Pulmonary edema and elevated left atrial pressure: four hours and beyond.

Cardiogenic pulmonary edema is caused by the increase in left atrial pressure when the left heart fails. The increased pressure causes rapid fluid accumulation within the lung interstitial spaces. However, over the following days to weeks, additional fluid may accumulate due to the deposition of excess lung connective tissue.

Role of propofol and its solvent, intralipid, in nitric oxide-induced peripheral vasodilatation in dogs.

BACKGROUND: The commercial propofol preparation in an intralipid solution causes marked vasodilatation. Both propofol and its solvent seem to stimulate the nitric oxide (NO) pathway. The role of intralipid in cardiac and regional haemodynamic changes induced by propofol and their respective interactions with the NO pathway was assessed. METHODS: Dogs were instrumented to record arterial pressure, heart rate, cardiac output, dP/dt (the first derivative of left ventricular pressure) and vertebral, carotid, coronary, mesenteric, hepatic, portal and renal blood flows. Experimental groups were as follows. Group 1 (control; n = 11): N-methyl-L-arginine (L-NMA) 20 mg kg-1 i.v.; Group 2 (n = 8): propofol (10 mg ml-1) 4 mg kg-1 i.v. bolus followed by 0.6 mg kg-1 min-1; Group 3 (n = 6): intralipid 0.25 ml kg-1 bolus followed by 0.06 ml kg-1 min-1. After 60 min, L-NMA was injected in Groups 2 and 3. RESULTS: Propofol induced increases in heart rate, coronary and carotid blood flows, and decreases in systemic vascular resistance and dP/dt. Intralipid increased renal blood flow, carotid vascular resistance and mesenteric vascular resistance. In the presence of intralipid, L-NMA-induced pressor response and systemic, carotid and renal vasoconstriction were more pronounced than in control dogs. CONCLUSIONS: Except for the coronary and carotid circulations, intralipid modulates the NO pathway in cardiac and regional blood flow.

Role of heparin and nitric oxide in the cardiac and regional hemodynamic properties of protamine in conscious chronically instrumented dogs.

BACKGROUND: Because protamine is administered to reverse heparin, a drug that might itself affect the pharmacologic properties of protamine, this study was designed to assess the properties of protamine alone and in the presence of heparin in conscious dogs. METHODS: Twelve dogs were instrumented to continuously record cardiac and regional hemodynamics. On separate occasions, a dose of protamine (0.5, 1, 3, 5, and 8 mg/kg) was randomly administered either alone or in the presence of heparin (ratio 100 IU/mg). Heparin (300 IU/kg) and protamine (3 mg/kg) were administered in the presence of N-methyl-L-arginine, a specific nitric oxide synthase inhibitor. Identical experiments were performed with protamine (8 mg/kg) in the absence of heparin on a separate occasion. RESULTS: Protamine alone produced limited cardiac and regional changes. In the presence of heparin, protamine produced hypotension at 3, 5, and 8 mg/kg, vasodilatation at 3 and 5 mg/kg, and a more pronounced dose-dependent increase in pulmonary pressure at 3, 5, and 8 mg/kg. Simultaneously, transient carotid vasodilatation at 3 and 5 mg/kg, coronary and hepatic vasodilatation at 3, 5, and 8 mg/kg, as well as a decrease in vertebral vascular resistance were recorded at 1, 3, and 8 mg/kg. Protamine produced an immediate increase followed by a secondary decrease in renal vascular resistance. Protamine-induced secondary pulmonary pressor effects were attenuated. In the presence of heparin, nitric oxide synthase blockade selectively attenuated protamine-induced immediate hypotension, systemic vasodilatation, and coronary, mesenteric, and hepatic vasodilations as well as the decrease in portal blood flow and accentuated the renal vasoconstriction. CONCLUSIONS: The presence of heparin accentuated the decrease in cardiac function induced by protamine as well as its effects on regional circulation. The data provide evidence that the nitric oxide pathway is involved in the systemic and selective regional heparin-protamine-mediated vasodilatation in conscious dogs.

Measurement of cardiac function in conscious rats.

