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Biomedical subjects

M Manohar

Publications and source records attributed to M Manohar.

At least 91 records · Page 5Linked to original sources
PubMed1984

Regional distribution of brain and myocardial perfusion in swine while awake and during 1.0 and 1.5 MAC isoflurane anaesthesia produced without or with 50% nitrous oxide.

Isoflurane has been hailed as the anaesthetic of the eighties. We examined the effects of isoflurane anaesthesia on regional distribution of brain and myocardial blood flow in 11 healthy isocapnic pigs using 15 micron diameter radionuclide labelled microspheres that were injected into the left atrium. Each animal was studied during five of the following six conditions: (i) unanaesthetised (control; n = 8); (ii) 1.45% end-tidal (ET; 1.0 MAC) isoflurane anaesthesia (n = 10); (iii) 2.18% ET (1.5 MAC) isoflurane anaesthesia (n = 9); (iv) 0.95% ET isoflurane + 50% N2O anaesthesia (equivalent to 1 MAC; n = 8); (v) 1.68% ET isoflurane + 50% N2O anaesthesia (equivalent to 1.5 MAC; n = 8); and (vi) 50% N2O alone (n = 8). The order of anaesthetised steps was randomised for each pig. At every step 50 to 55 min were allowed for equilibration with isoflurane, and for N2O 35 to 40 min were allowed for equilibration. Recovery periods of 60 min each were interposed between anaesthetised steps to allow pigs to recover towards control values. Control values of blood flow in the cerebrum, cerebellum, and brain-stem were 81 +/- 5, 87 +/- 8, and 64 +/- 6 ml X min-1 X 100 g-1, respectively. During 1.45% isoflurane anaesthesia, cerebral, cerebellar and brainstem blood flows were 120%, 152%, and 145% of respective control values. With 2.18% isoflurane, perfusion in these regions of the brain was 140%, 200%, and 226% of respective control values. Substitution of 50% N2O to maintain equipotent anaesthesia markedly exaggerated the increment in cerebral blood flow, while changes in cerebellar and brain-stem blood flow were similar. Cerebral blood flow during 0.95% isoflurane + 50% N2O and 1.68% isoflurane + 50% N2O anaesthesia was 137% and 210% of the control value, respectively. Regional brain blood flow was only insignificantly altered by 50% N2O alone. It is concluded that isoflurane caused dose-dependent vasodilatation in all regions of the brain, the magnitude being greater in the cerebellum and the brain-stem. The administration of N2O with isoflurane to maintain equipotent anaesthesia exaggerated cerebral vasodilatation, especially at deeper level of anaesthesia. Myocardial blood flow in isoflurane anaesthetised pigs decreased, especially in the inner layers, in a dose-related manner. The use of 50% N2O with isoflurane permitted higher heart rate, perfusion pressure, rate-pressure product, and transmural myocardial blood flow.

Anesthesia, Inhalation↗
PubMed1984

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.

Acidosis↗
PubMed1984

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)

Adrenal Glands↗
PubMed1984

Porcine regional brain and myocardial blood flows during halothane-O2 and halothane-nitrous oxide anesthesia: comparisons with equipotent isoflurane anesthesia.

Regional distribution of brain and myocardial blood flow were examined in 9 instrumented isocapnic normothermic swine, using 15-microns diameter radionuclide-labeled microspheres injected into the left atrium. Minimal alveolar concentration (MAC) of halothane required to prevent gross purposeful movement in response to a noxious stimulus in 50% of the pigs was found to be 0.70%. Measurements were made on each animal during nonanesthetized state (control), 1.0 and 1.5 MAC halothane anesthesia, and the equivalent of 1.0 and 1.5 MAC halothane anesthesia, using 50% N2O. The order of anesthetized steps was randomized for each pig. Recovery periods of 60 minutes were interposed between the anesthetic treatments. During halothane + 50% N2O anesthesia, heart rate, cardiac output, mean aortic pressure, and rate-pressure product were higher than comparable levels of halothane-O2 anesthesia. Halothane caused dose-dependent vasodilatation in all regions of the brain. Cerebral, cerebellar, and brain-stem blood flows at 1.5 MAC halothane were 135%, 135%, and 115% of respective control values. Substitution of 50% N2O to maintain same MAC dose markedly exaggerated the increment in porcine cerebral and brainstem blood flows, especially at 1.0 MAC when perfusions in these regions were 204% and 128% of respective control values. At 1.5 MAC anesthesia produced by halothane + 50% N2O, the cerebral, cerebellar, and brain stem perfusions were 153%, 146%, and 129% of control values. Transmural myocardial blood flow decreased from control value with both levels of halothane anesthesia, but with equivalent MAC anesthesia produced by halothane + 50% N2O, myocardial perfusion remained near awake values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Regional myocardial blood flow and coronary vascular reserve in unanesthetized ponies during pacing-induced ventricular tachycardia.

