Comparison of in vitro drug responses in airways of atopic dogs with and without in vivo airway hyperresponsiveness.

For comparison with previous studies in greyhounds and in the Basenji-Greyhound dog model of asthma (BG), basenji dogs were studied under identical conditions with respect to airway responsiveness to inhaled methacholine, cutaneous responses to intradermal antigen injection, and the sensitivity of isolated trachealis muscle to methacholine and isoproterenol. The relaxant effect of isoproterenol was assessed in trachealis muscle precontracted with methacholine (ED50). The basenji dogs resembled the BG dogs in that they showed multiple positive skin tests. Further, trachealis muscle showed a markedly reduced sensitivity to methacholine (pD2 6.64 +/- 0.10) (+/- S.E.) in vitro. However, basenji dogs resembled the greyhounds in requiring high concentrations of methacholine aerosols to produce a 2-fold increase in pulmonary resistance (1.68 mg/ml +/- 1.21). Thus, there were no significant correlations between sensitivity to methacholine in vitro and airway responsiveness to methacholine in vivo; however, the reduced sensitivity to methacholine in vitro in both basenji and BG dogs may be related to the marked atopy characteristic of both groups. In vitro sensitivity to isoproterenol was correlated (r = 0.82) with the concentration of methacholine needed to elicit the test contraction, but isoproterenol sensitivity in BG dogs was significantly less (p = .0027) than that predicted by the common regression line. This deficit in beta adrenergic function in trachealis muscle unrelated to atopy may be important in the in vivo airway hyperresponsiveness of BG dogs.

Extraplacental transfer of water in the sheep.

1. Ten pregnant ewes were operated on at 130 days of gestation. The fetal trachea was intubated with a double-lumen tube, an inflatable occluder was placed around the umbilical cord, vascular catheters were placed in the fetal carotid artery and jugular vein and in the maternal jugular vein, and multiple catheters were placed in the amniotic and allantoic sacs. 2. At 139 days gestation, the fetus was ventilated in utero, and the umbilical cord was occluded. The extrafetal fluids were circulated by means of roller pumps. Known activities of radio-iodinated human serum albumin, tritium-labelled water and 14C-labelled urea were injected into the amniotic and/or allantoic fluids. Samples were obtained at 30 min intervals for several hours. 3. Extrafetal fluid volumes were calculated from the albumin distribution volumes. The amounts of labelled water transferred to the maternal circulation were calculated from the changes in tracer concentrations in extrafetal fluids and fetal plasma. 4. No labelled albumin was detected in fetal or maternal plasma. The permeability-surface area product of labelled water at the combined amniotic and allantoic interfaces with the ewe was 28.2 +/- 2.8 ml/min (mean +/- S.E.M.). In five preparations the values could be separately calculated for amniotic and allantoic interfaces. The two mean values (19 +/- 4 and 12 +/- 1 ml/min) were not significantly different from each other. The permeability-surface area product at the combined interfaces with the fetus was 0.96 +/- 0.17 ml/min. Urea was so much less permeable than water that no reliable permeability-surface area products could be calculated in all of the preparations. 5. We calculated that the hydraulic conductivity of the combined extraplacental pathway is more than 0.5% of that of the placenta. Because the osmotic gradient across the extraplacental pathway is one to two orders of magnitude greater than that across the placenta, extraplacental transfer of water can significantly affect intrauterine water volume.

Arterial pressure after chronic reductions in suprarenal aortic flow in fetal lambs.

