Intravenous fluid administration and urine output during radical neck surgery.

This study examines perioperative urine output (UO) and hemodynamics in 24 patients who underwent radical head and neck surgery. The hypothesis tested was that "UO was not important in patients with normal renal function as long as hemodynamics were maintained." Intraoperatively, a "wet" group (13 patients) had generous amounts of intravenous (IV) fluid administered during surgery receiving 1,018 +/- 58 mL.h-1. The other "dry" group (11 patients) had fluids restricted to 426 +/- 23 mL.h-1. The intraoperative UOs for the wet and dry groups were 1.33 +/- 0.27 and 0.39 +/- 0.10 mL.kg-1 x h-1, respectively (p < 0.05). Postoperatively, the UOs for the wet and dry groups were 1.9 +/- 0.3 and 1.1 +/- 0.1 mL.kg-1 x h-1, respectively (p < 0.05). Perioperatively, there were no statistically significant differences between groups in systemic or pulmonary hemodynamics. Postoperatively, ordinary indices of renal function remained normal in both groups. We conclude that intraoperative oliguria due to moderate fluid restriction is not detrimental to renal outcome as long as systemic hemodynamics are maintained. Furthermore, not only does this relatively "dry" status not compromise hemodynamics, it affords the patient other benefits.

Effect of anesthetic induction agents on cardiovascular neuroregulation in dogs.

The goal of this study was to examine the hypothesis that intravenous anesthetic induction agents alter neuroregulation of the cardiovascular system. Additional goals were to investigate this in an animal model devoid of other drug effects. Healthy mongrel dogs had arterial catheters inserted and pneumatic occluders positioned around the thoracic aorta and inferior vena cava. After 10 to 14 days of recovery, neurocirculatory control mechanisms were assessed in the absence of anesthesia by recording changes in the RR interval of the electrocardiogram in response to alterations in systolic arterial pressure. Systolic pressure was manipulated over a range of 65 to 200 mm Hg by random occlusion of either the inferior vena cava (hypotension) or aortic (hypertension) occluders. The animals were then given bolus doses of either thiopental (20 mg/kg), diazepam (2 mg/kg), ketamine (5 mg/kg), or etomidate (1.2 mg/kg) on separate days and in random order. The arterial pressure alterations were repeated 3, 10, and 20 minutes after the drugs were given. Regression curves were calculated expressing the slope relation between RR interval and systolic pressure at awake control and each time point after drug administration. The responses were compared with control by repeat measures analysis of variance. Thiopental significantly decreased this slope relation for 10 minutes. Diazepam decreased this slope at 3 minutes only. Ketamine, like thiopental, decreased this slope for 10 minutes. Following etomidate, the slopes were similar to control. We conclude that thiopental, diazepam, and ketamine impair neurocirculatory control capabilities. The effect of diazepam is only transient, whereas that of thiopental and ketamine is longer, and etomidate does not affect these reflexes.

Effect of halothane on renal hemodynamics during normovolemia and acute hemorrhagic hypovolemia.

The effects of halothane on renal hemodynamics under both normovolemic and hypovolemic conditions were investigated in chronically instrumented conscious dogs whose homeostatic mechanisms were not altered by the presence of preexisting drugs. Renal blood flow and aortic pressure were assessed by prior implantation of Doppler ultrasonic flow probes on the renal artery and a catheter in the descending aorta. Administration of halothane to conscious normovolemic dogs (Group HN) resulted in 11-26% decreases in renal vascular resistance with no significant changes occurring in renal blood flow. In a second group of animals made hypovolemic while awake (Group AH), 30% of the blood volume was removed over one-half hour. In response to hemorrhage, these conscious animals' renal blood flow did not significantly change from the normovolemic control, and renal vascular resistance significantly decreased. With no further intervention, renal vascular resistance and renal blood flow remained unchanged from the level achieved after the 30% hemorrhage. A third group of animals (Group HH) was hemorrhaged in a manner similar to that of Group AH. They also showed no significant changes in renal blood flow and a significant decrease in renal vascular resistance in response to hemorrhage. Thereafter, administration of halothane, as in Group HN, to this group produced 11-23% decreases in renal vascular resistance with no significant decline in renal blood flow from the hypovolemic control levels established after hemorrhage. The author concludes the following: administration of halothane to normovolemic conscious dogs does not decrease renal blood flow; a moderate degree of acute hemorrhagic hypovolemia does not decrease renal blood flow in conscious dogs; and administration of halothane to acutely hypovolemic conscious dogs does not impair renal perfusion.

