C. Raner

Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine

Interactive effects between exogenous dopamine (DA) and isoflurane (I) combined with thoracic epidural blockade (TEA) were studied in dogs during chloralose anesthesia. The I–TEA intervention per se decreased heart rate (HR; 28%), mean arterial pressure (MAP; 63%), cardiac output (CO; 54%), left ventricular dP/ dt (LVdP/dt; 75%) and LVdP/dt/systolic arterial pressure (SAP; 42%). Prior to the I–TEA intervention, dopamine increased MAP, CO, LVdP/dt, LVdP/dt/SAP and stroke volume (SV) already at the dose 10 μg–kg‐1. min‐1 and, additionally, increased mean pulmonary artery pressure (MPAP) at the dose 20 μg–kg‐1. min‐1. During the I–TEA intervention, the DA–induced increases in MAP and systemic vascular resistance (SVR) were significantly higher than prior to I–TEA, as indicated by significant ANOVA interactive effects. At the dose 10 μg–kg‐1 min‐1, DA restored MAP, CO, LVdP/dt, LVdP/dt/SAP and SV to levels found before the I–TEA intervention, while HR was restored first at the dose 20 μg–kg‐1 –min‐1. At the dose 20 μg–kg‐1–min‐1, DA also increased MAP (39%), LVdP/dt (119%), LVdP/dt/SAP (73%), SVR (28%) and MPAP (70%) above levels prior to I–TEA. To conclude, exogenous dopamine effectively and dose–dependently counters cardiovascular depression induced by the anesthetic technique of combining I and TEA. The pressor and systemic vasoconstrictor actions of dopamine are potentiated by conjoint administration of I and TEA.

Autoregulation and vasodilator responses by isoflurane and desflurane in the feline renal vascular bed

Background: Inhalational anesthetics have agent‐specific effects on the renal circulation. This study investigated renal vasodilator responses produced by either autoregulation, 0.8% isoflurane (ISO) or 3.5% desflurane (DES).

Effects of isoflurane on feline intestinal blood flow during hemorrhage‐induced hypovolemia

The influence of isoflurane on intestinal reflex vasoconstriction during hemorrhage was investigated in cats (n= 10) during basal chloralose‐nitrous oxide anesthesia. Intestinal blood flow (IBF) was studied in a model with controllable intestinal perfusion pressures to exclude local myogenic vascular responses related to changes in intraluminal pressure. A jejunal segment, which was dissected free in situ, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio‐venous shunt. Intestinal perfusion pressure wds controlled by adjusting the shunt flow. IBF was measured (optical drop‐recording) before and after hemorrhage (8% of estimated blood volume). The protocol included steady‐state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% (MAC 1.0) isoflurane. IBF levels were consistently higher during isoflurane anesthesia than during basal chloralose anesthesia in the perfusion pressure range 75–150 mmHg (10.0–20.0 kPa). During basal anesthesia, a hemorrhage‐induced decrease in IBF was demonstrated throughout the perfusion pressure range 50 to 150 mmHg (6.7–20.0 kPa). The magnitude of the hemorrhage‐induced decrease in IBF was not significantly influenced by the addition of isoflurane. Thus, IBF, following hemorrhage, was significantly higher during isoflurane anesthesia than during basal chloralose anesthesia at perfusion pressures 50, 100, 125 and 150 mmHg (6.7, 13.3, 16.7 and 20.0 kPa).

Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor‐mediated mechanisms, dopamine effects were investigated in nine chloralose‐anesthetized dogs. The circulatory response to dopamine (0–40 μg · kg‐1 · min‐1) was studied before and during TEA, and during TEA after introducing the α1‐antagonist prazosin (0.3 mg · kg‐1), the α2‐antagonist rauwolscine (0.3 mg · kg‐1), and the β1‐antagonist metoprolol (0.5 mg · kg‐1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine‐induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre‐TEA levels at 10 μg · kg‐1 · min‐1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the β1‐blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding β1‐blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre‐TEA values by dopamine at 5–10 μg · kg‐1 · min‐1. The circulatory response to dopamine during TEA is mainly mediated by α1‐, α2‐ and β1‐adrenoceptor activation, and may be influenced by altered plasma catecholamine levels.

Effects of desflurane on systemic, preportal and renal circulatory responses to infra‐renal aortic cross‐clamping in the pig

Background: Different pharmacological approaches have been used in the control of cardiovascular responses to surgical infra‐renal aortic occlusion (AXC). The aim of the present study was to explore the modulatory effects of desflurane (DES) on these responses.

