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Biomedical subjects

C W Buffington

Publications and source records attributed to C W Buffington.

At least 37 records · Page 2Linked to original sources
PubMed1991

Altered load dependence of postischemic myocardium.

Intermittent myocardial ischemia can produce areas of postischemic ("stunned") myocardium in the heart of the human with coronary artery disease. These areas are no longer ischemic, but have diminished contractile performance. Although the effects of loading conditions on systolic contraction of normal, ischemic, and failing myocardium have been investigated in great detail, the way in which load affects contraction of postischemic myocardium is not known. The aim of this study was to determine in anesthetized dogs how loading conditions affect the systolic function of a region of myocardium after 10 min of ischemia and 1 h of reperfusion. Sets of piezoelectric crystals were implanted in a test zone and in a remote zone of myocardium. Measurements of systolic wall thickening were made during nine combinations of left atrial pressure (3, 6, and 9 cmH2O) and mean arterial pressure (70, 90, and 110 mmHg). One set of measurements was made under baseline conditions, and a second set was made after 10 min of coronary occlusion and 1 h of reperfusion. Ischemia and reperfusion reduced wall thickening in the test zone 36 +/- 3% and diminished the response to increases in preload. In contrast, the response of the test zone to changes in afterload was unchanged. An interaction between the test zone (in which depressed contraction was observed) and the surrounding myocardium (in which enhanced function was observed) produced the appearance of a regional wall motion abnormality as afterload increased. These results emphasize that the load dependence of postischemic myocardium differs from that of normal myocardium and must be taken into account in clinical studies in which regional contraction is used to monitor the heart for ischemia.

Animals↗
PubMed1990

Computer simulation of the hemodynamic determinants of myocardial oxygen supply and demand.

A computer program was developed that uses a mathematical model of the cardiovascular system to predict myocardial oxygen supply and demand as well as cardiac hemodynamics. This model combines the time-varying elastance model of the left ventricle, the modified Windkessel model of the arterial system, and the left ventricular pressure-volume area prediction of myocardial oxygen demand. The computer simulation permits independent control of variables, thus providing the opportunity to design "experiments" and to observe the results. The model predicts that tachycardia leads to reduced myocardial oxygen supply and increased demand. Hypertension caused by increased systemic vascular resistance increases supply more than it increases demand. On the other hand, increased contractility or left ventricular end-diastolic pressure increases demand more than supply, and may cause ischemia in the presence of coronary artery stenosis. The model is an aid in understanding how hemodynamic variables affect the balance between myocardial oxygen supply and demand. It can be used for education and to analyze study protocols prior to animal experimentation.

Animals↗
PubMed1989

The quotient of mean arterial pressure and heart rate predicts hypoperfusion of collateral-dependent myocardium.

This study tested the hypothesis that the quotient of mean arterial pressure (MAP) and heart rate (HR) (pressure divided by rate = PRQ) effectively predicts myocardial hypoperfusion in regions of myocardium supplied with blood via collateral vessels. Regression analysis of data gathered in a study of the effects of halothane and atrial pacing on the distribution of myocardial blood flow has discovered a strong relationship between the PRQ and the inner-to-outer flow ratio in the collateral-dependent zone (R = 0.78). A significant relationship was also found between PRQ and the ratio of subendocardial blood flow in the ischemic zone to subendocardial flow in the normally perfused zone (R = 0.61). These ratios demonstrate that hypoperfusion of the inner layers of the collateral-dependent zone occurred during the condition of hypotension combined with tachycardia; while normal flow distribution was present if MAP exceeded HR. Halothane (1% end-tidal) did not alter the distribution of coronary flow, indicating that halothane does not cause a coronary steal in this model. The results of this study support the concept that the PRQ is an effective predictor of myocardial hypoperfusion when flow to ischemic zones is delivered by collateral vessels in nonfailing, canine hearts.

Animals↗
PubMed1989

The magnitude and duration of direct myocardial depression following intracoronary local anesthetics: a comparison of lidocaine and bupivacaine.

Direct myocardial depression plays a role in the cardiovascular toxicity of local anesthetic agents, but this role is obscured by concomitant cardiac, systemic, and CNS events: seizures, hypoxia, acidosis, sympathetic activation, bradycardia, and A-V heart block. Direct injection of small bolus doses of lidocaine and bupivacaine into a branch of the left coronary artery was used to minimize these systemic effects. Regional contraction in the zone supplied by the coronary artery was measured with a sonomicrometer. Both agents caused a dose-dependent reduction in the extent of systolic contraction, and a 4.9:1 (lidocaine:bupivacaine) dose ratio produced a 50% depression of contraction. The duration of depression, taken as the time for 95% recovery of systolic contraction, was about 25% (P less than 0.05) longer with bupivacaine for an equal degree of depression. Coronary blood flow was reduced modestly by both agents. These results suggest that differences in the magnitude or duration of direct myocardial depression cannot explain the clinical perception that the cardiovascular toxicity of bupivacaine is greater than that of lidocaine.

