Regional Hemodynamic Variables Research Articles

Regional haemodynamic variables and perfusion index in the evaluation of sciatic nerve block: a prospective observational trial

ObjectiveWe determined whether regional haemodynamics and perfusion index (PI) could be reliable indicators of a successful sciatic nerve block (SNB).DesignProspective observational trial.SettingA tertiary teaching hospital in China from April 2020...

A Cardiovascular Mathematical Model of Graded Head-Up Tilt

A lumped parameter model of the cardiovascular system has been developed and optimized using experimental data obtained from 13 healthy subjects during graded head-up tilt (HUT) from the supine position to . The model includes descriptions of the left and right heart, direct ventricular interaction through the septum and pericardium, the systemic and pulmonary circulations, nonlinear pressure volume relationship of the lower body compartment, arterial and cardiopulmonary baroreceptors, as well as autoregulatory mechanisms. A number of important features, including the separate effects of arterial and cardiopulmonary baroreflexes, and autoregulation in the lower body, as well as diastolic ventricular interaction through the pericardium have been included and tested for their significance. Furthermore, the individual effect of parameter associated with heart failure, including LV and RV contractility, baseline systemic vascular resistance, pulmonary vascular resistance, total blood volume, LV diastolic stiffness and reflex gain on HUT response have also been investigated. Our fitted model compares favorably with our experimental measurements and published literature at a range of tilt angles, in terms of both global and regional hemodynamic variables. Compared to the normal condition, a simulated congestive heart failure condition produced a blunted response to HUT with regards to the percentage changes in cardiac output, stroke volume, end diastolic volume and effector response (i.e., heart contractility, venous unstressed volume, systemic vascular resistance and heart rate) with progressive tilting.

The influence of methysergide on 5-hydroxytryptamine-induced changes in regional distribution of blood flow.

Systemic and regional haemodynamic variables were measured at the baseline and after saline or 5-HT infusions (5 microgram kg-1 min-1, i.v.) or methysergide injections (0.5 mg kg-1, i.v.). Cardiac output and its complete distribution were measured by the radioactive microsphere (15 micrometer diam) technique. Although 5-HT did not change the systemic variables, methysergide caused a moderate increase in systolic and mean blood pressure and heart rate. 5-HT caused a substantial increase in gastric and a moderate increase in cerebral and myocardial blood flow at the expense of that to the lungs (arteriovenous shunt + bronchial flows), kidneys and skin. While methysergide was able to reduce the vascular responses to 5-HT in stomach, skin, kidneys, heart, lungs and brain, the drug itself, like 5-HT, decreased the number of microspheres reaching the lungs. Since a large number of 15 micron microspheres can escape through the arteriovenous anastomoses to lodge in the lungs it seems likely that both 5-HT and methysergide can reduce the 'non-nutrient' flow through these anastomoses.

Anestesia regional combinada con mascarilla laríngea Proseal en cirugía plástica periférica prolongada

The ProSeal laryngeal mask offers a better interface for controlled ventilation than does a traditional mask because of the ProSeal's improved airway seal and the possibility of draining the digestive tract. Limb reconstructive surgery is normally a long procedure involving the use of grafts or flaps located at a distance from the lesion. Regional anesthesia is therefore of limited use. We report a series of 24 adult patients who underwent peripheral plastic surgery under combined regional and general intravenous anesthesia and in whom the ProSeal mask was used. Data recorded included assessment of the airway and intubation difficulty, disease and duration of the procedure, type of regional anesthesia, respiratory and hemodynamic variables, patient satisfaction, laryngeal complications, and postoperative analgesia. All patients were adequately ventilated. One episode of bradycardia was controlled with atropine. In the immediate postoperative period, no patient presented laryngeal complications and only 1 patient reported significant pain (8 on a visual analog scale). The ProSeal mask was a good choice for use with combined regional-general anesthesia, ensuring control of the airway without causing complications. Analgesia was adequate in most cases.

