The background to the proposition that plankton be used as food in the United Kingdom during the Second World War.

Food shortages, particularly of proteins, in Britain during the Second World War led to the suggestion re-surfacing that marine plankton might be harvested on an industrial scale first as human food, then turning to its potential use as a supplement to stock and poultry feed. The notion emanated in the United Kingdom from Sir John Graham Kerr, at Glasgow University. He encouraged Alister Hardy, at Hull, to develop the idea and the natural testing ground was the Clyde Sea Area (given the extensive history of plankton research at Millport). Unpublished documents from the archives of the Scottish Association for Marine Science shed new light on the interactions behind the scenes of this project between Kerr, Hardy and the Millport Marine Station's then director, Richard Elmhirst. Elmhirst, who was sceptical about the feasibility of the plan from the outset, went along with it; not least as a way of attracting welcome research funding during lean times but also, doubtless, regarding it as his patriotic duty in case the proposal proved worthwhile.

Illustrations and the genesis of Barrett and Yonge's "Collins pocket guide to the sea shore" (1958).

Twenty nine items of correspondence from the mid-1950s discovered recently in the archives of the University Marine Biological Station Millport, and others made available by one of the illustrators and a referee, shed unique light on the publishing history of "Collins pocket guide to the sea shore". This handbook, generally regarded as a classic of its genre, marked a huge step forwards in 1958; providing generations of students with an authoritative, concise, affordable, well illustrated text with which to identify common organisms found between the tidemarks from around the coasts of the British Isles. The crucial role played by a select band of illustrators in making this publication the success it eventually became, is highlighted herein. The difficulties of accomplishing this production within commercial strictures, and generally as a sideline to the main employment of the participants, are revealed. Such stresses were not helped by changing demands on the illustrators made by the authors and by the publishers.

The sandhopper Talitrus saltator (Crustacea: Amphipoda) as a biomonitor of trace metal bioavailabilities in European coastal waters.

The amphipod crustacean Talitrus saltator is an established, easily accessible, biomonitor of trace metal bioavailabilities in coastal waters. We have carried out a geographically widespread collection of T. saltator from European shores, stretching from the north-west Atlantic through the Baltic to the Mediterranean. A primary aim of the work was to establish a database of accumulated trace metal concentrations (Cd, Cr, Cu, Fe, Mn and Zn) in this biomonitor. Statistical analysis has shown significant geographical differences in the bioavailabilities of all the metals, the most distinct being copper, iron and manganese. It has proved possible to identify unusually high accumulated concentrations of Cd, Cr, Cu, Fe, Mn and Zn in this biomonitor, indicative of high metal bioavailability at a particular site. These may serve as reference points for future biomonitoring programmes seeking to identify metal contamination in coastal waters.

Legal aspects of conserving native oysters in Scotland.

Native oysters (Ostrea edulis) historically supported valuable fisheries in Scotland, but are now absent from areas of former abundance on the east coast and occur mainly in isolated populations in west coast sea lochs. The main contemporary threat is from unauthorized gathering. In most places, the exclusive right to gather is retained by the Crown, as a remnant of the feudal system, but in some areas the right has been acquired by individuals or institutions. A temporary right to gather oysters may be obtained by permit from the proprietor, or through a Several or Regulating Order made under shellfish fisheries legislation. The right to gather oysters is separate from ownership of the foreshore or sea bed on which they are located. To receive the maximum legal protection, oyster beds must be marked out, or the rights to them otherwise adequately made known. Wild or formerly-cultivated oyster beds may not meet this criterion and, in any case, enforcement is difficult in remote locations. It has been proposed that there should be a statutory public right to gather oysters. Were this to be created, then strong conservation measures would need to be implemented to protect native oysters from eradication by uncontrolled gathering.

Prototype reflectivity analyses of hydrogen storage levels in single-walled carbon nanotubes.

A prototype case study is presented that examines the level of hydrogen content in H-SWNTs using the Surface Plasmon Resonance technique. The damping effect and the angular shift in the resonance minimum of an SWNT-gold interface due to the presence of hydrogen is analyzed using a parametric model, which is based on the concept of an effective permittivity. The new approach provides for a non-invasive analysis of the level of hydrogen content in H-SWNTs and is potentially extendable to other carbon-based hydrogen storage materials.