Vasodilator effects of desflurane and isoflurane in the feline small intestine

The influence of desflurane (DES) and isoflurane (ISO) on the intestinal vasculature was investigated in normoventilated cats (n=10) during basal chloralose anesthesia (control). We measured heart rate, mean arterial pressure (MAP) and intestinal blood flow (optical drop flowmetry). Intestinal vascular resistance (IVR) was derived. To avoid changes in local vascular tone related to alterations in transmural pressure gradients, intestinal arterial pressure was controlled and kept constant by a variable aortic clamp. Measurements were performed during control and during the administration of DES (3.5% and 7.0% end‐tidal) or ISO (0.8% and 1.6% end‐tidal). Each animal was exposed to both agents, prior to and after intestinal postganglionic denervation. In the innervated intestine, both DES and ISO dose‐dependently decreased IVR. At the high dose, DES (50±10% decrease in IVR) was a significantly more powerful vasodilator than ISO (37±12% decrease in IVR). In the denervated intestine, less pronounced vasodilations were produced by both DES and ISO, as compared to the innervated state, and there were, in this situation, no significant differences between agents concerning the magnitude of the vasodilation. As indicated by comparisons between the innervated versus the denervated state, both neurogenic and non‐neurogenic mechanisms contributed to the vasodilator responses. The vascular relaxation at the high dose was for ISO associated with a significantly more powerful non‐neurogenic vasodilation, and for DES associated with a significantly more powerful neurogenic vasodilation. This suggests that withdrawal of sympathetic neurogenic vasoconstrictor tone is more important for the vasodilation produced by DES than it is for ISO.

Dopamine or norepinephrine infusion during thoracic epidural anesthesia? Differences in hemodynamic effects and plasma catecholamine levels

Background:  During thoracic epidural anesthesia, an intravenous dopamine infusion augments the systemic pressure response and modifies plasma catecholamine levels. If such an altered response occurs when norepinephrine is infused is not clear. Therefore, dopamine and norepinephrine induced circulatory and catecholamine responses were studied before and during thoracic epidural anesthesia.

Local vascular effects of isoflurane during regional intestinal hypothermia in cats

The influence of isoflurane on intestinal blood flow (IBF) during regional intestinal hypothermia (28°C intraluminal temperature) was investigated in cats (n = 12) during basal chloralose‐nitrous oxide anesthesia. A jejunal segment, which was dissected free in situ and intermittently cooled in a saline bath, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio‐venous shunt. Intestinal perfusion pressures were controlled by adjusting the shunt flow. IBF was measured (optical drop‐recording) during regional normothermia and hypothermia. The protocol included steady‐state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% isoflurane. During normothermia, IBF levels were higher during isoflurane anesthesia than during basal chloralose anesthesia. Regional intestinal hypothermia induced no significant changes in IBF during basal chloralose anesthesia. However, the intestinal vasodilator effects of isoflurane, as shown during normothermia, were efficiently countered by regional cooling of the intestinal segment to 28°C. Accordingly, hypothermia IBF levels were similar, regardless of whether isoflurane was administered or not. This could have an impact on the choice of anesthetic techniques.

Interactive effects of isoflurane and amrinone in the feline intestinal and renal circulation

Interactive effects of the phosphodiesterase‐III inhibitor amrinone and isoflurane were investigated in cats. Cardiac output (thermodilution method), and intestinal (IBF) and renal (RBF) blood flows (optical flowmetry) were measured. Intestinal (IVR) and renal (RVR) vascular resistances were derived. To discriminate between pressure‐related local myogenic vascular responses and primary vascular drug effects, intestinal and renal perfusion pressures (50 mmHg; 6.7 kPa) were controlled. The protocol included steady‐state recordings with and without isoflurane in a randomized order, both before and after the administration of amrinone (2 mgkg‐1 i.v. + 2 mgkg‐1 i.v.). Amrinone induced no significant changes in IVR or RVR during basal chloralose anesthesia. During administration of 0.8% isoflurane, amrinone produced decreases in IVR and RVR, which were more pronounced than the vasodilator responses induced by this dose of isoflurane alone. On the other hand, with 1.6% isoflurane, amrinone did not add to the vasodilation. The cardiac effects of isoflurane and amrinone were small. Our data indicate that the vascular tone before administration of amrinone could be crucial for the vascular response of the drug and that isoflurane can significantly influence the regional circulatory effects of amrinone.

EFFECTS OF ISOFLURANE ON FELINE INTESTINAL BLOOD FLOW DURING HEMORRHAGE-INDUCED HYPOVOLEMIA

The influence of isoflurane on intestinal reflex vasoconstriction during hemorrhage was investigated in cats (n = 10) during basal chloralose-nitrous oxide anesthesia. Intestinal blood flow (IBF) was studied in a model with controllable intestinal perfusion pressures to exclude local myogenic vascular responses related to changes in intraluminal pressure. A jejunal segment, which was dissected free in situ, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio-venous shunt. Intestinal perfusion pressure was controlled by adjusting the shunt flow. IBF was measured (optical drop-recording) before and after hemorrhage (8% of estimated blood volume). The protocol included steady-state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% (MAC 1.0) isoflurane. IBF levels were consistently higher during isoflurane anesthesia than during basal chloralose anesthesia in the perfusion pressure range 75-150 mmHg (10.0-20.0 kPa). During basal anesthesia, a hemorrhage-induced decrease in IBF was demonstrated throughout the perfusion pressure range 50 to 150 mmHg (6.7-20.0 kPa). The magnitude of the hemorrhage-induced decrease in IBF was not significantly influenced by the addition of isoflurane. Thus, IBF, following hemorrhage, was significantly higher during isoflurane anesthesia than during basal chloralose anesthesia at perfusion pressures 50, 100, 125 and 150 mmHg (6.7, 13.3, 16.7 and 20.0 kPa).