Total Body Oxygen Consumption Research Articles

Response of plasma norepinephrine and epinephrine to dynamic exercise in patients with congestive heart failure

The activity of the sympathetic nervous system is increased at rest in patients with congestive heart failure. To determine whether this augmentation is carried over during dynamic upright exercise, 14 patients with congestive heart failure were stressed maximally during upright bicycle ergometry. Plasma norepinephrine and epinephrine levels were measured in the basal upright (sitting) posture before and during maximal exercise. The results were compared with those in six healthy control subjects before and during maximal exercise. Plasma norepinephrine increased during exercise from a mean (± standard error of the mean) of 650 ± 95 to 1,721 ± pg/ml in the group with heart failure. This increase was significantly less (p < 0.001) than that in the control group (from 318 ± 36 to 3,230 ± 418 pg/ml). However, for equivalent levels of total body oxygen consumption (V̇O 2), the group with heart failure had higher levels of plasma norepinephrine than the control group. Plasma epinephrine was similar in the two groups in the basal upright position (92 ±18 and 92 ± 26 pg/ml), but it increased more during exercise in the normal subjects (743 ± 210 pg/ml) than in the group with heart failure (167 ± 67 pg/ml) (p < 0.001). The percent increase in norepinephrine correlated with the percent change in V̇O 2 in the group with heart failure (r = 0.62, p < 0.02), but the percent change in epinephrine did not. There is, therefore, a disturbance in the sympathetic nervous system during exercise in patients with congestive heart failure. Although norepinephrine increases in such patients to a greater extent than in normal subjects at lower levels of exercise, the extremely high levels of norepinephrine and epinephrine generated by normal subjects during maximal upright exercise do not occur in patients with heart failure.

The pathophysiological profile of the acute cardiovascular toxicity of sodium fluoride

The intravenous infusion of sodium fluoride (2 mg/kg · min) into anesthetized rats caused a progressive fall in arterial blood pressure, cardiac output, heart rate and peripheral resistance. Respiratory rate increased during the first 20 min of infusion resulting in increased oxygen and decreased carbon dioxide blood concentrations. Total body oxygen consumption decreased after 30 min of NaF infusion by 29%, whereas the respiratory quotient (RQ) increased from 0.8 to 1.06. Death occurred afrer a mean dose of 79.6 ± 4.6 mg/kg NaF. The terminal cardiac event before death was atrioventricular block followed immediately by asystole. Artificial ventilation did not influence the cardiovascular and the lethal effects of fluoride infusion. The plasma concentrations of total and ionized calcium decreased upon NaF infusion. The infusion of extra calcium did not prevent NaF-induced cardiovascular failure but decreased plasma fluoride levels and increased the lethal dose of NaF by 17% (not significant). In isolated atria and perfused heart in vitro, NaF decreased the force of contraction in a dose-dependent manner. In conclusion, cardiovascular failurw resulting from the direct cardiodepressive and vasodilatating effects of fluoride (and not from respiratory depression or hypocalcemia) accounts for the lethal outcome of fluoride intoxication.

Determinants of total body oxygen consumption in adults undergoing cardiac catheterization.

Oxygen consumption was measured in 500 patients (151 F, 349 M, ages 12-84 yr.) undergoing routine cardiac catheterization. Sex, age, and heart rate were found to be the strongest predictors of oxygen consumption index (OCI). Males had higher OCI values than females at any age. Older patients of both sexes had lower OCI values than younger patients. Heart rate correlated directly with OCI. Treatment with propranolol correlated inversely with OCI. However, after correction for heart rate, there were no significant differences in OCI values between propranolol treated and nontreated patients. A linear regression equation was developed using combinations of variables to predict OCI, and tables are presented for predicting OCI in those patients in whom this variable cannot be directly measured.