Haemodynamic compromise during thoracoscopic/laparoscopic oesophagectomy.

Minimally invasive oesophagectomy is a relatively new procedure that is performed by means of thoracoscopy and laparoscopy. One stage of the procedure involves creation of a peritoneo-pleural communication in the presence of a pneumoperitoneum. In the case presented, severe hypotension occurred at this point. We believe this was caused by the escape of carbon dioxide from the peritoneal cavity into the right hemithorax, resulting in tension pneumothorax and cardiac tamponade. We believe this to be a predictable complication of this procedure but one that if expected, recognised and correctly managed, should not result in adverse outcomes.

Heart-lung interactions: the sigh and autonomic control in the bronchial and coronary circulations.

1. The Darwin hypothesis that human and animal expressions of emotion are the product of evolution and are tied to patterns of autonomic activity specified to progress the emotion remains under challenge. 2. The sigh is a respiratory behaviour linked with emotional expression in animals and humans from birth to death. The aim of the present study was to explore Darwin's hypothesis with respect to tied autonomic activity underlying sigh-induced changes in the bronchial and coronary circulations. 3. Awake dogs were prepared using pulsed ultrasonic flow probes on the right bronchial artery, parent intercostal artery and brachial artery, or on the right, circumflex and anterior descending coronary arteries. Central venous (CVP) and arterial pressures (AP) were measured; heart rate and flow conductances were derived. Three spontaneous sighs were monitored before and during random blockade of individual and combinations of cholinoceptors, alpha-adrenoceptors and beta-adrenoceptors using methscopolamine, phentolamine and propranolol infusions. The data were subject to a 2(3) factorial analysis. 4. A spontaneous sigh is marked by a transient fall and return (< 3 s) in CVP of 18 mmHg (from 4 +/- 1 to -14 +/- 2 mmHg), usually followed by apnoea lasting 23 +/- 2 s. There is an immediate tachycardia and small rise in AP (phase 1) then, during apnoea, bradycardia and a fall in AP (phase 2). During phase 2, bronchial and coronary blood flow and conductance rise two- to three-fold over 30s (peak at 8s). The vascular changes are absent in parent intercostal and brachial beds.

Effect of fentanyl on baroreflex control of circumflex coronary conductance.

1. Fentanyl, a synthetic mciro-opioid receptor agonist, is the preferred induction and maintenance anaesthetic agent in cardiac surgery. 2. Its actions on myocardial blood flow are poorly understood. There are reports of intra-operative myocardial ischaemia. Its reported actions on cardiorespiratory control vary widely, but do involve hypertension, bradycardia and peripheral vasoconstriction. 3. Accordingly, the postulate that fentanyl would cause coronary vasoconstriction and myocardial disadvantage was examined in awake dogs with a continuous wave Doppler flow probe mounted on the circumflex coronary artery. 4. Continuous intravenous infusion of fentanyl citrate (550 ng/kg per min) raised plasma concentrations of fentanyl to 3.37 ng/mL in a linear fashion at 20 min. There was a fall in core temperature of 0.7 degrees C and, although no apparent depression of ventilation or fall in arterial or coronary sinus PO2, there was a rise in PCO2 and H+ concentration. Some dogs salivated and panted transiently. Thus, fentanyl may reset temperature regulation in low doses but, at higher doses, is associated with metabolic acidosis. 5. In sinus rhythm, the arterial pressure of the dogs fell slightly, then rose to 115% of resting control. Circumflex flow and conductance rose early, then conductance steadily declined to 83%. Heart rate fell, then rose before returning to pre-infusion levels. The early circumflex coronary vasodilator effects, but not the later vasoconstrictor effects, were reduced in dogs with paced hearts. 6. In dogs with paced hearts, a dose-effect study using 138, 275, 550 and 1100 ng/kg per min fentanyl suggested that, at low plasma concentrations of 1-2 ng/mL, vasodilatation does occur in both coronary and systemic circulations; however, at higher doses, intense coronary and systemic vasoconstriction supervenes. 7. The dose-response effect of fentanyl on arterial baroreflex control of circumflex conductance was examined during the immediate 8 s circumflex vasodilator response to a step rise in aortic pressure caused by inflation of an intra-aortic balloon. At low plasma concentrations of fentanyl, baroreflex control of circumflex conductance appears to be enhanced but, with increasing plasma concentrations of fentanyl, appears to be depressed. 8. Therefore, the effects of fentanyl are dose dependent. At low plasma concentrations, left ventricular blood flow and its baroreflex control is enhanced but, at higher concentrations, it is depressed.