Effects of short-term simultaneous infusion of dobutamine and terlipressin in patients with septic shock: the DOBUPRESS study

BackgroundTerlipressin bolus infusion may reduce cardiac output and global oxygen supply. The present study was designed to determine whether dobutamine may counterbalance the terlipressin-induced depression in mixed-venous oxygen saturation (Svo2) in patients with catecholamine-dependent septic shock. MethodsProspective, randomized, controlled study performed in a university hospital intensive care unit. Septic shock patients requiring a continuous infusion of norepinephrine (0.9 μg kg−1 min−1) to maintain mean arterial pressure (MAP) at 70 (sd 5) mm Hg were randomly allocated to be treated either with (i) sole norepinephrine infusion (control, n=20), (ii) a single dose of terlipressin 1 mg (n=19), or (iii) a single dose of terlipressin 1 mg followed by dobutamine infusion titrated to reverse the anticipated reduction in Svo2 (n=20). Systemic, pulmonary, and regional haemodynamic variables were obtained at baseline and after 2 and 4 h. Laboratory surrogate markers of organ (dys)function were tested at baseline and after 12 and 24 h. ResultsTerlipressin (with and without dobutamine) infusion preserved MAP at 70 (5) mm Hg, while allowing to reduce norepinephrine requirements to 0.17 (0.2) and 0.2 (0.2) μg kg−1 min−1, respectively [vs1.4 (0.3) μg kg−1 min−1 in controls at 4 h; each P<0.001]. The terlipressin-linked decrease in Svo2 was reversed by dobutamine at a mean dose of 20 (8) μg kg−1 min−1 [Svo2 at 4 h: 59 (11)% vs 69 (12)%, P=0.028]. ConclusionsIn human catecholamine-dependent septic shock, terlipressin (with and without concomitant dobutamine infusion) increases MAP and markedly reduces norepinephrine requirements. Although no adverse events were noticed in the present study, potential benefits of increasing Svo2 after terlipressin bolus infusion need to be weighted against the risk of cardiovascular complications resulting from high-dose dobutamine.

Systemic and regional hemodynamic effects of enalaprilat infusion in experimental normotensive sepsis

Angiotensin-converting enzyme inhibitors have been shown to improve splanchnic perfusion in distinct shock states. We hypothesized that enalaprilat potentiates the benefits of early fluid resuscitation in severe experimental sepsis, particularly in the splanchnic region. Anesthetized and mechanically ventilated mongrel dogs received an intravenous infusion of live Escherichia coli over a period of 30 min. Thereafter, two interventions were performed: fluid infusion (normal saline, 32 mL/kg over 30 min) and enalaprilat infusion (0.02 mg kg(-1) min(-1) for 60 min) in randomized groups. The following groups were studied: controls (fluid infusion, N = 4), E1 (enalaprilat infusion followed by fluid infusion, N = 5) and E2 (fluid infusion followed by enalaprilat infusion, N = 5). All animals were observed for a 120 min after bacterial infusion. Mean arterial pressure, cardiac output (CO), portal vein blood flow (PVBF), systemic and regional oxygen-derived variables, and lactate levels were measured. Rapid and progressive reductions in CO and PVBF were induced by the infusion of live bacteria, while minor changes were observed in mean arterial pressure. Systemic and regional territories showed a significant increase in oxygen extraction and lactate levels. Widening venous-arterial and portal-arterial pCO2 gradients were also detected. Fluid replacement promoted transient benefits in CO and PVBF. Enalaprilat after fluid resuscitation did not affect systemic or regional hemodynamic variables. We conclude that in this model of normotensive sepsis inhibition of angiotensin-converting enzyme did not interfere with the course of systemic or regional hemodynamic and oxygen-derived variables.