Anesthetics, Local↗
PubMed1988

The prevalence of steal-prone coronary anatomy in patients with coronary artery disease: an analysis of the Coronary Artery Surgery Study Registry.

Coronary steal requires a specific anatomic arrangement of coronary occlusion, collateral vessels, and stenosis of the artery supplying the collaterals. The prevalence of this anatomic variant, steal-prone coronary anatomy, was investigated in 16,249 patients with coronary artery disease whose angiograms were carefully recorded as part of the Coronary Artery Surgery Study (CASS). Almost half of the angiograms had one or more total occlusions, and, of these, about 80% had angiographically visible collateral supply to the area distal to the occlusion. Of subjects with an occlusion and collaterals, about 60% had a hemodynamically significant stenosis of the artery supplying the collateral vessels. In summary, 23% of the patients in the CASS Registry demonstrated steal-prone coronary anatomy. Thus, coronary steal could possibly affect almost a quarter of the patients with coronary artery disease having anesthesia. Studies that seek clinical evidence of harm from coronary steal must be done in that subset of patients with coronary artery disease with steal-prone anatomy.

Angiography↗
PubMed1988

Atrial natriuretic factor may mediate the renal effects of PEEP ventilation.

Mechanical ventilation with PEEP decreases urine output and urinary sodium excretion. Observed changes in cardiac output, renal blood flow, renin release, and antidiuretic hormone (ADH) secretion do not adequately explain the renal effects of PEEP. Altered release of atrial natriuretic factor (ANF), which is natriuretic and diuretic, may complete this explanation. The following hypothesis was tested: a PEEP-induced decrease in transmural right atrial pressure decreases ANF release, and this mechanism mediates subsequent alterations in renal function. Seven female mongrel dogs were anesthetized with halothane and their lungs ventilated mechanically for three consecutive 40 min periods of 0 PEEP, 10 cmH2O PEEP, and 0 PEEP. Addition of 10 cmH2O PEEP during mechanical ventilation decreased right atrial dimension and transmural right atrial pressure while intracavitary right atrial pressure was increased. Urine output was significantly decreased during PEEP, as were absolute and fractional excretion of sodium and osmolar clearance. PEEP ventilation resulted in a consistent and significant decline in plasma ANF concentration (82 +/- 11 to 62 +/- 11 pg/ml, P less than 0.05). Hemodynamic parameters, renal function, and ANF concentration returned to control values after cessation of PEEP. A second series of experiments in five dogs demonstrated a close temporal relationship between changes in atrial dimension or atrial transmural pressure, plasma ANF concentration, and urine output or sodium excretion. The results of this study demonstrate that PEEP-induced decreases in atrial distension resulted in decreased ANF release, which may mediate, in part, the antinatriuretic and antidiuretic effects of PEEP.

Animals↗
PubMed1987

Isoflurane induces coronary steal in a canine model of chronic coronary occlusion.

The hypothesis that isoflurane causes coronary steal was investigated in a canine model of chronic coronary occlusion. An ameroid constrictor was implanted in dogs to stimulate the development of intercoronary collateral vessels. During an acute experiment 3-4 weeks following implantation, heart rate, mean arterial pressure, and total coronary flow were held constant, and flow distribution was measured with microspheres in the presence and absence of isoflurane. Contractile function of the collateral-dependent zone and myocardial lactate extraction were also measured. Isoflurane produced a decrease in collateral flow and a decrement in collateral zone contraction, while, at the same time, enhancing flow in the normally perfused zone. In a second series of animals, isoflurane was found to have effects similar to those of adenosine, an arteriolar dilator known to produce coronary steal. In contrast, neither halothane nor nitrous oxide caused flow alterations or dysfunction of the collateral-dependent zone.

Adenosine↗
PubMed1987

Lack of direct coronary vascular effects of Escherichia coli endotoxin in dogs.