The goal of this study was to establish that 1. blood velocity profile in the rat aorta is parabolic, and 2. measure of left ventricular thickening fraction can be used in rats. Spontaneously hypertensive and normotensive Wistar Kyoto rats were instrumented with a 20-MHz pulsed Doppler flow probe around the thoracic aorta and a 20-MHz pulsed Doppler thickening probe on the left ventricle. Doppler frequency shifts were measured throughout the entire aorta diameter, and individual blood velocity profiles were constructed. It was demonstrated that blood velocity in the ascending aorta of rats is laminar; therefore, cardiac output can be measured using the pulsed Doppler method. In Wistar Kyoto rats, left ventricular thickening fraction was 24 +/- 1% and 25 +/- 1%, 2 and 3 weeks following surgery. In spontaneously hypertensive rats, left ventricular thickening fraction was 22 +/- 2%. Halothane depressed left ventricular thickening fraction, whereas isoproterenol increased left ventricular thickening fraction in conscious rats. Thus, pulsed Doppler technique is a valuable tool for evaluating cardiovascular function in conscious rats.

Comparison of cardiac and regional hemodynamic responses to N-methyl-L-arginine and aminoguanidine infusions in conscious pigs.

The aim of this study was to elucidate cardiac and regional hemodynamics using a nonspecific inhibitor of the constitutive and inducible nitric oxide synthase (NOS), N-methyl-L-arginine (L-NMA), and a specific inhibitor of the inducible NOS, aminoguanidine, in conscious pigs. Animals were divided into two groups. After hemodynamics were stabilized, animals in group 1 (n = 5) received an infusion of L-NMA at 300 microg/kg per min, i.v., over 60 min, and group 2 (n = 5) received an infusion of aminoguanidine, infused at 1 mg/kg per min over 60 min. Hemodynamic parameters including arterial blood pressure, heart rate, cardiac output, dP/dt, and carotid, coronary, hepatic, portal, mesenteric, and renal blood flows were continuously recorded before and 5, 15, 30, 45, 60, and 120 min after L-NMA infusion or aminoguanidine infusion, or both. The L-NMA vasopressor response (20%) was associated with a significant increase in systemic vascular resistance (45%). Carotid, hepatic, and renal vascular resistance increased significantly by 95%, 110%, and 20%, respectively, at 60 min after L-NMA infusion. Finally, heart rate, cardiac output, dP/dt, and portal and mesenteric blood flows remained unchanged after L-NMA infusion. In contrast, aminoguanidine infused at 1 mg/kg per min over 60 min did not change systemic arterial blood pressure or regional blood flow in conscious pigs. Furthermore, aminoguanidine had no effect on acetylcholine vasodilator effects. In conclusion, the lack of pressor effects and of agonist-stimulated NO production induced by aminoguanidine suggests that aminoguanidine is a weak inhibitor of the constitutive NOS. Compared with L-NMA, the selectivity of aminoguanidine may decrease possible side effects that could occur as a result of inhibition of constitutive NOS.

Antinociceptive and cardiovascular properties of esmolol following formalin injection in rats.

PURPOSE: To assess the role of esmolol, a beta1 receptor blocker, in the modulation of pain in the absence of anesthesia. METHODS: Rats were chronically instrumented to record mean arterial blood pressure (MAP) and heart rate (HR). Animals were divided into three groups. Group 1 [esmolol high (EH) 150 mg x kg(-1) x hr(-1); n = 9], Group 2 [esmolol low (EL) 40 mg x kg(-1) x hr(-1); n = 7] and Group 3 saline (n = 9). Formalin 5% was injected in the rat hind paw. Formalin-induced lifting, MAP and HR were recorded at five minute intervals for 35 min after formalin injection. RESULTS: Formalin was associated with an early (Phase 1; 0-5 min) and late nociceptive response (Phase 2; 10-35 min). Esmolol did not affect Phase 1. Although low dose esmolol had minimum effects on nociceptive Phase 2, it was diminished with high dose esmolol. Formalin induced biphasic increases in MAP and HR. Although esmolol did not affect the initial increase in MAP, high dose esmolol blunted the secondary increase in MAP Both low and high doses of esmolol inhibited formalin-induced tachycardia during the first 30 min. CONCLUSION: Our data suggest that esmolol leads to analgesia and reduction of cardiovascular responses to pain.

Effects of N-methyl-L-arginine on cardiac and regional blood flow in a dog endotoxin shock model.