Systemic and regional hemodynamic effects of enalaprilat infusion in experimental normotensive sepsis

Angiotensin-converting enzyme inhibitors have been shown to improve splanchnic perfusion in distinct shock states. We hypothesized that enalaprilat potentiates the benefits of early fluid resuscitation in severe experimental sepsis, particularly in the splanchnic region. Anesthetized and mechanically ventilated mongrel dogs received an intravenous infusion of live Escherichia coli over a period of 30 min. Thereafter, two interventions were performed: fluid infusion (normal saline, 32 mL/kg over 30 min) and enalaprilat infusion (0.02 mg kg-1 min-1 for 60 min) in randomized groups. The following groups were studied: controls (fluid infusion, N = 4), E1 (enalaprilat infusion followed by fluid infusion, N = 5) and E2 (fluid infusion followed by enalaprilat infusion, N = 5). All animals were observed for a 120 min after bacterial infusion. Mean arterial pressure, cardiac output (CO), portal vein blood flow (PVBF), systemic and regional oxygen-derived variables, and lactate levels were measured. Rapid and progressive reductions in CO and PVBF were induced by the infusion of live bacteria, while minor changes were observed in mean arterial pressure. Systemic and regional territories showed a significant increase in oxygen extraction and lactate levels. Widening venous-arterial and portal-arterial pCO2 gradients were also detected. Fluid replacement promoted transient benefits in CO and PVBF. Enalaprilat after fluid resuscitation did not affect systemic or regional hemodynamic variables. We conclude that in this model of normotensive sepsis inhibition of angiotensin-converting enzyme did not interfere with the course of systemic or regional hemodynamic and oxygen-derived variables.

Effects of levosimendan on systemic and regional hemodynamics in septic myocardial depression

Calcium desensitization plays an important part in the pathophysiology of septic myocardial depression. We postulated that levosimendan, a new calcium sensitizer, would be beneficial in sepsis-induced cardiac dysfunction. Prospective, randomized, controlled study in two university hospital intensive care units. Twenty-eight patients with persisting left ventricular dysfunction related to septic shock after 48 h of conventional treatment including dobutamine (5 microg/kg per minute). After 48 h of conventional treatment patients were randomized to receive a 24-h infusion of either levosimendan (0.2 microg/kg per minute, n=15) or dobutamine (5 microg/kg per minute, n=13). Data from right heart catheterization, echocardiography, gastric tonometry, laser-Doppler flowmetry, and lactate concentrations and creatinine clearance were obtained before and after the 24-h drug infusion. Dobutamine did not change systemic or regional hemodynamic variables. By contrast, at the same mean arterial pressure levosimendan decreased pulmonary artery occlusion pressure and increased cardiac index. Levosimendan decreased left ventricular end-diastolic volume and increased left ventricular ejection fraction. Levosimendan increased gastric mucosal flow, creatinine clearance, and urinary output while it decreased lactate concentrations. These findings show that levosimendan improves systemic hemodynamics and regional perfusion in patients with septic cardiac dysfunction under conditions where administration of 5 microg/kg dobutamine per minute is no longer efficacious. Accordingly, our results suggest that levosimendan can be an alternative to the strategy of increasing the dose of dobutamine under such conditions.

Gonadectomy and Androgen Replacement Alter Cardiac Performance in Conscious Adult Male Rats

Gender disparities in cardiac function have been described. Yet the extent to which gender related differences in cardiac performance are due to the presence of sex-specific biological factors are unclear. We used a longitudinal study aimed at examining whether castration and androgen replacement affects cardiac performance in conscious adult male rats. Adult male rats were implanted with Piezoelectric transit-time gauges and radio telemetry devices to measure regional myocardial segment length and hemodynamic variables before and after castration and after androgen replacement. Androgen withdrawal accelerated average heart rates by 7% (p = 0.010). Heart rate was lowered to intact values when androgens were restored to normal physiological levels (p = 0.004). Mean arterial pressure was not affected by androgen deprivation and androgen replacement. However, androgen withdrawal produced a 40% decrease in the velocity of circumferential shortening and a 46% reduction in the rate of myocardial relaxation. Androgen supplementation completely restored contractile function. These results provide the first evidence that androgen withdrawal and androgen replacement produces dramatic alterations on cardiac performance in conscious animals and demonstrates the significance of androgens as a cardioregulatory hormone in males. Sex steroids are likely contributors to gender-related differences in cardiac function.