Experiments were performed on 13 fetal lambs of 126 days gestational age. Seven days after surgery, suprarenal aortic blood flow was reduced to 70% of control with an inflatable occluder for a period of at least 4 days. This produced an almost constant aortic pressure difference of 35 mmHg across the occluder. Plasma renin activity (PRA) rose in the next hour from 6 to 42 ng.ml-1.h-1 (P less than 0.01) but decreased to a level that was statistically insignificantly above normal by the next day. PRA as a function of lower body arterial blood pressure showed rapid adaptation. Upper body arterial blood pressure was statistically significantly elevated by 5 mmHg within 5 min and continued to rise while plasma renin activity was falling. Femoral artery blood pressure dropped immediately but returned to near normal within 1 h and remained there. The long-term upper body hypertension was irreversible with a 30-min infusion of saralasin. Subrenal aortic flow reduction caused none of these changes. We conclude that the fetal kidneys can regulate arterial blood pressure upward but that the long-term effect does not depend solely on a direct vasoconstrictive action of angiotensin.

Fetal O2 consumption in sheep during controlled long-term reductions in umbilical blood flow.

Electromagnetic flow sensors and inflatable occluders were placed on the distal aortas of nine fetal lambs of 111-124 days gestation; indwelling vascular catheters were placed in a lower body artery and vein and the common umbilical vein. After a control period of 7.6 +/- 2.1 (SD) days, distal aortic flow was reduced to about 60% of control flow; placental flow fractions of distal aortic flow were 77 +/- 5%, control; 69 +/- 11% during flow reduction. Duration of the flow reductions was 9.6 +/- 6.5 days. Fetal O2 consumption fell from 6.4 +/- 1.5 to 5.3 +/- 1.1 ml X min-1 X kg-1 (P less than 0.02) as umbilical blood flow was reduced from 202 +/- 47 to 116 +/- 36 ml X min-1 X kg-1 (P less than 0.001). Least-squares polynomial regression analysis showed that O2 consumption was a linear function of umbilical blood flow (P less than 0.01). With regard to long-term fetal O2 consumption, there was no evidence for a margin of safety in fetal umbilical blood flow.

Comparison of drug responses in vivo and in vitro in airways of dogs with and without airway hyperresponsiveness.

Basenji-greyhound (BG) dogs demonstrate marked nonspecific airway hyperresponsiveness. To assess the possible contribution of an abnormal sensitivity of airway smooth muscle to this phenomenon, we studied the in vitro contractile responses to methacholine and histamine and the relaxant response to isoproterenol in trachealis muscle from five BG dogs with airway hyperresponsiveness in vivo and from five greyhound dogs that served as a control population. Isoproterenol responses were determined against a half-maximal methacholine contraction. Aerosol methacholine concentrations required to produce a 2-fold increase in pulmonary resistance were 0.07 +/- 0.02 (+/- S.E.) mg/ml in BG dogs and 0.67 +/- 0.26 mg/ml in greyhounds; pD2 values for methacholine-induced contraction of cervical trachealis muscle were 7.03 +/- 0.11 in BG dogs and 7.50 +/- 0.11 in greyhounds. A significant (P less than .01) negative correlation was found between methacholine sensitivity in vivo and in vitro. Aerosol concentrations of histamine required to produce a 2-fold increase in pulmonary resistance were 0.19 +/- 0.06 mg/ml in BG dogs and 1.44 +/- 0.43 mg/ml in greyhounds; pD2 values for histamine were identical in BG dogs (4.95 +/- 0.08) and greyhounds (5.05 +/- 0.19). Isoproterenol pD2 values were less in the trachealis muscle (cervical) of BG dogs (6.76 +/- 0.10) than in that of greyhounds (7.93 +/- 0.16), but this is probably a consequence of the higher concentration of methacholine needed to contract BG muscles. We conclude that the airway hyperresponsiveness of BG dogs does not reflect an increased sensitivity of airway smooth muscle per se.

Transmural coronary vasodilator reserve and flow distribution in unanesthetized calves sojourning at 3500 m.