Effects of anaesthesia on regional coronary control mechanisms.

1. The regional coronary circulation is under the control of local metabolic and myogenic factors, but is also influenced by autonomic systems, including sympathetic and parasympathetic nerves. 2. General anaesthetic agents influence not only local control through changes in metabolic demand, but also neural control through suppression of autonomic influence. 3. Anaesthetic agents have differing effects on reflex control systems, which are dependent on coronary territory and ventricular rate. 4. Effects of anaesthesia should be taken into account when interpreting results in anaesthetized models of coronary control.

Airway thermal volume in humans and its relation to body size.

The objective of this study was to investigate the influence of volume ventilation (VE) and cardiac output (Q) on the temperature of the expired gas at the distal end of the endotracheal tube in anesthetized humans. In 63 mechanically ventilated adults, we used a step decrease in the humidity of inspired gas to cool the lungs. After change from humid to dry gas ventilation, the temperature of the expired gas decreased. We evaluated the relationship between the inverse monoexponential time constant of the temperature fall (1/tau) and either VE or Q. When VE was increased from 5.67 +/- 1.28 to 7.14 +/- 1.60 (SD) l/min (P = 0. 02), 1/tau did not change significantly [from 1.25 +/- 0.38 to 1.21 +/- 0.51 min-1, P = 0.81]. In the 11 patients in whom Q changed during the study period (from 5.07 +/- 1.81 to 7.38 +/- 2.45 l/min, P = 0.02), 1/tau increased correspondingly from 0.89 +/- 0.22 to 1. 52 +/- 0.44 min-1 (P = 0.003). We calculated the airway thermal volume (ATV) as the ratio of the measured values Q to 1/tau and related it to the body height (BH): ATV (liters) = 0.086 BH (cm) - 9. 55 (r = 0.90).

Effects of hypertonic saline on regional function and blood flow in canine hearts during acute coronary occlusion.

Small-volume resuscitation using hypertonic saline (7.5%) is effective for various types of shock. Recently, hypertonic saline has been proposed for fluid management in patients with impaired cardiovascular function. Whether hypertonic saline is safe in the compromised heart during coronary occlusion is not known. We examined the effects of hypertonic saline at 4 mL.kg-1 on myocardial function and blood flow during acute coronary occlusion. In anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers. Myocardial contractility was assessed using percent of systolic shortenings measured in both normal or ischemic regions. Blood flow distribution was measured using radioactive microspheres. Percent of systolic shortening and blood flow in the normal myocardium, unaltered by coronary occlusion, increased significantly after hypertonic saline from 11.0 +/- 1.1% to 13.7 +/- 1.4% and from 120 +/- 13 mL.min-1.100 g-1 to 169 +/- 13 mL.min-1.100 g-1, respectively. In the ischemic myocardium, occlusion of the left anterior descending coronary artery markedly decreased percent of systolic shortening from 13.0 +/- 1.2% to 9.3 +/- .9% and blood flow from 98 +/- 13 mL.min-1.100 g-1 to 19 +/- 10 mL.min-1.100 g-1. At peak effect of hypertonic saline contractility and blood flow in the ischemic myocardium decreased to 7.4 +/- .8% and 12 +/- 5 mL.min-1.100 g-1, respectively. Five of the nine dogs developed premature ventricular beats during hypertonic saline infusion. However, no significant changes were observed when normal saline was given at equivalent volumes to hypertonic saline in six dogs. Hypertonic saline was associated with significant increases in heart rate (from 116 +/- 3 beats.min-1 to 129 +/- 5 beats.min-1) and cardiac output (from 2.54 +/- .17 L.min-1 to 3.32 +/- .26 L.min-1). Except for an improved perfusion in the skin, hepatic arterial, and coronary beds, blood flow to the muscle, spleen, jejunum, kidney, and brain was not significantly altered by hypertonic saline. Our data demonstrates variant effects of hypertonic saline on either normal or ischemic myocardium. Whereas contractile function and blood flow in the normal myocardium were improved after hypertonic saline infusion, further decreases in blood flow and contractile function in region distal to coronary occlusion could lead to worsening of ischemic injury. These data suggest that hypertonic saline may be deleterious in hearts with impaired contractile function caused by ischemia.