Gut luminal endotoxin reduces ischemia-reperfusion injury of the small gut in germ-free pigs.

Translocation of luminal bacteria and their products through the intestinal mucosa during ischemia-reperfusion (I/R) may modify I/R injury. To test this hypothesis, 16 germ-free pigs were studied prior to and after clamping the superior mesenteric artery (SMA) and 12 pigs served as controls. Nine pigs in the I/R and 5 in the control group received endotoxin intragastrically, 60 min before baseline. Gut absorption of an inert indicator (polyethyleneglycol [PEG] 3350), gut intraluminal PCO2 (tonometry), and systemic and regional hemodynamic variables were measured up to 4 h after baseline. Gut blood flow was stopped during clamping, some reactive hyperemia occurred up to 30 min after declamping in the I/R groups, independently of prior endotoxin administration. Gut intraluminal-arterial PCO2 gradients were elevated in I/R versus control groups during I and for some time during R, prior endotoxin had no effect. However, in controls without and with luminal endotoxin, PEG urinary excretion, as percentage of the dose administered, was 0.12 +/- 0.12 and 0.17 +/- 0.07, respectively, while it measured 1.82 +/- 0.70 in the I/R group and 0.55 +/- 0.37% in the I/R and endotoxin groups, respectively (P< 0.001). The data suggest that gut luminal endotoxin ameliorates I/R injury of the gut wall in germ-free pigs, without altering changes in gut perfusion adequacy and systemic hemodynamics.

Hemodynamic, sympathetic and angiotensin II responses to PEEP ventilation before and during administration of isoflurane.

Positive end-expiratory pressure (PEEP) ventilation and isoflurane anesthesia may opposingly affect the sympathetic nervous and renin-angiotensin systems. This study was performed to elucidate the modulatory effects of isoflurane anesthesia on the neurohumoral and cardiovascular responses to PEEP. Renin-angiotensin and sympathetic nervous activity were investigated in mechanically ventilated, normovolemic, chloralose anesthetized pigs before and during administration of 1.4% isoflurane. Arterial angiotensin II (AII) concentrations were measured and systemic, mesenteric, hepatic and renal spillover of norepinephrine (NE-SO) were calculated using isotope dilution. Regional hemodynamic variables were investigated in parallel. PEEP10 alone moderately elevated AII levels (+12.5 +/- 4.9 pg/ml, P < 0.05) and increased systemic (+22 +/- 2.9 pmol.min.100 g-1, P < 0.05) and notably mesenteric (+32 +/- 9.6 pmol.min.100 g-1, P < 0.05) NE-SO. Blood flow decreased in all vascular beds studied. Except for in the liver, isoflurane generally reduced NE-SO compared to baseline but did not change AII concentrations. Strikingly, the sympathoexcitatory response to PEEP10 was inhibited, whereas AII increased markedly (+284 +/- 64 pg/ml, P < 0.05) during PEEP10 and isoflurane. Renal blood flow was significantly more reduced during PEEP10 and isoflurane compared to PEEP10 alone, whereas the magnitude of reductions were similar in the other vascular beds. The data suggest that renin-angiotensin activation is important to attenuate the impact of PEEP ventilation on cardiovascular performance during administration of the sympathodepressant isoflurane. Interference with the renin-angiotensin system may cause cardiovascular decompensation in isoflurane anesthetized patients subjected to PEEP-ventilation.

How sympathetic tone maintains or alters arterial pressure.