PURPOSE: Indirect evidence suggests a decrease in organ perfusion as a result of nitric oxide (NO) inhibition in endotoxic shock. Cardiac and regional hemodynamic responses to N-methyl-L-arginine (L-NMA), a nonspecific inhibitor of constitutive and inducible nitric oxide synthase (NOS), were assessed in nine conscious dogs subjected to endotoxin. MATERIALS AND METHODS: Lipopolysaccharide (LPS) was titrated to a maximum of 200 microg/kg, IV, over 45 minutes. L-NMA was given in a dose of 20 mg/kg, IV. Hemodynamic parameters were recorded for 6 hours following L-NMA administration. RESULTS: LPS induced significant decreases in mean arterial blood pressure (MAP), cardiac output (CO), first derivative of left ventricular pressure (dP/dt), coronary blood flow, carotid blood flow, mesenteric blood flow, renal blood flow, and a significant hepatic vasodilation. L-NMA fully reversed the effects of LPS on MAP, heart rate, dP/dt, coronary and carotid blood flow, and reversed mesenteric blood flow and hepatic blood flow at 1 and 3 hours, respectively. L-NMA partially overcame the LPS-induced decrease in renal blood flow at 30 minutes and 1 hour. Except for mesenteric and carotid circulation, L-NMA did not change regional vascular resistance. CONCLUSIONS: It is likely that constitutive NOS is implicated in immediate cardiac, carotid, mesenteric, and renal vascular changes, whereas inducible NOS accounted for delayed responses in hepatic and coronary circulation.

Effects of hyperbaric hyperoxia on cardiac and regional hemodynamics in conscious dogs.

BACKGROUND: Although evidence of systemic vasoconstriction has been reported both in animal models and in humans, the regional hemodynamic effects of hyperbaric hyperoxia have not been well characterized. METHODS: In the present study, we report the effects of hyperoxia (normobaric and hyperbaric) on simultaneous measurements of cardiac and regional hemodynamics in the chronically instrumented conscious dog. RESULTS: Hyperbaric hyperoxia (202 kPa) produced significant decreases in heart rate (12%) and cardiac output (20%) and a significant increase in systemic vascular resistance (30%). Carotid artery blood flow decreased significantly (18%) whereas coronary, hepatic, renal and mesenteric flows remained unchanged. CONCLUSIONS: Our data show that the hyperoxic vasoconstriction is limited to the cerebral and peripheral vascular beds. Additionally, blood flow to major organs is well preserved in the face of hyperoxia-induced decreases in cardiac output. Consequently, we postulate that a redistribution of blood flow from peripheral vascular beds (e.g., skin, muscle, bone) to major organs occurs during hyperbaric hyperoxia.

Cardiovascular deconditioning and venous air embolism in simulated microgravity in the rat.

BACKGROUND: Astronauts conducting extravehicular activities undergo decompression to a lower ambient pressure, potentially resulting in gas bubble formation within the tissues and venous circulation. Additionally, exposure to microgravity produces fluid shifts within the body leading to cardiovascular deconditioning. A lower incidence of decompression illness in actual spaceflight compared with that in ground-based altitude chamber flights suggests that there is a possible interaction between microgravity exposure and decompression illness. HYPOTHESIS: The purpose of this study was to evaluate the cardiovascular and pulmonary effects of simulated hypobaric decompression stress using a tail suspension (head-down tilt) model of microgravity to produce the fluid shifts associated with weightlessness in conscious, chronically instrumented rats. METHODS: Venous bubble formation resulting from altitude decompression illness was simulated by a 3-h intravenous air infusion. Cardiovascular deconditioning was simulated by 96 h of head-down tilt. Heart rate, mean arterial blood pressure, central venous pressure, left ventricular wall thickening and cardiac output were continuously recorded. Lung studies were performed to evaluate edema formation and compliance measurement. Blood and pleural fluid were examined for changes in white cell counts and protein concentration. RESULTS: Our data demonstrated that in tail-suspended rats subjected to venous air infusions, there was a reduction in pulmonary edema formation and less of a decrease in cardiac output than occurred following venous air infusion alone. Mean arterial blood pressure and myocardial wall thickening fractions were unchanged with either tail-suspension or venous air infusion. Heart rate decreased in both conditions while systemic vascular resistance increased. CONCLUSIONS: These differences may be due in part to a change or redistribution of pulmonary blood flow or to a diminished cellular response to the microvascular insult of the venous air embolization.