Central and regional hemodynamic effects of intravenous isosorbide dinitrate, nitroglycerin and nitroprusside in patients with congestive heart failure

A triple crossover random design was used to compare the central and regional hemodynamic effects of intravenous isosorbide dinitrate, nitroglycerin and nitroprusside in 10 patients with low output congestive heart failure. Isosorbide dinitrate and nitroglycerin were infused in dose increments of 0.8 μg/kg body weight per min up to 4.0 μg/kg per min and nitroprusside in increments of 0.4 μg/kg per min up to 2.0 μg/kg per min. The central and regional hemodynamic responses of isosorbide dinitrate and nitroglycerin were similar;both effected a 10 to 35 percent reduction in pulmonary capillary wedge pressure, systemic blood pressure and vascular resistance and pulmonary arterial pressure and resistance with a 7 to 22 percent increase in stroke volume and cardiac output. Nitroprusside elicited a similar decrease in pulmonary capillary wedge pressure with a greater reduction (15 to 45 percent) in systemic blood pressure and resistance and pulmonary arterial pressure and resistance and greater augmentation of stroke volume and cardiac output (20 to 40 percent). Arterial oxygen saturation remained unchanged with isosorbide dinitrate and nitroglycerin and decreased slightly with nitroprusside. None of the drugs altered total body oxygen consumption. All three drugs decreased limb vascular resistance and elevated limb blood flow proportional to the degree of change in systemic vascular resistance and cardiac output. Isosorbide dinitrate and nitroglycerin did not alter renal vascular resistance, so that a mild reduction in renal blood flow was noted as systemic blood pressure decreased. Nitroprusside decreased renal vascular resistance; however, the concomitant decrease in arterial pressure resulted in no net change in renal blood flow. None of the three drugs altered hepatic blood flow or vascular resistance. In low output congestive heart failure, these three drugs effect similar responses in preload, nitroprusside causing a greater change in afterload. Preferential vasodilation of regional vascular beds was noted with limb flow greater than hepatic and renal flow with isosorbide dinitrate and nitroglycerin and limb flow much greater than renal and greater than hepatic flow with nitroprusside.

Cardiopulmonary resuscitation

The physical stress on the rescuer performing cardiopulmonary resuscitation (CPR) was assessed utilizing the ECG, rate pressure product (RPP), and total body oxygen consumption (VO2). Six healthy physicians served as rescuers. Only a submaximal physical effort was required to perform good CPR, as demonstrated by the heart rate and VO2 changes. However, the effect was enough to generate a mean rescuer RPP approaching 20,000 with 2 of the rescuers well over 20,000. These data suggest that CPR might elicit ischemic symptoms in a rescuer with coronary artery disease.

Effects of thiopentone on cardiac performance, coronary hemodynamics and myocardial oxygen consumption in chronic ischemic heart disease.

Thiopentone was administered as induction agent for general anesthesia to eight patients with stable ischemic heart disease; 6 mg/kg of the drug induced decrease in arterial blood pressure (-27%), systematic vascular resistance (-20%), stroke volume index (-14%), mean pulmonary arteriolar occlusion pressure (-15%) and left ventricular stroke work index (-38%), while heart rate increased by 10% and cardiac output remained unchanged. Total body oxygen consumption decreased by 30%. Myocardial oxygen consumption decreased by 39% with unchanged or decreased myocardial oxygen extraction and myocardial lactate uptake decreased by 40%. Arterial and coronary sinus hypoxanthine levels were unchanged and no ST-T-segment changes or dysrhythmias were recorded. In the present experimental setting, the results indicate that thiopentone substantially decreased myocardial oxygen requirements. In spite of the marked reduction in coronary perfusion, myocardial oxygen demand was matched by supply, myocardial dysoxia was not induced and cardiodepression was clinically negligible. Rate pressure product was a poor indicator of changes in myocardial oxygen consumption after thiopentone administration.

Oxygen Transport to Tissue under Normovolemic Moderate and Extreme Hemodilution during Coronary Bypass Operation

Oxygen transport to tissue was studied in 12 patients undergoing coronary bypass operation under normovolemic moderate and extreme hemodilution. Normovolemic moderate hemodilution (15 ml per kilogram of body weight), carried out immediately after induction of anesthesia, decreased the mean hematocrit from 0.43 to 0.33. Simultaneously, the cardiac index and the left ventricular filling pressure increased slightly but the systemic oxygen transport was reduced by 20%. The subcutaneous tissue oxygen tension (Po 2) was approximately 40 mm Hg after induction of anesthesia and underwent a transient increase during moderate hemodilution. During cardiopulmonary bypass and extreme hemodilution, the mean hematocrit declined to 0.16. Concurrently, the mean tissue Po 2 fell sharply and reached a minimum of 14 mm Hg at deepest hypothermia. After decannulation and reinfusion of autologous blood, the Po 2 rose to 30 mm Hg. In general, total-body oxygen consumption changed along with tissue Po 2. Blood lactate concentration underwent a clear increase in the early phase of extracorporeal circulation and remained rather stationary thereafter. No perioperative myocardial infarctions were encountered, and each patient made an uneventful recovery.