Regional myocardial blood flow (MBF; 15-micron-diam radionuclide-labeled microspheres) was studied in six unanesthetized calves sojourning at 3500 m (PB = 500 mm Hg) for 53 +/- 2 days. These high-altitude (HA)-exposed calves were studied during chronic hypoxemia (PaO2 = 48 +/- 1 mm Hg), maximal coronary vasodilation, and during acute normoxemia (PaO2 = 91 +/- 1 mm Hg). Nine calves born and raised at sea level (SL) were also studied at matched PaO2 during chronic normoxemia, maximal coronary vasodilation, and acute hypoxemia to serve as control. Marked pulmonary hypertension and right ventricular (RV) hypertrophy were present in HA calves. Left ventricular (LV) MBF of HA calves during chronic hypoxemia (1.05 +/- 0.11 ml X min-1 X g-1) was similar to that of normoxemic SL calves (1.11 +/- 0.06 ml X min-1 X g-1) but MBF in their hypertrophied RV (1.65 +/- 0.21 ml X min-1 X g-1) exceeded that in normoxemic SL calves (0.47 +/- 0.06 ml X min-1 X g-1). More interesting was the finding that RV and LV MBF of HA calves did not change between chronic hypoxemia and acute normoxemia. By contrast, acute hypoxemia of a similar degree caused a dramatic increase in RV as well as LV MBF of SL calves. Minimal LV coronary vascular resistance was similar in the two groups of calves. This meant that functional cross-sectional area of LV coronary vascular bed was not altered in response to sojourn at HA. Minimal RV coronary vascular resistance of HA calves was also not different from that of SL calves. This means that functional cross-sectional area of the RV coronary vascular bed in HA calves increased proportionately with the increase in their RV mass.

Flow through the foramen ovale of the fetal and new-born lamb.

Right and left atrial pressures were measured in eight chronically instrumented fetal and neonatal lambs. Flows were measured with a combination of electromagnetic flow sensor and microsphere techniques. Three of the fetuses were ventilated in utero during the measurements. Four fetuses were studied as neonates immediately after spontaneous term delivery and one was studied as a normal fetus in utero. Data from these preparations were augmented with seven sets of previously reported data from normal fetuses in utero for analysis. Linear least-squares regression analysis demonstrated that inferior caval vein flow into the right atrium was inversely related to right atrial pressure. This flow could not be demonstrated to depend on the velocity of blood in the inferior caval vein. Non-linear least-squares regression analysis of foramen ovale flow as a function of a power of the flow in the inferior caval vein revealed that the square of the velocity of blood in the inferior caval vein predicted foramen ovale flow. Of the two forces that determine foramen ovale flow in the fetus, pressure difference and kinetic energy, the latter was far larger than the former. These results support the theory that the fetal foramen ovale is maintained in an open position by the kinetic energy of the blood in the inferior caval vein.

Regional blood flow changes in response to near maximal exercise in ponies: a review.

In recent years, increasing attention has been focused on the physiological responses of the horse to maximal exercise. Cardiovascular response in near maximally exercised galloping ponies (heart rate 225 +/- 7 beats/min; whole body oxygen consumption 122 +/- 12 ml/min/kg) comprised a marked increase in blood flow to the cerebellum, myocardium, diaphragm and the working muscles, while renal blood flow decreased precipitously. Cerebral and brainstem perfusion did not vary from resting values. Transmural homogeneity of myocardial blood flow persisted during near maximal exercise. It was reported that tachycardia of exercise contributed about one-third of the total increment in left ventricular coronary blood flow. Considerable unutilised coronary vasodilator capacity was also demonstrated in near maximally exercised ponies and it was suggested that maximally exercising ponies were not limited from further exertion because of the coronary circulation.

Vasography, its indications and complications.

A retrospective study was undertaken of the results of vasography in 440 male partners of infertile marriages who had undergone scrotal exploration and in a group of 42 men with a variety of genital tract disorders. Abnormalities were observed in 10% of 265 azoospermic men and in 4% of 175 other men with infertility. There was no evidence that vasography caused damage to the vas deferens and no oligozoospermic man became azoospermic. A high incidence radiological of abnormalities was seen in haemospermia but the incidence of abnormalities in selected men with ejaculatory problems or testicular pain was low.