Small-volume resuscitation using hypertonic saline improves organ perfusion in burned rats.

Resuscitation using small volumes (3-5 mL/kg) of 7.5% hypertonic saline (HTS) is effective for hemorrhagic shock. Whether HTS is beneficial for the initial resuscitation of burn injury is not clear. We compared the hemodynamic effects of HTS versus lactated Ringer's solution (LR) and examined organ tissue perfusion during burn resuscitation (R). Full thickness scald burn (35% of total body surface area) was induced in pentobarbital-anesthetized rats. Regional blood flows were measured using radioactive microspheres before and 30 min after burn, and after R with either HTS (4 mL/kg) or LR (at a dose required for equivalent restoration of arterial blood pressure). Data from the HTS-or LR-resuscitated groups were compared to those from a nonresuscitated group (n = 10 in each group). Mean arterial pressure decreased 30% after burn (from 120 +/- 4 to 84 +/- 5 mm Hg, mean +/- SEM) and returned toward baseline (112 +/- 7 mm Hg) at 10 min after R with HTS (4 mL/kg) or LR (22.6 +/- 0.7 mL/kg), but subsequently decreased to 100 +/- 7 mm Hg with HTS and 105 +/- 5 mm Hg with LR at 30 min. In contrast to LR, resuscitation using HTS was associated with tachycardia. Blood flows to the skin and muscle of the normal or burn regions did not change after fluid resuscitation as compared to a nonresuscitated group. Fluid resuscitation transiently increased intestinal perfusion. Similar improvements in blood flow to the spleen were observed with HTS and LR at 10 min after R (from 128 +/- 10 to 156 +/- 15 and from 113 +/- 10 to 145 +/- 26 mL.min-1 x 100 g-1, respectively). However, at 30 min after R, splenic perfusion in the LR group was not different from that in the nonresuscitated group. Blood flows to the brain and kidney increased 39% and 42%, respectively, with HTS. HTS was also associated with pronounced improvements in blood flows to the heart (from 346 +/- 20 to 631 +/- 37 mL.min-1 x 100 g-1), liver (from 36 +/- 2 to 62 +/- 4 mL.min-1 x 100 g-1), and testis (from 29 +/- 2 to 43 +/- 2 mL.min-1 x 100g-1). Resuscitation using HTS was associated with rapid improvement in organ tissue perfusion in anesthetized rats subjected to burn injury. In comparison to LR, greater increases in blood flows to the heart, kidney, liver, and testis were observed with HTS. The results suggest that significant improvement in blood flow distribution can be achieved using HTS at less than one fifth the volume of LR for the initial treatment of burn shock.

The relationship between systolic pressure and stroke volume describes myocardial contractility.

OBJECTIVE: To develop a method of measuring end-systolic elastance from information obtained outside the ventricle and thereby simplify its transduction. DESIGN: Prospective, within-animal comparative analysis. SETTING: University-based laboratory study. PARTICIPANTS: Six mixed-breed dogs. INTERVENTIONS: Instrumentation included minor axis sonomicrometry, ascending aortic flow probe, aortic and ventricular pressure transducers, and constricting cuffs on the vena cavae and aorta. MEASUREMENTS AND MAIN RESULTS: Elastance was determined from the equation PES = EES (VED - VES), where VED - VES is stroke volume and PES is end-systolic arterial pressure. EES was derived from both preload and afterload manipulation. Cardiac performance indices were calculated automatically by computer under conditions of varying load and inotropy. This extraventricular method of elastance calculation was compared by linear regression and analysis of variance to preload recruitable stroke work, traditional EES determination (using ventricular dimension instead of volume), and LVdP/dt at 50 mmHg. EES measured from the aortic sites correlated well with the other contractility indicators (p < 0.003 in all cases) and demonstrated more sensitivity and stability under loading manipulation than traditional EES. A strong relationship between the change in stroke volume and end-systolic ventricular diameter during acute aortic constriction (r = 0.924, p < 0.0001) was observed, and the mean r value for the individual outflow elastance measurements was 0.97 +/- 0.02. CONCLUSIONS: In this study, measurement of EES from the ventricular outflow tract during progressive aortic constriction produced results more consistent and descriptive than EES by traditional techniques and has the potential for obtaining elastance measurements from possibly less invasive techniques.