Total body and splanchnic thermogenesis in curarized man during a short exposure to cold.

To investigate thermoregulation independent of muscular contractions in adult man during a short period of exposure to cold, five examinations were carried out on four individuals who were unconscious due to persistent brain damage and who were totally curarized during the exposure. An increase was found in total body oxygen consumption of 0.043 mmol . kg-1 (range 0.038-0.049) or 25%, in plasma noradrenaline of 5.05 nmol . 1-1 (range: 2.48-6.73) or 132%, and in plasma non-esterified fatty acids of 0.6 mmol . -1 (range: 0.049-0.095) or 44%. No changes occurred in plasma adrenaline or plasma glucose. Splanchnic oxygen consumption increased and contributed significantly to that of the total body in only one of the four cases. These results indicate that regulatory nonshivering thermogenesis exits in adult man not acclimatized to cold, that it is mediated by noradrenaline, that the major fuel substrate for the increased energy demand is the triglycerides from the fat stores, and that the splanchnic area contributes only irregularly and to a small degree to this part of thermogenesis.

Hemodynamic and cardiometabolic effects of prenalterol in patients with gram negative septic shock.

The hemodynamic effects of prenalterol, a new inotropic agent, were investigated in 10 patients with gram negative septic shock. In four of the patients, coronary sinus blood flow (CSF) and myocardial oxygen and lactate extraction were also determined. After baseline hemodynamic measurements, prenalterol was infused intravenously over a 10-min period to a total dose of 150 micrograms/kg. All patients responded within 15 min after completion of prenalterol infusion by increasing mean arterial pressure from 57 +/- 11 to 75 +/- 20 mmHg (7.58 +/- 46 to 9.97 +/- 2.66 kPa), (+32%), (P less than 0.01) and cardiac index from 2.65 +/- 0.40 to 3.80 +/- 0.47 1.min-1.m-2, (+44%) (P less than 0.001). There was no change in heart rate or systemic vascular resistance, nor were any arrhythmias recorded. The urinary output increased significantly. After prenalterol, CSF increased from 185 +/- 14 to 246 +/- 14 ml.min-1, (+33%), (P less than 0.001) and myocardial oxygen and lactate extraction rose from 19.8 +/- 2.1 to 26.6 +/- 2.1 ml O2.min-1, (+34%) (P less than 0.001) and from 33.2 +/- 2.3 to 44.7 +/- 2.1 mumol.min-1, (+35%), (P less than 0.001), respectively. The total body oxygen consumption increased from 287 +/- 13 to 348 +/- 23 ml O2.min-1, (+21%), (P less than 0.01) and the arterial lactate concentration decreased from 5.61+/- 0.55 to 3.94 +/- 0.16 mmol.l-1, (-30%), (P less than 0.01), suggesting improved tissue perfusion. The results demonstrate that prenalterol is a potent, highly selective inotropic agent inducing the same magnitude of increase in blood pressure and cardiac output as reported for dopamine in septic shock.

Hemodynamic and Metabolic Responses to Upright Exercise in Patients with Congestive Heart Failure: Treatment with Nitroglycerin Ointment

Although a vasodilator drug might favorably alter hemodynamics in resting, supine patients with heart failure, it must be determined if the drug has any unfavorable as well as favorable effects under extremes of real life stress situations normally encountered by ambulatory patients, especially upright exercise. An adverse response might occur with the addition of pharmacologic vasodilation to the metabolic arteriolar dilation accompanying upright exercise. In order to evaluate these factors in a controlled environment, seven NYHA class 2-3 patients with congestive heart failure without angina pectoris or stenotic valvular lesions performed upright bicycle exercise preand postadministration of a maximally-tolerated dose of 2 percent nitroglycerin ointment, determined previously by titration. Nitroglycerin therapy resulted in slightly improved cardiac performance at two given submaximal workloads. Also noted was, at a higher workload, a decreased ratio of arteriovenous oxygen difference to cardiac index suggestive of increased circulatory reserve. Pulmonary capillary wedge pressure, total body oxygen consumption, plasma catecholamines, and blood lactates did not show a statistically significant change after use of nitroglycerin ointment, nor were symptoms of fatigue or dyspnea improved during exercise. It is concluded that nitroglycerin ointment does not remarkably improve hemodynamics or alter nutritional blood flow to exercising muscle at a submaximal upright workload. From our data and that of others, it is concluded that nitroglycerin ointment can be given safely to heart failure patients to improve resting supine hemodynamics without adversely affecting upright exercise performance or hemodynamics.