Porcine systemic and regional organ blood flow during 1.0 and 1.5 minimum alveolar concentrations of sevoflurane anesthesia without and with 50% nitrous oxide.

Effects of sevoflurane anesthesia on organ blood flow were examined in nine healthy isocapnic pigs using 15-mumol diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of sevoflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was found to be 2.66 +/- 0.20%. Hemodynamic measurements were made on each pig during the following five conditions: awake (control); 1.0 MAC of sevoflurane anesthesia; 2.66% (1.0 MAC) sevoflurane + 50% N2O anesthesia; 1.5 MAC of sevoflurane anesthesia; and 3.99% (1.5 MAC) sevoflurane + 50% N2O anesthesia. Dose-related decrease in cardiac output, mean aortic pressure and left ventricular work occurred with sevoflurane anesthesia but heart rate was unchanged. Addition of 50% N2O to either of the pre-established sevoflurane concentrations did not change heart rate or the cardiac output, but with 3.99% sevoflurane mean aortic pressure decreased further. Unlike isoflurane and halothane which increase porcine brain blood flow, cerebral blood flow decreased to a similar level with both levels of sevoflurane anesthesia. Whereas cerebellar perfusion was unaltered with both levels of sevoflurane anesthesia, brain-stem blood flow decreased to a similar level from the control value. However, during 3.99% sevoflurane anesthesia, brain-stem blood flow exceeded that at 2.66% sevoflurane anesthesia. Addition of N2O to pre-established concentrations of sevoflurane increased regional brain blood flow but cerebral and brain-stem blood flow exceeded awake value only during 2.66% sevoflurane + 50% N2O anesthesia. Transmural myocardial blood flow decreased in a dose-dependent manner during sevoflurane anesthesia but the subendocardial/subepicardial perfusion ratio remained at control value.(ABSTRACT TRUNCATED AT 250 WORDS)

Porcine brain and myocardial perfusion during enflurane anesthesia without and with nitrous oxide.

Brain and myocardial blood flow (MBF) were examined in 10 previously instrumented swine during isocapnic conditions using 15 micron in diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of enflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 1.66%. In pigs, 50% nitrous oxide decreased enflurane requirement for 1.0 MAC anesthesia by 0.82%. Each animal was studied during the following conditions: (a) unanesthetized (control); (b) 1.0 MAC enflurane anesthesia (1.66% end-tidal concentration); (c) 1.5 MAC (2.49%) enflurane anesthesia; (d) the equivalent of 1.0 and 1.5 MAC anesthesia produced by enflurane (0.84 and 1.67%) plus 50% nitrous oxide. Cerebral and total brain blood flow values were the same as control values during both levels of enflurane anesthesia. However, blood flow in the brainstem and cerebellum exhibited a dose-related increase; the increment of 28% for each of these regions at 1.5 MAC achieved statistical significance. Vascular resistance in all regions of the brain decreased with enflurane anesthesia. Substitution of 50% nitrous oxide for enflurane to maintain the same level of anesthesia markedly increased cerebral blood flow. At 1.0 and 1.5 MAC anesthesia produced using enflurane plus 50% nitrous oxide, cerebral blood flow was 151 and 183% of the control value, respectively. During enflurane plus nitrous oxide anesthesia equivalent to 1.5 MAC, cerebellar and brain stem blood flow were 135 and 180% of respective control values. MBF in all regions decreased in a dose-related manner with enflurane anesthesia. At 1.5 MAC enflurane, perfusion values in the walls of the left and the right ventricles were 52 and 59% of respective control values. During both levels of enflurane plus 50% nitrous oxide anesthesia, transmural MBF in all regions remained close to awake values. Subendocardial/subepicardial perfusion ration in both ventricles exceeded 1.00 during all steps of the protocol, thereby suggesting that subendocardial O2 delivery kept pace with O2 demand. These experiments have demonstrated that usage of 50% N2O with enflurane to produce equipotent anesthesia resulted in a dramatic increase in cerebral blood flow while MBF remained near awake value.