Comparative effects of nitric oxide inhibition on the coronary vasomotor responses to etomidate, propofol, and thiopental in anesthetized dogs.

We examined the hypothesis that the coronary vasomotor responses to etomidate (ETO), propofol (PRO), and sodium thiopental (STP) are mediated through contrasting effects on the resting nitric oxide (NO)-dependent vasodilator tone that opposes adrenergic vasoconstrictor activity in the intact dog. Circumflex flow (CxF) responses to randomized intracoronary microinjections (0.3 mL) of normal saline (NS), alkalinized saline (AS), intralipid (IL), adenosine (ADE, 17 micrograms), acetylcholine (ACh, 1.25 micrograms), ETO (6, 12, 60 micrograms), PRO (30, 60, 300 micrograms), and STP (75, 150, 750 micrograms) were quantified in eight isoflurane-anesthetized dogs with fixed ventricular rates (100 bpm). Injections were repeated during intravenous (IV) infusion (50 mg/kg + 1 mg.kg-1.min-1) of NG-nitro-L-arginine methyl ester (L-NAME). ADE and ACh transiently increased CxF to 305% +/- 20% (P < 0.001) and 310% +/- 29% (P < 0.001) of resting values, respectively. ETO had no effect, whereas PRO (300 micrograms) provoked small transient increases in CxF to 135% +/- 4% (P < 0.05) of control. Responses to STP (750 micrograms) were characterized by momentary decreases to 74% +/- 4% (P < 0.001), followed immediately by increases to 183% +/- 11% (P < 0.001) of resting values; NS AS, and IL had no effect. The momentary decreases with STP (750 micrograms) were significantly augmented during NO inhibition with CxF declining to 49% +/- 7% (P < 0.001) of resting values, whereas the secondary increase was unchanged. With L-NAME, CxF responses to ACh were attenuated to 32% +/- 3% (P < 0.001) of control, whereas responses to ADE, ETO, and PRO were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional myocardial function during contiguous ischaemia in an anaesthetized canine model: comparison of six methods of measurement.

During acute myocardial ischaemia, the function of the unaffected muscle is the primary determinant of residual cardiac performance. We compared six methods of measuring regional function in the remaining non-ischaemic segment after acute ligation of the left anterior descending (LAD) coronary artery in 16 dogs. Preparation included left ventricular micromanometers, regional sonomicrometer transducers to measure segment length and wall thickness, caval occluders and left atrial catheters for injection of radioactive microspheres to measure regional blood flow. Pulmonary artery, central venous and systemic arterial pressures were measured and regional coronary venous blood was collected for direct myocardial oxygen consumption (VO2) calculations. Under basal high-dose fentanyl-neuromuscular blocker anaesthesia, the LAD was occluded after addition of halothane or isoflurane at 0.5 or 1.5 MAC concentrations. Regional myocardial function of the non-ischaemic segment was assessed by the following computer-derived indices: percent systolic wall thickening (% WT), velocity of shortening (vs), percent systolic shortening (%SS), regional stroke work (RSW), regional preload recruitable stroke work (RPRSW) and regional end-systolic elastance (Ees). No index demonstrated enhanced function in the non-ischaemic segment after LAD ligation and all monitors, except Ees, were sensitive to depression of function represented by a decrease in values after administration of halothane and isoflurane (P < 0.05). Ees values increased with the addition of isoflurane and remained constant with halothane. Circulating concentrations of catecholamines were unchanged after ischaemia, while inhalation agents caused a decrease in the concentrations of adrenaline and dopamine (P < 0.05), but not noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of nitric oxide synthesis causes systemic and pulmonary vasoconstriction in isoflurane-anesthetized dogs.