To examine the effects of tachycardia on coronary circulation, transmural distribution of myocardial blood flow (MBF, 15-micron diameter radionuclide-labeled microspheres) was studied in six healthy adult ponies at rest (heart rate = 60 +/- 7 beats . min-1), during ventricular pacing at 150 and 200 beats . min-1, as well as with ventricular pacing at 250 beats . min-1 before and during maximal coronary vasodilatation (iv adenosine infusion; 4 mumole . kg-1 . min-1). Mean aortic pressure and cardiac output were unchanged from control values with ventricular pacing. Whereas ventricular pacing at 150 and 200 beats . min-1 resulted in a progressive uniform increase in transmural MBF and well-maintained endo:epi perfusion ratio, pacing at 250 beats . min-1 did not result in a further increase in MBF compared to pacing at 200 beats . min-1 and the left ventricular (LV) subendocardial:subepicardial (endo:epi) perfusion ratio was significantly less than 1.00 (0.87 +/- 0.05). Blood flow to the LV papillary muscles and subendocardium was significantly less than that recorded at 200 beats . min-1. The LV endo:epi perfusion ratio with ventricular pacing at 250 beats . min-1 during adenosine infusion resulted in a decrease in mean aortic pressure (63% of control value) and a marked further reduction in blood flow to the LV papillary muscles as well as the LV subendocardium, while MBF increased dramatically in the LV subepicardium compared to values observed during ventricular pacing at 250 beats . min-1 alone. This resulted in a LV endo:epi perfusion ratio of 0.39 +/- 0.09. By contrast, transmural right ventricular (RV) MBF increased significantly and the RV endo:epi perfusion ratio was well maintained. These data demonstrate that coronary vasomotion functions to maintain LV subendocardial blood flow in the pony myocardium at a heart rate of 200 beats . min-1, while at 250 beats . min-1 exhaustion of coronary vasodilator reserve in the deeper layers limits further increase in MBF.

Adenosine↗
PubMed1983

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.

Adenosine↗
PubMed1983

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.

Animals↗
PubMed1983

Systemic distribution of blood flow in swine while awake and during 1.0 and 1.5 MAC isoflurane anesthesia with or without 50% nitrous oxide.

To examine the effects of isoflurane on systemic distribution of cardiac output, organ/tissue blood flow was measured in 11 isocapnic pigs using 15-micrometer diameter radionuclide-labeled microspheres injected into the left atrium. Measurements were made on each pig during five of the following six conditions; awake (control); 1.0 MAC (1.45% end-tidal)isoflurane anesthesia; 1.5 MAC (2.18% end-tidal) isoflurane anesthesia; 0.95% end-tidal isoflurane and 50% N2O anesthesia equivalent to 1.0 MAC; 1.68% end-tidal isoflurane and 50% N2O anesthesia equivalent to 1.5 MAC; and 50% N2O administration. The order of anesthetized steps was randomized. A period of 60 min was interposed between anesthetized steps to allow pigs to recover towards control values. Mean aortic pressure decreased in a dose-related manner during isoflurane anesthesia, whereas cardiac output decreased only during 1.5 MAC isoflurane anesthesia and heart rate remained unchanged. The addition of N2O attenuated the hypotensive effects of isoflurane and cardiac output was maintained near control values because of increased heart rate. Brain blood flow increased in a dose-dependent manner with isoflurane anesthesia, but myocardial blood flow exhibited a dose-related decrease. The addition of 50% N2O to maintain the same total MAC anesthesia resulted in a larger increase in brain blood flow especially at 1.5 MAC, while myocardial blood flow was maintained near control value. Rate-pressure product and myocardial blood flow at 1.5 MAC anesthesia were higher when N2O was used with isoflurane. While blood flow and fraction of cardiac output going to the adrenal glands were unaltered during isoflurane-N2O anesthesia, blood flow increased at 1.5 MAC isoflurane anesthesia. Splenic blood flow and splenic fraction of cardiac output were increased at both MAC levels of isoflurane as well as isoflurane-N2O anesthesia whereas blood flow to the stomach, small intestine, diaphragm, skeletal muscle, and adipose tissue decreased from control values. Renal, hepatic arterial, and cutaneous blood flow remained unaltered. Fifty percent N2O in the presence of a residual end-tidal isoflurane concentration of 0.20% caused heart rate to increase from control levels, while cardiac output and mean aortic pressure were unaltered. Brain blood flow increased by 27% above control values, but perfusion in the myocardium, adrenal glands, spleen, kidneys, liver, and skin was unchanged. Stomach, small intestine, skeletal muscle, and diaphragm blood flows decreased from control values, whereas perfusion of adipose tissue increased.

Anesthesia, Inhalation↗
PubMed1982

Respiratory effects of pregnancy and progesterone in Jersey cows.