Effects of hypoxia and shock on transcutaneous PO2 values in dogs.

Transcutaneous Po2 (PtcO2) was measured with transcutaneous oxygen electrode sensors and correlated with Pao2, Pvo2, cardiac output, and O2 delivery during changes in FIO2 and standardized hypovolemic shock in anesthetized dogs. Simultaneously, cardiorespiratory variables were measured: intravascular pressures, arterial and mixed venous gases, and cardiac output. Before the shock experiments, these physiologic variables were measured while the FIO2 was varied from 0.21–1.0. Then the FIO2 was held constant while the animal was subjected to hemorrhagic shock and resuscitation. PtcO2 followed PaO2 values (r = 0.96) during variations in the FIO2 when the cardiac output was in the normal range. The 95% response time was less than 15 sec. In the active hemorrhage stage, PtcO2, Pvo2, and cardiac output simultaneously decreased. As the cardiac output dropped, the PtcO2 fell from values near that of the PaO2 and approached the falling PvO2. At the point of 20 torr, the PtcO2 fell below the PvO2. During these shock experiments, when the PtcO2 was greater than 20 torr, the PvO2 was less than PtcO2, but when the PtcO2 was less than 20 torr, the PvO2 was greater than the PtcO2. This PtcO2-PvO2 crossing point corresponded to a cardiac output of 25–30% of the control and a decrease in total body oxygen consumption of 30%. With fluid resuscitation, the PtcO2 responded more quickly at first than the increase in cardiac output. Throughout the shock period, the PaO2 did not vary significantly from the preshock control value. The oxygen delivery was the variable that the PtcO2 followed most closely during the entire hypoxia and hemorrhagic shock experiments, rw = 0.82. It was concluded that the PtcO2 is an accurate, noninvasive, continuous method for monitoring peripheral oxygen delivery and a valuable tool for the study of disturbed circulation in various shock states. In the latter conditions, it does not follow PaO2, but rather, oxygen delivery.

OXYGEN TRANSPORT DURING DOPAMINE INFUSION IN DOGS

Catecholamines increase not only oxygen delivery to tissues but also oxygen consumption (VO2). The effect of an infusion of dopamine hydrochloride has been studied at two doses, each in six dogs. Dopamine 10 micrograms kg-1 min-1 caused an increase in haemoglobin concentration and altered cardiac output, oxygen availability and total body oxygen consumption such that oxygen availability ratio increased and (CaO2-CVO2) decreased although these changes were not statistically significant. Dopamine 30 micrograms kg-1 min-1 increased (P less than 0.05) heart rate, haemoglobin concentration and CaO2 and significantly reduced stroke volume and VD/VT. Although oxygen availability increased, increases in oxygen consumption were greater and this resulted in a statistically insignificant reduction in oxygen availability ratio and an increase in (CaO2-CVO2). Terminating the dopamine infusion resulted in significant (P less than 0.05) decreases in cardiac output, PVO2, CaO2), oxygen availability and oxygen consumption and an increase in (CaO2-CVO2). It was concluded that maximum oxygen delivery occurs at a lower dose than that required to produce the maximum increase in oxygen consumption.

Exercise performance after septal myotomy and myectomy in patients with obstructive hypertrophic cardiomyopathy

The effect of left ventriculomyotomy and myectomy on exercise capacity and cardiac function in patients with obstructive hypertrophic cardiomyopathy has not previously been determined. In this study, 29 patients were evaluated during graded treadmill exercise before and after operation. Postoperatively, 27 of 29 patients reported symptomatic improvement and had greatly reduced left ventricular outflow gradient. Twenty-five of 28 patients (89 percent) attained higher exercise levels after operation, arid this was accompanied by an increase in total body oxygen consumption from 16 to 21 ml/min per kg ( P < 0.005). A significant increase in cardiac index during maximal exercise also accompanied this improved exercise performance (5.0 to 5.7 liters/min per m 2, P < 0.05). The increase in maximal cardiac index was associated with greater desaturation of mixed venous blood (34 to 24 percent, P < 0.02) in patients with preoperative angina. At a given level of mixed venous oxygen saturation (30 percent), overall mean cardiac index was higher postoperatively (4.6 to 5.2 liters/min per m 2, P < 0.05). These results suggest that, although several mechanisms probably contribute to symptomatic improvement after myotomy and myectomy, enhanced cardiac performance plays an important role in the majority of patients.