After chronic sympathectomy or sinoaortic denervation (SAD), arterial pressure (AP) becomes extremely unstable, especially because of movement-related depressor episodes. The simultaneous measurement of AP and regional blood flows in sympathectomized and SAD rats indicates that these depressor episodes are accompanied by strong regional vasodilations, possibly involving an autoregulatory component. The sympathetic nervous system, mainly through baroreflex modulation of its activity, overrides these responses and thereby, considerably limits the AP variability. In the conscious unrestrained rat, AP fluctuates in a narrow range (variation coefficients calculated over 1-hour beat-to-beat recordings are typically approximately 5%). This variability of AP involves sympathetically-mediated pressor episodes that are coupled to behavior and alerting environmental stimuli. Regarding the latter, studies in SAD rats point to an opposing interaction between centrally-induced sympathoexcitation and baroreflex activation. Another component of normal AP variability appears as an oscillation centered around 0.4 Hz. Spectral analysis of AP and regional hemodynamic variables indicates that this oscillation is secondary to rhythmic fluctuations in the vasomotor sympathetic tone that are synchronized by the arterial baroreceptor reflex. It is concluded that both stability and normal variability of AP critically depend on the baroreflex control of the sympathetic vascular tone.

Influence of Thiopental, Etomidate, and Propofol on Regional Myocardial Function in the Normal and Acute Ischemic Heart Segment in Dogs

The effects of 30-min infusions of thiopental (20, 30, 40, 50, 60, and 70 mg.kg-1.h-1), etomidate (2.4, 3.6, 7.2, 9.6, 12, and 14.4 mg.kg-1.h-1), and propofol (6, 9, 12, 15, 18, and 21 mg.kg-1.h-1) on regional hemodynamic variables in the normal and acute ischemic heart segment were studied in dogs using ultrasonic segment length gauges. The three agents were associated with a dose-dependent decrease in end-diastolic length, indicating a decrease in left ventricular filling. This effect was most pronounced for propofol. At the doses tested, etomidate did not significantly alter regional myocardial function. Thiopental, however, was associated with a dose-dependent decrease in systolic shortening, which was significantly greater in the ischemic segment. These findings confirm the hemodynamic stability seen with etomidate and show that thiopental depresses myocardial function more in the acute ischemic heart than in the normal heart. The decrease in systolic shortening associated with propofol was similar in the normal and in the acute ischemic heart segment.

Hemodynamic responses to vasopressinergic antagonism in water-deprived conscious rats.

Experiments were performed on conscious, chronically instrumented rats to determine the role of arginine vasopressin (AVP) on the systemic and regional hemodynamic effects of 48-h water deprivation. Arterial and venous catheters as well as pulsed Doppler flow probes were implanted in rats to measure cardiac output (CO), mesenteric blood flow (MBF), renal blood flow (RBF), or hindquarter blood flow (HQBF). After adequate recovery from surgey, euhydrated animals were administered a specific V1-vasopressinergic antagonist [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg iv], a combined V1, V2-antagonist [d(CH2)5DTyr(Et)VAVP, 30 micrograms/kg iv], or saline vehicle (100 microliter/100 g). Neither antagonist was associated with any change in mean arterial blood pressure (MABP), heart rate (HR), systemic or regional flow or vascular resistance. All animals were subsequently water deprived for 48 h, at which time the experiments were repeated. Dehydration was associated with an increase in plasma AVP levels, hematocrit, and MABP but with a decrease in HR. Administration of either the combined V1, V2-antagonist or vehicle had no effect on any systemic or regional hemodynamic variables measured after 48-h dehydration. In contrast, although MABP, CO, MBF, and RBF were unaffected, V1-antagonism resulted in elevated HR, increased HQBF, and decreased hindquarter vascular resistance. In conclusion, AVP does not have a major effect on systemic hemodynamics in the dehydrated rat. However, certain beds may be affected by the relatively moderate levels of plasma AVP elicited during dehydration.

Systemic and regional hemodynamic effects of leukotrienes D4 and E4 in the conscious rat.