The postulate that the hemodynamic changes produced by isoflurane (1.5%) involve release of nitric oxide (NO) was examined. Fifteen dogs were anesthetized with thiamylal (15 mg/kg) and ventilated with isoflurane and oxygen. Catheters were inserted for measurement of aortic pressure, pulmonary artery pressures, and determination of cardiac output. Left thoracotomy was performed and complete heart block was induced by injection of 37% formaldehyde (0.3 mL) into the atrioventricular node; ventricular rate was fixed at 100 beats/min by external pacing. An apical microtransducer was inserted into the left ventricle (LV) via the apex for measurement of left ventricular pressure (LVP) and its first derivative (dP/dt). Flow probes were mounted on the left circumflex (Cx) and anterior descending (AD) coronary arteries. Measurements were obtained before (control period) and during NO inhibition using IV NG-nitro-L-arginine methyl ester (L-NAME) by a 50 mg/kg bolus plus 1 mg/kg/min. Infusion of L-NAME caused immediate and sustained increases in mean arterial pressure to 145 +/- 3% (P < 0.001), mean pulmonary arterial pressure to 128 +/- 5% (P < 0.001), pulmonary capillary wedge pressure to 144 +/- 8% (P < 0.001), coronary perfusion pressure to 163 +/- 4% (P < 0.001), systemic vascular resistance to 209 +/- 9% (P < 0.001), pulmonary vascular resistance to 142 +/- 12% (P < 0.005), anterior descending flow to 115 +/- 4% (P < 0.005), and circumflex flow to 113 +/- 3% (P < 0.01) of control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Preparation of the intensive care patient for major surgery.

Improved methods for monitoring and treating critically ill patients have increased the number of surgical candidates with multiorgan system impairment. Whereas such patients may have been considered "too sick to undergo surgery" in the past, many such patients linger in the intensive care unit unless definitive therapy is accomplished. Specific attention to review of the patient's preoperative preparation for surgery on a system-by-system basis may improve outcome substantially. The need for possible mechanical ventilation prior to transport to the operating room must receive particular attention. Pneumothorax, if present, must be treated prior to institution of positive-pressure ventilation so progression to tension pneumothorax can be avoided. Deficits in the circulating blood volume must be identified and corrected preoperatively if possible. A need for enhancement of cardiac output or alteration of vascular tone requires pulmonary arterial catheterization and indicates an increased operative risk. Metabolic abnormalities such as disturbances of acid-base balance, sodium or potassium concentration, and endocrinopathies are identified and corrected as much as possible prior to operation. Antibiotics are instituted as appropriate. Replacement of the red blood cell mass is dictated primarily by anticipated or actual blood loss. Factors of coagulation are infused on a replacement basis as necessary. Great care must be taken during transport to the operating room, as maintenance of intravascular monitoring devices, therapeutic infusions, and mechanical ventilation must continue during transport. Precautions must be taken to avoid hypothermia during transport and institution of anesthesia. Critical illness mandates specific considerations of the anesthetic agents to be utilized.

Role of systemic arterial pressure, heart rate, and derived variables in prediction of severity of myocardial ischemia during acute coronary occlusion in anesthetized dogs.

The present study examined the postulate that the quotient of mean systemic arterial pressure and heart rate predicts the severity of myocardial ischemia during occlusion of the left anterior descending coronary artery. Studies were performed in open-chest fentanyl-anesthetized dogs before and during halothane (n = 8) or isoflurane (n = 8) anesthesia. The pressure-rate quotient (PRQ) decreased significantly in both groups during incremental increases in halothane or isoflurane to 68% and 57% of control values at 0.5 MAC and to 41% and 38% at 1.5 MAC for halothane and isoflurane, respectively. Myocardial lactate production was unchanged from the ischemic region, and no correlation between the PRQ and myocardial lactate production was observed. In contrast, heart rate correlated significantly (r = 0.376; P less than 0.05) with lactate production. The product of systolic systemic arterial pressure and heart rate (rate-pressure product) correlated with blood flow (r = 0.493; P less than 0.001) and with oxygen consumption (r = 0.571; P less than 0.001) in the normal myocardium. A weak correlation (r = 0.330; P less than 0.05) of rate-pressure product with myocardial lactate production from the ischemic region was observed. There were no correlations between the PRQ and myocardial lactate production from the ischemic region or indices of blood flow distribution (i.e., inner/outer ratio in the ischemic region or ischemic/normal ratio). The relationship of hemodynamic variables to measurements of regional myocardial metabolism was independent of background anesthetic agent of depth of anesthesia. The current data suggest that heart rate changes are weakly predictive of severity of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular function during induced hypotension by fenoldopam or sodium nitroprusside in anesthetized dogs.