Bovine regional brain blood flow during sojourn at a simulated altitude of 3500 m.

Regional distribution of brain blood flow (15 micron diameter radionuclide labelled microspheres injected into the left atrium) was studied in 6 unanesthetized calves during the 7th-8th weeks of exposure to a simulated altitude of 3500 m (PB = 500 mm Hg). Measurements were made during chronic hypoxemia (PaO2 = 48 +/- 1 mm Hg) and acute normoxemia (PaO2 = 91 +/- 1 mm Hg). Five calves, born and raised at sea level, were also studied in a similar manner during normoxemia (PaO2 = 86 +/- 2 mm Hg) and at 12 and 22 min of acute hypoxemia (PaO2 = 49 +/- 1 mm Hg) to serve as controls. Acute hypoxemia in sea level calves resulted in a marked uniform increase in blood flow to all regions of the brain and the brain O2 delivery remained similar to its normoxemic value. By comparison, however, blood flow in all regions of the brain in calves sojourning at 3500 m remained unchanged between hypoxemia and normoxemia. In these calves brain O2 delivery decreased during hypoxemia. These experiments demonstrated that blood flow in the bovine brain-stem and cerebellum behaved in the same manner as in the cerebrum during exposure to acute as well as chronic hypoxia. It is suggested that there are likely to be differences in adaptation of bovine cerebral circulation to acute vs chronic hypoxia.

Blood-gas tensions and acid-base status in ponies during treadmill exercise.

Blood-gas tensions and acid-base status were examined in 8 healthy grade ponies at rest (heart rate = 55 +/- 3 beats/min) and during moderate (fast trot; heart rate = 155 +/- 3 beats/min) and severe (gallop; heart rate = 218 +/- 7 beats/min) exercise performed on a treadmill. Arterial oxygen tension and hemoglobin-oxygen saturation of exercising ponies did not change from the resting values. Arterial oxygen content increased markedly during exercise, as a consequence of increased hemoglobin concentration. The total oxygen content, as well as the saturation of hemoglobin with oxygen in the mixed venous blood, decreased at each intensity of exercise. Arterial carbon dioxide tension decreased with moderate (16%) and severe (29%) exercise, indicating hyperventilation. In galloping ponies, during steady-state severe exercise marked metabolic acidosis developed, as indicated by a sharp increase in the arterial concentration of lactic acid (11.6 +/- 1.3 mM/L during severe exercise vs 0.6 +/- 0.3 mM/L at rest). This increase in lactate was accompanied by a decrease in arterial pH and bicarbonate concentration.

Distribution of blood flow during moderate and strenuous exercise in ponies (Equus caballus).

Blood flow to the brain, heart, kidneys, diaphragm, and skeletal muscles was studied at rest and during graded treadmill exercise, using radionuclide-labeled microspheres (15 microns diameter), in 11 healthy adult ponies. Hemodynamic changes brought about by exercise included marked increases in cardiac output, mean aortic pressure, left ventricular end-diastolic pressure, and right ventricular systolic and end-diastolic pressures. Blood flow to the brain stem and cerebral hemispheres was unchanged during both moderate exercise (heart rate = 154 +/- 3 beats/min) and severe exercise (heart rate = 225 +/- 7 beats/min). Despite marked hypocapnia during severe exercise, cerebellar blood flow increased by 32% above control value (94 +/- 7 ml/min/100 g). Myocardial blood flow increased transmurally with both levels of exercise. The endo:epi (inner:outer) perfusion ratio for the left ventricle and the interventricular septum decreased during exercise. It was, however, not different from unity. During severe exercise, renal blood flow decreased to 19% of its control value. Blood flow to the diaphragm exceeded that to the skeletal muscles during both intensities of exercise. Blood flow to the exercising muscles of the brachium and thigh increased by 31- to 38-fold during moderate exercise and by 70- to 76-fold during severe exercise. It is concluded that the cardiovascular response to strenuous exercise in the pony included an increase in blood flow to the cerebellum, myocardium, diaphragm, and exercising skeletal muscles, while blood flow was diverted away from the kidneys. It would appear that the pony's cardiovascular response to severe exercise is similar to that of persons.