The effect of leukotrienes (LTs) D4 and E4 on systemic and regional hemodynamic variables were studied in the conscious rat (n = 5-9). Renal (R), mesenteric (M), and hindquarter (HQ) blood flow (BF) were monitored by directional pulsed Doppler velocimetry, and mean arterial blood pressure (MAP) and heart rate were recorded through a catheter in the femoral artery. In a separate series of experiments, cardiac index (CI) was measured by the thermodilution method. Systemic injection of LTD4 or LTE4 (0.1-10 micrograms/kg) produced dose-dependent pressor responses; BF in the M, HQ, and R vessels declined, due to increased vascular resistance (VR) at the following order: M much greater than HQ greater than R. Low doses of LTD4 or LTE4 produced vasodilation in the HQ area. Infusion of LTD4 (3 micrograms X kg-1 X min-1) for 10 min produced progressive and pronounced vascular constriction in the M and HQ regions along with reduction in BF. The LTD4 infusion also markedly decreased CI with a concomitant rise in total peripheral resistance index (TPRI). Indomethacin (5 mg/kg iv) pretreatment did not modify any of the hemodynamic effects of LTD4 or LTE4. FPL 55712 (10 mg/kg iv) and LY 171883 (30 mg/kg iv), two different LT-receptor antagonists, partially blocked the constriction effects of these LTs. LY 171883, but not FPL 55172, blocked the HQ vasodilation produced by LTE4. LY 171883 alone increased HQ-BF and reduced HQ-VR. These data indicate that LTD4 and LTE4 are potent constrictors of the M vascular bed, but at low doses they also produce dilation of the HQ blood vessels. Furthermore, no escape from the effects of prolonged infusion of the LTs was demonstrated in this species. Finally, the hemodynamic responses to LTD4 and LTE4 in the conscious rat are independent of cyclooxygenase products of LTs and are only partially blocked by FPL 55712 or LY 171883. These studies taken together suggest a differential distribution of multiple LT receptors in the rat vasculature.

Reversal of depressant effects of propranolol on the left ventricular pump function by nifedipine in dogs with chronic ischaemia.

The aim of this study was to clarify the combined effects of propranolol and nifedipine on the regional wall motion and haemodynamic variables of the heart in dogs with chronic ischaemia. After an injection of propranolol the heart rate and stroke volume significantly decreased (from 128(18) beats X min-1 to 113(12) beats X min-1 and from 15.1(3.1) ml to 12.2(2.6) ml respectively) and the left ventricular end diastolic pressure and systemic vascular resistance in systole increased significantly (from 7.3(1.5) mmHg to 10.0(1.8) mmHg and from 8.61(1.42) kPa X litre-1 X min-1 to 11.80(1.59) kPa X litre-1 X min-1 respectively). In the regional myocardium the end diastolic length increased significantly in both border and normal zones (7(3)% and 4(2)% respectively) and the percentage systolic shortening in the normal zone decreased significantly from 18.0(3.1)% to 15.1(2.9)%. In the border and infarcted zones the percentage systolic shortening or systolic lengthening did not change. The administration of nifedipine resulted in significant decreases in left ventricular systolic pressure and in systemic vascular resistance (from 122(17) mmHg to 105(14) mmHg and from 11.80(1.59) kPa X litre-1 X min-1 to 6.63(1.24) kPa X litre-1 X min-1 respectively) and stroke volume increased to 18.2(4.4) ml. The percentage systolic shortening in the border and normal zones improved significantly to 9.8(3.2)% and 19.2(3.7)% respectively without any change in end diastolic length and left ventricular end diastolic pressure. In the infarcted zone no significant change in systolic lengthening or end diastolic length was seen. Thus impaired left ventricular pump function induced by propranolol was reversed by nifedipine.

Regional hemodynamic effects of clonidine in congestive heart failure.

Regional and central hemodynamic variables were ascertained in 10 patients with congestive heart failure before and after the oral administration of clonidine. Following the 0.2 mg dose, renal, hepatic, and limb blood flow remained unaltered, whereas a reduction was noted in heart rate (10%), mean systemic (14%), and pulmonary capillary wedge pressures (27%). Cardiac index and systemic vascular resistance fell slightly, however the changes were not statistically significant. Higher dose clonidine (0.4 mg) elicited similar regional hemodynamic effects whereas systemic vascular resistance significantly diminished (21%) and cardiac index remained unchanged. In congestive heart failure, the central antihypertensive agent, clonidine, effects a significant reduction in preload (left ventricular filling pressure) and afterload (systemic blood pressure) without markedly altering other central and regional hemodynamic variables.