Cardiac and regional hemodynamic interactions between halothane and nitric oxide synthase activity in dogs.

BACKGROUND: In vitro, halothane appears to affect the role played by nitric oxide in the regulation of vascular tone and cardiac function. In vivo, the results of the interactions between halothane and the nitric oxide pathway remain controversial. The authors investigated the effects of halothane on the cardiac and regional hemodynamic properties of N-methyl-L-arginine (NMA), a specific nitric oxide synthase inhibitor, in dogs. METHODS: Twenty-five dogs were chronically instrumented. Aortic pressure, the first derivative of left ventricular pressure, cardiac output, heart rate, and carotid, coronary, mesenteric, hepatic, portal and renal blood flows were continuously recorded. N-methyl-L-arginine was infused intravenously at 20 mg/kg over 1 min in awake dogs (n = 11) and in 1.2% halothane-anesthetized dogs (n = 10). As a control group, the remaining four dogs were studied awake and during 1.2% halothane for 2 h in the absence of NMA. RESULTS: In awake dogs, NMA produced a sustained pressor response (34%) and systemic vasoconstriction (40%) associated with a decrease in cardiac output (16%). Regional circulation changes included an immediate and transient increase in carotid (43%) and coronary (237%) blood flows and a subsequent decrease in carotid blood flow (25%). Hepatic and mesenteric blood flows also decreased, by 43% and 16%, respectively. Except for the coronary circulation, regional vascular resistance increased significantly. Halothane did not affect the pressor response to NMA but did blunt the cardiac output changes. Consequently, the systemic vasoconstriction after nitric oxide synthase inhibition was of shorter duration and of lesser magnitude during halothane anesthesia. Halothane also blunted the carotid, mesenteric, and renal vasoconstriction induced by NMA. Finally, in 1.2% halothane-anesthetized dogs, NMA induced a coronary vasoconstriction. CONCLUSIONS: Halothane minimally interferes with the systemic and regional hemodynamic consequences of nitric oxide synthase blockade. The nature and magnitude of the interaction depend on the territory in which they occur.

Cardiopulmonary changes with moderate decompression in rats.

Sprague-Dawley rats were compressed to 616 kPa (a) for 120 min then decompressed at 38 kPa/min to assess the cardiovascular and pulmonary responses to moderate decompression stress. In one series of experiments the rats were chronically instrumented with Doppler ultrasonic probes for simultaneous measurement of blood pressure, cardiac output, heart rate, left and right ventricular wall thickening fraction, and venous bubble detection. Data were collected at baseline, throughout the compression/decompression protocol, and for 120 min post decompression. In a second series of experiments the pulmonary responses to the decompression protocol were evaluated in non-instrumented rats. Analyses included blood gases, pleural and bronchoalveolar lavage (BAL) protein and hemoglobin concentration, pulmonary edema, BAL and lung tissue phospholipids, lung compliance, and cell counts. Venous bubbles were directly observed in 90% of the rats where immediate post-decompression autopsy was performed and in 37% using implanted Doppler monitors. Cardiac output, stroke volume, and right ventricular wall thickening fractions were significantly decreased post decompression, whereas systemic vascular resistance was increased suggesting a decrease in venous return. BAL Hb and total protein levels were increased 0 and 60 min post decompression; pleural and plasma levels were unchanged. BAL white blood cells and neutrophil percentages were increased 0 and 60 min post decompression and pulmonary edema was detected. Venous bubbles produced with moderate decompression profiles give detectable cardiovascular and pulmonary responses in the rat.

Cardiovascular effects of NG-methyl-L-arginine in chronically instrumented conscious dogs.

The cardiovascular effects of nitric oxide blockade were examined in five conscious chronically instrumented dogs. The hypothesis tested was that nitric oxide release plays a role in vascular tone and regional organ blood flow under physiological conditions. Aortic pressures; the first derivative of the left ventricular pressure; cardiac output (CO); heart rate; and carotid, coronary, renal, hepatic, and portal blood flows were recorded before and after bolus injection of 5, 10, and 20 mg/kg of NG-methyl-L-arginine (L-NMA). In response to L-NMA, mean arterial pressure increased by 7, 20, and 35%, respectively, in a dose-dependent manner, whereas CO decreased. CO reduction was sustained at the highest dose, whereas peripheral blood flows were not altered. These data suggest that blocking basal nitric oxide synthesis by administering L-NMA leads to a modest dose-dependent pressor response despite a marked and sustained reduction in CO recorded at the highest dose of L-NMA. Moreover, within our dose range, although the nitric oxide synthase inhibition provides a significant pressor response, it does not alter the resting carotid, coronary, renal, hepatic, and portal blood flows.