Unanesthetized Jersey cows were studied during both pregnant (5-9 months) nonlactating states, and nonpregnant lactating states; and also following treatment with progesterone (Pr). The pH, PCO2 and PO2 of aortic blood, VE and f were measured and the mixed expired gas was analyzed. The following significant changes from the nonpregnant state occurred during pregnancy: PaCO2 = -3.2 mm Hg, pHa = +0.02 unit, VT = -0.44 L, f = +7 breaths/min, and VE/VCO2 = +9.7. Concomitant with the respiratory studies, serum Pr levels were determined by radioimmunoassay (RIA) in 11 nonpregnant and 5 pregnant cows, and in 6 nonpregnant, lactating cows prior to and on days 3, 5 and 10 of treatment with Pr (500 mg, i.m., twice daily). Minute ventilation (VE, L X min-1 X kg-1, BTPS) was positively correlated (r = +0.59) and PaCO2 was negatively correlated (r = -0.64) with endogenous serum Pr levels of non-pregnant and pregnant cows. However, exogenous Pr did not significantly alter these parameters or pHa, despite mean serum levels nearly twice (23.6 +/- 10.2 ng/ml) those observed in pregnant cows (12.7 +/- 3.7 ng/ml). The increased ventilation during pregnancy in Jersey cows, shown in this study, does not appear to be related to Pr as exogenous Pr failed to induce hyperventilation. The correlation of increased ventilation with endogenous Pr levels therefore suggests that the mode of in vivo Pr release, or different compound, simultaneously released, could be the stimulus.

Animals↗
PubMed1982

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.

Animals↗
PubMed1982

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.

Altitude Sickness↗
PubMed1982

Radiographic characterization of diaphragmatic excursion in halothane-anesthetized ponies: spontaneous and controlled ventilation systems.

A radiograph technique for identification of diaphragmatic segments and quantitation of their contribution to total diaphragmatic function was developed. five anesthetized ponies were studied on 3 separate occasions. Studies were made of the ponies in left lateral recumbency at 2 anesthetic levels (1 and 2 minimal alveolar anesthetic concentrations; halothane) and under spontaneous and controlled ventilation systems. General pattern of diaphragmatic displacement was unchanged by increased depth of anesthesia. Controlled ventilation altered the pattern of diaphragmatic displacement. Diaphragmatic displacement and regional volume changes were a function of active contraction or passive movement.

Anesthesia↗
PubMed1982

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.

Animals↗
PubMed1981

A technique for catheterisation of the coronary sinus in adult ponies (Equus caballus).

Long-term catheterisation of the coronary sinus using a specially designed catheter was accomplished in 6 ponies via a right lateral thoracotomy. The catheter comprised a 10 to 12 cm long stiff segment (Teflon) joined to a 100 cm length of pliable medical grade (vinyl) tubing. Catheters were kept functional up to 10 weeks postoperatively. Location of the catheter tip was verified by determining the oxygen tension of anaerobically withdrawn blood samples. Normal values of oxygen tension of the coronary sinus blood in ponies were similar to those reported for the dog, whereas oxygen content was significantly lower.

Animals↗
PubMed1981

Blood flow in the hypertrophied right ventricular myocardium of unanesthetized ponies.

To examine the effects of right ventricular (RV) hypertrophy on regional myocardial blood flow and coronary vascular reserve, hemodynamics and myocardial blood flow (15-micrometers radio-nuclide-labeled microspheres) were studied in 12 unanesthetized adult ponies before and during intravenous isoproterenol HCl infusion (1 microgram.kg-1.min-1). Six ponies served as controls, whereas in each of the others the main pulmonary artery (PA) had been banded 35-90 days prior to the study. Marked RV hypertrophy was present in PA-banded animals. In these ponies, there was a significant increase in RV systolic pressure (147%), heart rate (88%), RV tension-time index (279%), and RV myocardial blood flow (137%), while their RV coronary vascular resistance was only 40% of that for control ponies. Blood flow in right side of the interventricular septum was also significantly higher in the PA-banded ponies. Endo/epi perfusion ratio exceeded 1.00 for both ventricular freewalls in all animals. With isoproterenol infusion, there was a marked increase in myocardial blood flow in both groups. However, in PA-banded ponies the endo/epi flow ratio decreased precipitously below 1.00 in both ventricular freewalls. In control ponies this did not happen in the RV freewall, and RV coronary vascular resistance decreased to 19% of its control value. In PA-banded ponies, the magnitude of decline in RV coronary vascular resistance was much smaller, only 32% of that for control ponies. It is concluded that, unlike in LV hypertrophy, transmural myocardial blood flow per unit mass is much higher in the hypertrophied RV myocardium of adult resting ponies, and this higher RV perfusion occurs at the expense of curtailed RV coronary vascular reserve.

Animals↗