, placental blood flow did not decrease, and fetal blood gases remained at normal prebypass levels during and after fetal cardiac bypass. We propose that production of vasoactive prostaglandins is responsible for the increased placental vascular resistance and decreased placental blood flow observed after fetal cardiac bypass. An understanding of the mechanism responsible for the increased placental vascular resistance seen after fetal cardiac bypass will be an important first step before clinical application.     

Hemodynamic responses to alfentanil in halothane-anesthetized dogs

Alfentanil is an opioid that has been used both as a sole anesthetic and in conjunction with other inhalation anesthetics. However, its effects on myocardial performance and regional blood flow are not clearly known. Using sonomicrometry and radioactive microsphere techniques, we examined the hemodynamic responses to alfentanil when given as a loading dose (45 micrograms/kg) followed by continuous infusion (3 micrograms X kg-1 X min-1) in dogs anesthetized with halothane. Similar plasma levels of alfentanil were observed after the loading and infusion doses, and both techniques of administration produced a significant reduction in arterial pressure without change in global or regional function of the left ventricle. Although cardiac output and left ventricular end-diastolic pressure remained unchanged, heart rate and systemic vascular resistance decreased significantly after the loading dose and recovered slightly when alfentanil was infused continuously. Despite the systemic hypotension, alfentanil did not alter perfusion to the heart, brain, muscle, and skin; however, blood flow to the renal cortex and the arterial supply to the liver decreased by 25 and 60%, respectively. Reduction in blood flow to the kidneys and the liver suggests that alfentanil should be used with caution when normal function of these organs is in question.     

The effect of haemorrhage on renal blood flow and intrarenal flow distribution

Bleeding of dogs to constant arterial pressure of 90 mm/g and 60 mmHg respectively decreased renal blood flow in proportion to pressure reduction. There was no evidence of autoregulation of renal blood flow or of selective renal vasoconstriction. With the radioactive microsphere technique a moderate shift of blood flow from the outer to the inner cortex was observed. In the renal 133Xe wash-out curves exponent 1(attributed to the elimination of the indicator from the cortex) was more reduced than exponents 2 and 3 (medulla). These findings may not indicate a redistribution of renal blood flow through resistance changes in specific parts of the renal vasculature but may represent the consequences of focal cortical ischaemia, most prominent in the outer cortex.     

Indomethacin and pancreatic blood flow. An experimental study in pigs

Indomethacin has been reported to decrease pancreatic blood flow. The drug has been used as an analgesic in acute pancreatitis. As decreased blood flow to the pancreas may detrimentally affect the outcome of acute pancreatitis, we investigated the effects of indomethacin on blood flow in the normal porcine pancreas. Regional blood flows, with special reference to the pancreatic flow, were studied with radioactively labelled microspheres in ketamine-anesthetized pigs before and after intravenous administration of indomethacin 2 mg/kg during 10 min. A transient decrease of cardiac output was seen during the infusion. Basal pancreatic blood flow was significantly increased 10 and 30 min after administration of indomethacin. No significant changes were found in small-intestinal or renal blood flow. We conclude that indomethacin does not reduce blood flow in normal porcine pancreas.