Effects of thiopental and ketamine on cardiac function during moderate hemorrhage in chronically instrumented rats.

This study was designed to assess the effects of thiopental and ketamine on cardiac function after a blood loss of 2 ml/100 g of body weight. In nine Sprague-Dawley rats, a catheter was placed in the abdominal aorta, a pulsed Doppler probe was positioned around the thoracic aorta, and a wall-thickness probe was sutured onto the left ventricle. On three occasions, all rats were studied awake, during thiopental anesthesia, and during ketamine anesthesia. In awake rats, a 30% blood loss resulted in an immediate, transient hypotension (49%) and a prolonged decrease in cardiac output (39%) and stroke volume (28%). No significant changes were observed in the wall-thickening fraction, which is an index of cardiac contractility, and in the heart rate. The effect of thiopental on cardiovascular responses to moderate hemorrhage was minimal. Although ketamine did not affect the hypotensive response to moderate hemorrhage, it did accentuate systemic vasoconstriction and cardiac depression as indicated by a decrease in cardiac output (57%), stroke volume (49%), and wall thickness (47%).

Hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration and enflurane, halothane or isoflurane in chronically instrumented dogs.

To assess the hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration [Ca2+] and enflurane (2.5%), halothane (1.2%) or isoflurane (1.6%), seven dogs were chronically instrumented to measure heart rate (HR), aortic, left atrial and left ventricular (LV) pressures, and cardiac output (CO). [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. Verapamil was infused at 3 micrograms.kg-1 x min-1 (loading dose 200 (awake), 150 (isoflurane) or 100 (enflurane and halothane) micrograms.kg-1), giving mean verapamil concentrations around 75 (range of means: 66-84 ng.ml-1). Verapamil produced mostly minor changes in the cardiovascular effects of changing [Ca2+] in both awake and anesthetized dogs, indicating mostly additive effects. Verapamil induced a decrease in HR at high [Ca2+] and abolished an increase in mean aortic pressure at both low and high [Ca2+] awake. Verapamil exaggerated the decrease in CO and stroke volume (SV) induced by low [Ca2+] during enflurane anesthesia and abolished the increase in CO induced by low [Ca2+] and exaggerated the increase in SV and LV dP/dtmax induced by high [Ca2+] during halothane anesthesia.

Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.

To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.

Comparative effects of halothane, enflurane, and isoflurane at equihypotensive doses on cardiac performance and coronary and renal blood flows in chronically instrumented dogs.

In order to compare equihypotensive effects of the three available volatile anesthetics, halothane, enflurane, and isoflurane, dogs were chronically instrumented for measurement of: arterial, left ventricular, and left atrial blood pressures; rate of rise of left ventricular blood pressure; myocardial wall thickening (pulsed Doppler); cardiac output (pulmonary artery electromagnetic flow meter); and coronary and renal blood flows (pulsed Doppler flow meters). All three anesthetics were administered on different days in random order to each dog (n = 10) at doses necessary to decrease mean arterial pressure to 70 and 45 mmHg and two intermediate arterial blood pressures. Changes in cardiac function and regional blood flows were compared to the awake resting state and between anesthetics using analysis of variance and paired t tests. All three anesthetics produced increases in heart rate and decreases in left ventricular dP/dt, myocardial thickening fraction, and stroke volume with the hypotension. The decreases in cardiac performance were similar among the anesthetics except at the high dose (mean arterial pressure = 45 mmHg). During this profound hypotension, cardiac performance was better maintained during isoflurane anesthesia and most depressed by enflurane anesthesia. Coronary and renal blood flows were well preserved with all three anesthetics even at mean arterial pressures of 45 mmHg. Our results suggest that isoflurane may be more beneficial than halothane or enflurane for producing profound intentional hypotension (less than 50 mmHg mean arterial pressure), although extrapolation from animal experiments to the clinical situation should be used with caution.

Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in conscious, chronically instrumented dogs and their interactions with ganglionic blockade.

To assess the hemodynamic effects of acute changes in extracellular ionized calcium concentration, [Ca2+], seven dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) pressures, cardiac output, and coronary and renal blood flows. [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. This protocol was performed in the conscious dogs with and without ganglionic blockade (chlorisondamine 2 mg.kg-1). LV dP/dtmax decreased at low [Ca2+] and increased at high [Ca2+] during all conditions. The other hemodynamic variables measured were only slightly changed by changing [Ca2+] without ganglionic blockade and surprisingly even less with ganglionic blockade. Therefore, the lesser hemodynamic effects induced by acute changes in [Ca2+] in the conscious compared with anesthetized dogs cannot be explained by the depressant effects of the anesthetics upon the autonomic nervous system. We have suggested that the binding of Mg2+ to citrate may be of importance for the minor hemodynamic effects in the conscious dogs.

The ouabain-dependent Na(+)-K+ pump and the brain renin-angiotensin system.

The present study investigated the role of ouabain-dependent inhibition of the Na(+)-K+ pump and stimulation of the brain renin-angiotensin system by looking at 1) the short-term and long-term effects of ouabain on arterial blood pressure, and 2) the acute and chronic effects of angiotensin II (ANG II) intraventricularly (i.c.v.) on the release of an endogenous inhibitor of the Na(+)-K+ pump. Ouabain infused subcutaneously in a dose of 1.5 mg.kg-1. 24 h-1 for 7 days did not affect arterial blood pressure in rats, whereas increases in both blood pressure and weight were observed in rats infused with ouabain at the same dose for a 4-week period. Plasma supernate obtained from pentobarbital-anesthetized dogs acutely treated with ANG II (1 microgram i.c.v. every 30 min for 2 h) induced a 44% decrease in the ouabain-sensitive 86Rb uptake by the rat tail artery which was prevented by pretreatment with saralasin i.c.v. Plasma supernate obtained from dogs that were infused for 4 days with ANG II (20 ng/min i.c.v.) and received saline as the drinking fluid also reduced by 34% the ouabain-sensitive 86Rb uptake by the rat tail artery. The present study provides evidence that chronic inhibition of the Na(+)-K+ pump for 4 weeks leads to the development of hypertension and that the release of an endogenous inhibitor of the Na(+)-K+ pump is implicated in the hypertension resulting from chronic stimulation of the brain angiotensin-system and an increase in sodium chloride intake.

Comparison of the effects of isoflurane and desflurane on cardiovascular dynamics and regional blood flow in the chronically instrumented dog.

Seven mongrel dogs were chronically instrumented for the measurement of aortic and left ventricular blood pressures, cardiac output, left ventricular wall thickening, left ventricular dP/dt, and circumflex coronary, renal, hepatic and portal blood flows under the influence of desflurane (D) and isoflurane (I). Administration of the two anesthetics, was randomized, as was the order of the concentrations administered. Each dog was studied awake and at 1.2, 1.4, 1.75, and 2.0 MAC of each anesthetic on different days. Both anesthetics decreased mean arterial pressure, stroke volume, systemic vascular resistance, left ventricular dP/dt, and wall thickness. The decreases were dose-dependent for mean arterial pressure (percent of awake values: D 78, I 85 at 1.2 MAC, and D 67, I 69 at 2.0 MAC); stroke volume (D 66, I 72 at 1.2 MAC, and D 52, I 57 at 2.0 MAC); dP/dt (D 61, I 64 at 1.2 MAC, and D 46, I 49 at 2.0 MAC); and WT (D 68, I 70 at 1.2 MAC, and D 47, I 60 at 2.0 MAC). Systemic vascular resistance decreased approximately the same at 1.2 MAC (D 71, I 87%) as at 2.0 MAC (D 71, I 79%). Heart rate increased but also not in a dose-dependent fashion (percent of awake values: D 177, I 145 at 1.2 MAC, and D 176, I 155 at 2.0 MAC). Coronary blood flow was increased by both anesthetics at all concentrations (percent of awake values: I 136 at 1.2 MAC and 161 at 2.0 MAC of awake, and D 131 at 1.2 MAC and 138 at 2.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)