Transmural coronary vasodilator reserve and flow distribution during severe exercise in ponies.

Transmural distribution of myocardial blood flow and coronary vasodilator reserve (15-microns-diam radionuclide-labeled microspheres) was studied in 11 adult, healthy ponies at rest and during moderate and severe exercise performed on a treadmill (heart rate 56 +/- 4, 154 +/- 3, and 225 +/- 7 beats . min-1, respectively.). Exercise resulted in a marked increase in cardiac output, mean aortic pressure, right ventricular (RV) systolic and end-diastolic pressure, left ventricular (LV) end-diastolic pressure, and the maximum rate of rise of LV pressure LV (dP/dtmax). Accompanying these changes was a pronounced increase in transmural myocardial perfusion. During severe exercise, subendocardial/subepicardial (endo/epi) perfusion ratio for the LV (0.99 +/- 0.02) decreased significantly from control value (1.27 +/- 0.03) but it was not significantly different from 1.00. With adenosine infusion during severe exercise, transmural myocardial blood flow throughout the cardiac ventricles was able to increase significantly further (delta from severe exercise to severe exercise with adenosine, 75% for LV, 68% for septum, and 57% for RV) despite the fact that heart rate, aortic pressure, and RV and LV end-diastolic pressures were unaltered. During severe exercise with adenosine, endo:epi perfusion ratios were 1.11 +/- 0.15 and 1.32 +/- 0.10 for LV and RV, respectively. In the LV, the coronary vasodilator reserve was found to be the least in papillary muscles, where the increment in blood flow during severe exercise with adenosine was only 46% above severe exercise without adenosine. Coronary vasodilator reserve was largest in the middle layers of the LV myocardium (88%). With adenosine infusion during severe exercise, coronary vascular resistance in both LV and RV decreased significantly from that observed during severe exercise alone (27 +/- 2 and 30 +/- 2 mmHg . ml-1 . min . g, respectively) to levels observed during maximal coronary vasodilation induced by adenosine infusion at rest (20 +/- 2 and 18 +/- 2 mmHg . ml-1 . min . g, respectively). These data clearly demonstrate that there remains a marked coronary vasodilator reserve transmurally in the pony myocardium during severe exercise.

Organ blood flow and distribution of cardiac output in nonanesthetized swine.

Organ blood flow and distribution of cardiac output (CO) were determined in awake resting swine, using radionuclide-labeled 15-micrometer diameter microspheres. Absolute values of blood flow (per 100-g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 45.46 +/- 2.64% of the resting CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.13%, 3.04%, 12.95%, 4.27%, and 18.71%, respectively.

Systemic and regional blood flow distribution in unanesthetized swine and swine anesthetized with halothane + nitrous oxide, halothane, or enflurane.