Cardiovascular Changes After Weight Reduction in Obesity Hypertension

Intravascular volumes and systemic and regional hemodynamic variables were measured before and after weight reduction in 12 patients with obesity and essential hypertension. These findings were compared with those in nine patients who did not have any weight loss. Reduction of mean arterial pressure significantly correlated with the fall in total body weight (r = 0.46, p less than 0.05). Total circulating and cardiopulmonary blood volumes were significantly reduced (p less than 0.05 and p less than 0.01, respectively), and these changes permitted a decreased venous return and cardiac output (p less than 0.01). This fall in cardiac output was directly related to a contracted total blood volume (r = 0.49, p less than 0.05) and decreased cardiopulmonary blood volume (r = 0.52, p less than 0.05). Patients who did not lose weight showed no changes in any of these hemodynamic measurements. In addition, weight loss was associated with reduced resting circulating levels of plasma norepinephrine (p less than 0.01), suggesting that diminished adrenergic function may also be related to weight reduction and its associated fall in arterial pressure.

Systemic and regional hemodynamic characteristics of bilateral cellophane perinephritis hypertension in conscious rabbits.

Using the radioactive microsphere technique, systemic and regional hemodynamic variables were measured in normotensive rabbits and in rabbits with bilateral cellophane perinephritis hypertension. An average decrease in cardiac output of 18 percent was measured in the hypertensive rabbits as a result of a reduction in stroke volume; heart rate remained unchanged. Thus, in the established phase, hypertension was maintained by the elevated total peripheral resistance. A redistribution of cardiac output was observed in the hypertensive rabbits; a significantly higher fraction was received by the brain, small intestine and heart. The weight normalized blood flow to the kidneys, spleen, skeletal muscles, bones and fat was significantly decreased while an increase in vascular resistance was observed in the hypertensive rabbits in all the organs investigated. A negative correlation existed between the weight of the left ventricle and the blood flow to the left ventricle in hypertensive rabbits, suggesting inadequate coronary perfusion as myocardial hypertrophy becomes more pronounced.

Effect of neuromuscular blocking agents pancuronium bromide and its monoquaternary analogue Org NC 45 on regional blood flow and cardiac metabolism in pigs

AbstractThe effects of pancuronium bromide (60, 120, 300, and 600 μg.kg−1, i.v.) and its monoquaternary analogue Org NC 45 (300,750, and 1500 μg.kg−1, i.v.) on the systemic and regional hemodynamic variables were studied in the anesthetized pig. Pancuronium exhibited a dose‐dependent positive chronotropic and inotropic activity. The enhanced oxygen requirement of the myocardium was successfully met by a combination of higher blood supply to, and oxygen extraction by, the tissue. No changes were noticed in cerebral, renal or hepatic arterial blood flow. On the other hand, Org NC 45, which unlike pancuronium lacks vagolytic and sympathomimetic actions, did not cause an increase in heart rate or left ventricular dP/dtmax (LV dp/dtmax). Instead, in the two highest doses (750 and 1500 μg.kg−1) Org NC 45 decreased arterial blood pressure, LV dP/dtmax and the blood supply to the brain, kidneys, and liver. Neither compounds showed any effect on cardiac metabolism of glucose, lactate, or free fatty acids (FFA), although arterial blood glucose concentration did decrease following the two highest doses of each compound. Since Org NC 45, in a dose of 300 μg/kg−1, which is seven to ten times the ED90 for neuromuscular paralysis in man, is completely devoid of systemic and regional hemodynamic effects, and pancuronium in similar dose ratio is not, Org NC 45 might be preferred for use in cardiac anesthesia.