Influence of different anesthetic agents on the release of cholecystokinin in dogs.

The purpose of this study was to investigate the effect of pentobarbital, halothane, and chloralose anesthesia on the endogenous release of cholecystokinin-33 (CCK-33) in dogs prepared with duodenal fistulas. Release of CCK-33 was induced by intraduodenal infusion of a medium-chain triglyceride (corn oil, 1 gm/kg/hr). Plasma CCK-33 concentrations were measured by means of a specific radioimmunoassay. Pentobarbital and chloralose were administered intravenously, and halothane was administered by a vaporizer (semiclosed technique), with O2 and N2O used as carriers. No incidence of hypotension was found with the use of these anesthetic agents. Basal concentrations of plasma CCK-33 were elevated, although not significantly, during pentobarbital or chloralose anesthesia. In conscious dogs (control study), peak plasma CCK-33 concentrations of 529 +/- 53 pg/ml were measured 30 minutes after intraduodenal infusion of fat. Under pentobarbital anesthesia, peak plasma CCK-33 concentrations of 452 +/- 264 pg/ml were found 80 minutes after infusion of fat. Under halothane anesthesia, fat-induced release of CCK-33 was abolished, whereas chloralose anesthesia did not influence fat-induced release of CCK-33. These findings may have implications for the design of future studies of gastrointestinal physiology. In CCK-33 studies that require anesthesia, chloralose appears to be an appropriate anesthetic agent.

Alteration of renal hemodynamics by thiopental, diazepam, and ketamine in conscious dogs.

Renal hemodynamic changes associated with thiopental, diazepam, and ketamine were studied in conscious dogs after previous surgical placement of an aortic catheter and a Doppler ultrasonic flow probe on the left renal artery. Thiopental, 10 mg/kg, changed blood pressure minimally whereas 20 mg/kg significantly decreased blood pressure by 5% to 10%. Renal blood flow initially increased significantly, then returned to control levels after both doses. Renal resistance was not significantly altered by 10 mg/kg of thiopental whereas 20 mg/kg significantly reduced resistance by 10%. Diazepam, 1 and 2 mg/kg, caused transient increases in arterial pressure of approximately 10%. Renal blood flow significantly decreased 5% to 10% from control levels with both doses. Renal resistance did not change with the 1-mg/kg dose of diazepam, but 2 mg/kg of diazepam increased it by 8% to 12%. Ketamine, 2.5 and 5 mg/kg, elevated arterial pressure 20% to 40%. Renal blood flow increased significantly by 10% to 15% with both doses of ketamine. This effect lasted longer with the large dose. Renal resistance was significantly elevated by the 2.5-mg/kg dose of ketamine, whereas 5 mg/kg did not alter this variable. In conclusion, each of these drugs maintains renal blood flow reasonably well in an unanesthetized animal. However, ketamine appears to be more beneficial than thiopental, which in turn, is superior to diazepam in this regard. Little dose-response effect was evident for any of the drugs. Furthermore, it should be noted that changes in arterial pressure can be misleading when perfusion of this vascular bed is considered.

Morphine effects on cardiac output and regional blood flow distribution in conscious dogs.