In order to study the distribution of cardiac output during various anesthetic regimens, we measured regional organ blood flow using 15 micrometers diameter radionuclide-labeled microspheres injected into the left atrium. Studies were carried out in nine pigs during resting unanesthetized state (control), during halothane (inspired concentration = 1.25 per cent) + nitrous oxide (50 per cent) anesthesia, during halothane (inspired concentration = 2.25 per cent) anesthesia, and during enflurane (inspired concentration = 4.0 per cent) anesthesia. The order of the last two treatments [halothane (2.25 per cent) and enflurane (4.0 per cent)] was randomized among the nine pigs. All anesthetic steps employed intermittent positive-pressure ventilation to maintain PaCO2 close to control values. Animals were allowed to recover towards the control state before changing to the next anesthetic regimen. Forty-five minutes were allowed for equilibration with each anesthetic regimen before hemodynamic measurements were made. In unanesthetized resting swine blood flow received by brain, cardiac ventricles, kidneys, liver (via hepatic artery), gastrointestinal tract, and skeletal muscle was 63.70 +/- 5.56, 128.56 +/- 14.92, 280.89 +/- 19.72, 21.95 +/- 3.25, 148.55 +/- 15.29 and 13.76 +/- 4.12 ml . min-1 . 100 g-1, respectively (mean +/- SEM). Corresponding values for the percentage of cardiac output received by the brain, cardiac ventricles, kidneys, liver (via hepatic artery), and gastrointestinal tract were 1.13 +/- .08, 3.04 +/- 0.13, 12.95 +/- 1.54, 4.27 +/- 0.76, and 18.71 +/- 0.91 per cent, respectively. Cardiac output and mean arterial blood pressure decreased significantly from control values with each of the three anesthetized steps. The decrease in cardiac output was greatest with the halothane anesthesia and least with halothane + N2O. Blood flow per unit weight of the cardiac, renal, and splanchnic tissues decreased significantly with each anesthetic regimen whereas brain blood flow and hepatic arterial blood flow were unaltered from control values. Thus, the per cent cardiac output received by the brain had increased with halothane (119 per cent) and enflurane (102 per cent) anesthesia while it was unaltered from the heart, renal, and splanchnic organs. Percentage of total cardiac output received by liver via the hepatic artery increased by 162 per cent during halothane anesthesia and 133 per cent during enflurane anesthesia, when compared to control values. During halothane + nitrous oxide anesthesia, the per cent of cardiac output going to the brain was not increased significantly. It is concluded that cardiac output as well as individual organ/tissue blood flow was better maintained during halothane + nitrous oxide anesthesia in comparison to halothane or enflurane anesthesia.

Regional myocardial blood flow and coronary vascular reserve in unanesthetized young calves exposed to a simulated altitude of 3500 m for 8--10 weeks.

We determined regional myocardial blood flow (15-micrometer tracer microspheres) and hemodynamics in nine normal calves, seven calves with right ventricular (RV) hypertrophy induced by pulmonary artery banding (PAB) at sea level, and five calves exposed to simulated high altitude (HA) of 3,500 m (PB = 500 mm Hg) for 8--10 weeks. Progression of RV hypertrophy was very rapid in HA calves. RV weight:body weight ratio of 2.74 +/- 0.20 g/kg at 8--10 weeks of sojourn at HA significantly exceeded that in PAB calves (1.98 +/- 0.11 g/kg) 20 weeks post-banding. All calves were studied unanesthetized at sea level before (control) and during maximal coronary vasodilation (iv adenosine; 4 microM/kg per min). Normal and HA calves were also studied during acute hypoxemia (PaO2: 42 +/- 1 mm Hg) induced by administration of 12--13% O2 + N2 in the inhaled gas. RV myocardial blood flow was significantly increased only in PAB calves, whereas in HA calves it was similar to that in normal calves. Left ventricular (LV) mass and blood flow were identical in three groups of calves. Polycythemia did not occur in HA calves. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, despite very fast progression of RV hypertrophy in HA calves, functional cross-sectional area of the RV coronary vascular bed kept pace with the increase in cardiac mass. Minimal coronary vascular resistance per unit weight of the left ventricular myocardium was also identical in three groups of calves. This suggested that chronic hypoxemia by itself did not cause an increase in the functional cross-sectional area of the LV coronary vascular bed. Acute hypoxemia resulted in a significant increase in myocardial blood flow in all calves, but in HA calves, RV endo:epi perfusion ratio decreased below 1.00. Transmural RV myocardial blood flow and RV systolic pressure in HA calves during acute hypoxemia significantly exceeded that in normal calves.