Fenoldopam, a selective dopamine1 receptor agonist, has been recommended for induced hypotension because it effectively lowers arterial blood pressure and improves renal perfusion. We examined cardiovascular functions during hypotension induced by fenoldopam or sodium nitroprusside. In eight halothane-anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers for the assessment of LV contractility using the analysis of the pressure-diameter relationship. Blood flow distribution was measured by radioactive microspheres. Doses of fenoldopam and nitroprusside were titrated to reduce mean arterial blood pressure to 60 mm Hg. After 40 min of hypotension, fenoldopam and nitroprusside caused similar increases in heart rate (17% +/- 4% vs 19% +/- 10%, respectively) and decreases in systemic vascular resistance (-24% +/- 5% vs -27% +/- 4%). Hypotension induced by fenoldopam was associated with higher LV end-diastolic pressure (4.4 +/- 0.6 vs 2.5 +/- 1.1 mm Hg) and end-systolic meridional wall stress (33.0 +/- 4.3 vs 17.8 +/- 2.1 g/cm2) when compared with nitroprusside. There were no significant changes in cardiac output and cardiac contractility as expressed by the slope (Ees) of the LV end-systolic pressure-diameter relationship, velocity of shortening of the diameter, and percentage of wall thickening of the LV. In contrast to nitroprusside, which decreased renal blood flow from 197 +/- 19 to 163 +/- 15 mL/min, renal blood flow increased during fenoldopam-induced hypotension from 187 +/- 20 to 239 +/- 18 mL/min. The increase in renal perfusion was similar in upper, middle, and lower regions of the kidney; however, it was more in the medulla compared with the cortex (37% +/- 17% vs 25% +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)

No evidence for blood flow redistribution with isoflurane or halothane during acute coronary artery occlusion in fentanyl-anesthetized dogs.

The present study examines the postulate that isoflurane, in contrast to halothane, causes redistribution of blood flow away from an ischemic myocardial region through vasodilation of adjacent normally perfused myocardium. The study was performed in open-chest dogs anesthetized with fentanyl; ischemia was induced by occlusion of the left anterior descending coronary artery. At 0.6% alveolar concentration, isoflurane increased transmural blood flow to 125% of control values (P less than 0.05) in the normal region without concomitant changes in blood flow to the ischemic region or in the endocardial/epicardial flow ratio in the ischemic region. The evidence excludes either transmural steal or regional redistribution phenomena. Myocardial blood flow variables returned to control values at 1.8% isoflurane, and no blood flow redistribution effects were evident. In contrast, whereas halothane 0.4% caused no significant effect on myocardial blood flows, an alveolar concentration of 1.2% decreased transmural blood flow to normally perfused left ventricle to 70% of control (P less than 0.05). Regional myocardial oxygen consumption in the normal and ischemic areas decreased at higher alveolar concentrations and was unchanged at the lower concentrations for both agents. Myocardial lactate production from the ischemic region was unchanged with either agent, suggesting that, in terms of metabolic changes, neither agent worsened ischemia during sustained occlusion of the left anterior descending coronary artery. The present data show no evidence for worsening of myocardial ischemia with either isoflurane or halothane. Isoflurane causes a relatively greater increase in perfusion compared to myocardial oxygen consumption of normally perfused myocardium; nevertheless, sufficient coronary vascular reserve remains in the native collateral circulation so that myocardial metabolic supply-and-demand relationships during ischemia are not further compromised.