This study documents the changes in selected regional hemodynamics occurring in response to large doses of intravenous morphine. It was performed in normal conscious dogs. Their cardiovascular systems was unaltered by the presence of other drugs or recent surgery. The animals had been surgically prepared previously by implantation of chronic indwelling electromagnetic and Doppler ultrasonic flow probes on the aorta and the cranial mesenteric, renal and iliac arteries and placement of aortic catheters. Morphine, 1 mg/kg, produced mesenteric vascular dilation (30 per cent maximum decrease in resistance), renal vascular dilation (11 per cent maximum decrease in resistance) and nonsignificant changes in iliac vascular resistance. Morphine, 3 mg/kg, resulted in a similar amount of renal dilation (maximum 12 per cent decrease in resistance) but constricted the mesenteric vasculature (maximum 120 per cent increase in resistance) and the iliac vasculature (68 per cent maximum increase in resistance). These changes were observed despite the lack of sustained major changes in cardiac output, blood pressure, total peripheral resistance, or heart rate. It is therefore concluded that morphine has only minimal effects on systemic hemodynamics, but has significant effects when the alterations it produces in regional hemodynamics are considered. Such alterations may be physiologically significant when perfusion to these individual organs is a concern. The minimal systemic effects of high dose morphine is a phenomenon, for the most part, common to both dogs and humans. Whether similar regional hemodynamics changes as these occur in humans cannot be determined at this time since continuous flow monitoring techniques have, as yet, not been applied to humans.

Generalized cardiovascular and regional hemodynamic effects of meperidine in conscious dogs.

Changes in both total cardiovascular function and regional hemodynamics associated with large doses of intravenous meperidine were studied in conscious dogs in the absence of other drugs or recent surgery. The animals had previously been surgically prepared by placement of aortic catheters and implantation of chronic indwelling electro-magnetic and Doppler ultrasonic flow probes on the aorta and on mesenteric, renal, and iliac arteries. Meperidine, 2 mg/kg, produced mild renal vascular dilation (10% maximum decreases in resistances and 5% increases in blood flow), but did not alter the resistances and flows in the mesenteric or iliac vascular beds. Meperidine, 6 mg/kg, again resulted in renal dilation (maximum 22% decreases in resistance and 18% increase in blood flow). The iliac vasculature also dilated (maximum 39% decreases in resistance and 40% increases in blood flow). However, the mesenteric vasculature constricted (89% increases in resistance and 40% decreases in blood flow). Following 2 mg/kg of meperidine cardiac output and aortic pressure decreased significantly while total peripheral resistance increased significantly. Heart rate remained unchanged. Following 6 mg/kg of meperidine total peripheral resistance and aortic pressure decreased significantly while heart rate increased. Cardiac output increased during the first part of the observation period then subsequently decreased significantly. It is concluded that in unmedicated dogs meperidine has significant effects on total cardiovascular function and on regional blood flow.

Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex.

The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. After general anesthesia with sodium pentobarbital, or after section of the ipsilateral carotid sinus nerve, carotid chemoreceptor stimulation with nicotine, 0.2 microgram/kg, failed to induce a detectable hemodynamic effect. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.

A simple method to increase the FDO2 of resuscitator bags.

Four resuscitator bags were studied to see if the delivered fractional oxygen percentage (FDO2) could be affected by manually controlling the inherent reexpansion rate of the bag so as to allow a greater entrainment of oxygen rather than air into the bag. Flow rates of oxygen into the bag were varied: 5, 10, 15, and 20 liter/min. For each flow rate, bag refill (reexpansion) times were varied: 1, 2, 4 sec. The results show that such a maneuver will effectively increase the FDO2 of the bags at all flow rates tested--in certain instances to values greater than 0.8. This maneuver would be important to resuscitation situations where it is desirable to achieve better patient oxygenation.

Cardiorespiratory effects of Pseudomonas and E. coli endotoxins in the awake dog.

A comparison of the cardiovascular and respiratory effects of Pseudomonas aeruginosa and Escherichia coli endotoxins was investigated in the unanesthetized dog. Animals were anesthetized with halothane for placement of cardiovascular catheters and then allowed to awaken prior to collection of control data and experimentation. One group of 12 animals was given E. coli endotoxin (5 mg/kg), another group of 13 received Pseudomonas endotoxin (8 mg/kg). Variables were collected for 6 h after endotoxin injection. A third group of 13 animals serving as sham animals received no endotoxin. When major cardiovascular variables, such as arterial blood pressure, cardiac output, right atrial pressure, and left ventricular pressure and dP/dt were monitored, it was seen that the basic patterns of response to endotoxins were quite similar, with differences between groups being primarily quantitative. Analysis of respiratory data showed that animals receiving Pseudomonas developed an earlier respiratory response. Nevertheless, blood gas data were similar in the two groups.