Conditioning Effects of Chronic Infusions of Dobutamine

We studied the conditioning effects of chronic infusion of dobutamine and exercise training in three groups of chronically instrumented dogs. One group was infused with normal saline, a second group was infused with dobutamine (40 mug/kg per min), and the third group was exercised on a treadmill at 4 mph, up a 10 degrees incline. Each group was either infused or exercised for 2 h a day, 5 d a week for 5 consecutive wk. Resting heart rate and arterial blood lactate concentration, measured at weekly intervals, decreased progressively in the dobutamine and exercise groups, but not in the group that received normal saline infusion. Cardiovascular responses to submaximal treadmill exercise were not changed by 5 wk of normal saline infusion. However, the increases in heart rate, cardiac output, mean aortic blood pressure, arterial blood lactate, plasma renin activity, and norepinephrine concentration during exercise were significantly smaller after 5 wk of conditioning with either dobutamine or exercise training. After conditioning, the increases in arteriovenous oxygen difference during exercise were larger in the latter two groups, but the increases in total body oxygen consumption did not differ before and after conditioning. To assess ventricular function, we intravenously infused methoxamine both before and after conditioning. The slope of the line that related systolic aortic blood pressure and mean left atrial pressure increased in the animals conditioned with either dobutamine or exercise, indicating enhanced myocardial contractility. Left ventricular blood flow was lower in these two groups of animals than it was in the normal saline group. Left ventricular weight did not differ among the three groups. Our results show that chronic infusion of dobutamine produced cardiovascular and metabolic conditioning effects like those produced by exercise training, and further suggest that sympathetic stimulation during exercise plays a role in physical conditioning.

EFFECT OF HYPOTENSION INDUCED WITH SODIUM NITROPRUSSIDE ON CANINE CORONARY ARTERIAL FLOW

In seven dogs anaesthetized with pentobarbitone, coronary and pulmonary artery blood flows were measured using electromagnetic flow meters. The infusion of a 0.01% solution of sodium nitroprusside caused an initial small increase in mean coronary artery flow which returned to control as the arterial pressure decreased. No changes were noted in cardiac output nor were further changes observed in coronary flow. Heart rate was increased consistently during the hypotension and left ventricular dp/dt max was reduced as were coronary and total peripheral resistances. There were no significant changes in myocardial or total body oxygen extraction or consumption.

CANINE CORONARY BLOOD FLOW RESPONSES TO HYPOXAEMIA: THE INFLUENCE OF HALOTHANE

Electromagnetic flow meters were used to measure blood flow in the coronary and pulmonary arteries of six anaesthetized dogs following thoracotomy. Halothane 1% (v/v) caused a reduction in arterial pressure, coronary artery flow, cardiac output and myocardial and total body oxygen consumption and an increase in coronary vascular resistance. Hypoxaemia caused large increases in coronary artery flow during both cardiac systole and diastole, but not until PaO2 was less than 5.3 kPa. This response was not influenced by the presence of halothane. Although myocardial oxygen availability and consumption were maintained during hypoxaemia, total body oxygen availability and consumption were markedly reduced.

Metabolic control of the circulation. Effects of acetate and pyruvate.

Chloralose-anesthetized dogs were infused intravenously with either Tris-acetate or Tris-pyruvate at 0.0375, 0.075, and 0.15 mmol/kg per min successively, each for 20 min. Acetate infusion increased cardiac output, left ventricular dP/dt and dP/dt/P, and coronary blood flow, while pyruvate infusion did not. Infusions of either substance increased arterial blood and skeletal muscle concentrations of citrate and malate, but only acetate infusion increased the tissue AMP content and decreased the ATP:AMP ratio. The increase in cardiac output produced by acetate was accompanied by an increase in total body oxygen consumption and a decrease in the difference between arterial and mixed venous blood oxygen. Myocardial oxygen consumption increased during acetate infusion, but the decrease in myocardial oxygen extraction and the increase in coronary sinus blood oxygen saturation suggest that an active coronary vasodilation which was not a result of the increased cardiac work, occurred. The concentration of hypoxanthine in the coronary sinus and the content of myocardial adenosine increased, which suggests that the increase in coronary blood flow was caused by the vasodilator action of adenosine released from the myocardium, and that adenosine production is not necessarily tied to PO(2). These systemic and coronary hemodynamic changes also occurred when acetate (0.075 mmol/kg per min) was infused into conscious dogs. Acetate infusion also increased blood flow to the gastrointestinal tract, kidneys, intercostal muscle, and diaphragm. These changes were not affected by propranolol pretreatment, but were abolished by pretreatment with fluoroacetate which reduced acetate oxidation. These results suggest that the circulatory stimulation produced by acetate was not caused by increases in tricarboxylic acid cycle intermediates. Instead, it was probably related to the increased cleavage of ATP to AMP that accompanies activation of acetate to acetyl CoA, and was not mediated via beta-adrenergic receptors. It is speculated that hemodynamic changes may occur in patients who undergo hemodialysis with acetate-containing dialysate. Hemodynamic changes of ethanol may also be brought about by acetate, which is one of the intermediates that accumulates during ethanol metabolism.

Opsonic alpha2 surface binding glycoprotein therapy during sepsis.

A pronounced depletion of an opsonic protein for hepatic reticuloendothelial (RE) phagocytosis has been demonstrated in critically ill trauma patients. This opsonic alpha(2) surface binding (SB) glycoprotein has immunologic identity and a similar amino acid composition to cold insoluble globulin (CIg). Since CIg can be concentrated in cryoprecipitate, it was utilized as a readily available source of opsonic alpha(2)SB glycoprotein for replacement therapy after injury with documented hypoopsonemia. Six septic patients (2 multiple trauma, 2 thermal burn, and 2 intra-abdominal abscess) were studied to test whether cryoprecipitate infusion would restore this humoral component. Pre- and posttherapy opsonin levels were determined by bioassay and electroimmunoassay. In all patients, severe opsonin depletion was reversed following cryoprecipitate infusion. All patients had a rapid improvement in febrile state, normalization of leukocyte levels, and improvement in pulmonary function as evidenced by decreasing requirements for end expiratory pressure at lowered levels of inspired oxygen. One patient was studied more extensively and demonstrated an increase in cardiac output, limb blood flow, total body and limb oxygen delivery, total body and limb oxygen consumption and a progressive decrease in pulmonary shunt fraction. Thus, opsonic alpha(2)SB glycoprotein deficiency can be reversed by cryoprecipitate infusion in critically ill septic injured patients. Replacement of this humoral factor may be an important therapeutic modality in prevention of multiple organ failure, but it should be administered only after documentation of hypoopsonemia in traumatized patients.

ACUTE COLD EXPOSURE AND THE METABOLISM OF GLUCOSE AND SOME OF ITS PRECURSORS IN THE LIVER OF THE FED AND FASTED SHEEP

Measurements of total body oxygen consumption, visceral and hepatic blood flow, oxygen consumption, exchanges of amino acids, lactate, pyruvate and glucose were made on sheep fed 3--6 h or 21 h before the experiment and exposed for 3 h to a neutral environment (15 degrees C) or a cold environment (0.5 to 4 degrees C with clipped coat and wind speed 2 m.s-1). Recent feeding significantly increasedd the total oxygen consumption and the oxygen consumption of the viscera and liver. No general release of amino acids from the viscera or uptake by the liver after feeding was detected although the arterial plasma concentration of essential amino acids did increase significantly after feeding. The plasma concentration of most non-essential amino acids also increased except that of glycine, which decreased significantly. Cold exposure increased the total oxygen consumption and reduced the respiratory quotient significantly. Release of amino acids from the viscera was stimulated by cold exposure. There was a variable increase in the hepatic uptake of lactate and alanine when the sheep were fasted and cold-exposed. The liver's glucose output doubled and the blood (arterial) glucose concentration significantly increased in the cold.

Altered hemodynamic responses to acute hypoxemia in spontaneously hypertensive rats.

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.