This study explored the hypothesis that coronary vascular injury and dysfunction result from intracoronary administration of Escherichia coli endotoxin (0.025 to 0.025 to 0.4 mg/kg) in dogs. Peak hyperemic coronary flow following a 15-sec period of stopped flow and the maximum flow in response to adenosine were used to estimate coronary vascular reserve. The wet-to-dry ratio of myocardial tissue was used to estimate extravascular water content as an indicator of vascular leak due to endothelial injury. Intracoronary saline was used as a control. Peak reactive hyperemia and maximum flow at constant coronary pressure were not different in the animals receiving intracoronary endotoxin (n = 6) and the animals receiving saline (n = 5) during 4 hr following treatment. In addition, wet-to-dry ratios were similar in these two groups. These data fail to support the hypothesis that endotoxin, per se, produces coronary vascular injury of sufficient magnitude to produce myocardial dysfunction.

Animals↗
PubMed1987

Adrenergic coronary vasoconstriction during myocardial underperfusion.

The effects of adrenergic alpha-receptor-mediated coronary vasoconstriction were examined in the presence of coronary stenosis and during experimental coronary hypoperfusion. Adrenergic coronary vasoconstriction was observed to operate even in the presence of coronary stenosis to limit oxygen delivery to the heart and increase myocardial oxygen extraction, but this vasoconstrictor effect did not result in myocardial lactate production. During constant coronary pressure perfusion the transmural distribution of alpha-receptor coronary vasoconstriction was determined with microspheres. A uniform transmural distribution of alpha-receptor-mediated vasoconstriction was observed at normal and subnormal perfusion pressures. During constant flow hypoperfusion, which permits transmural coronary steal, the left ventricular inner/outer blood flow ratio was more favorable with alpha-receptors intact than with alpha-receptors blocked. These findings indicate that alpha-receptor-mediated coronary vasoconstriction has an unexpected beneficial effect by lessening transmural steal during coronary hypoperfusion.

Animals↗
PubMed1986

Impaired systolic thickening associated with halothane in the presence of a coronary stenosis is mediated by changes in hemodynamics.

Myocardial ischemia results when halothane is administered to animals with severe coronary stenosis. This study was done to separate the effect of halothane, per se, on myocardial ischemia from indirect cardiovascular effects, primarily hypotension, that might cause ischemia by altering the oxygen supply-demand balance. Eight dogs underwent sterile surgery for implantation of sonomicrometer crystals and atrioventricular (A-V) heart block. One week later, each dog was anesthetized with morphine and chloralose. Heart rate was controlled by ventricular pacing and altered in five steps from 50 to 150 beats/min. Arterial blood pressure was controlled by blood withdrawal or phenylephrine infusion at four levels of arterial pressure (60 to 120 mmHg). Regional myocardial contraction was measured at each of the resulting 20 points as an indicator of myocardial ischemia. Twenty points were collected under each of four conditions in each animal: control, halothane (1% inspired), stenosis, halothane plus stenosis. Systolic thickening in the presence of stenosis was divided, on a point-by-point basis, by values obtained in the absence of stenosis to obviate the direct effects of blood pressure and heart rate on thickening. A separate normalization was done for data obtained in the presence of halothane. The normalized data demonstrate impaired systolic contraction at low arterial pressures and high heart rates. Multiple regression analysis failed to demonstrate a significant effect of halothane on systolic contraction once the effects of blood pressure, heart rate, and the negative inotropic effect of halothane were taken into account. Thus, the contraction failure that occurred during halothane and severe stenosis was mediated by changes in hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Hemodynamic determinants of ischemic myocardial dysfunction in the presence of coronary stenosis in dogs.

The effects of arterial blood pressure and heart rate on myocardial contraction were studied in a canine model of coronary stenosis. Systolic thickening of a region of myocardium supplied by a cannulated coronary artery was used as a measure of oxygen shortage. A glass stenosis in an external perfusion circuit that provided blood to the cannulated vessel was used to limit coronary flow. Mean arterial pressure was controlled by a blood reservoir and phenylephrine infusion and stabilized at four levels: 60, 80, 100, and 120 mmHg. At each blood pressure level, heart rate was increased by ventricular pacing in steps from 50 to 150 beats/min. Systolic thickening was measured at each of the resulting 20 combinations of blood pressure and heart rate. Measurements were made before cannulation, to serve as an unstenosed control, and following cannulation in the presence of moderate and severe stenoses. In the presence of the severe stenosis, ischemic dysfunction occurred when mean arterial pressure was decreased to 60 mmHg. At this pressure, dysfunction was most dramatic at rapid heart rates. In contrast, hypertension to a mean arterial pressure of 120 mmHg was well tolerated in these nonfailing hearts. Importantly, no single value of either blood pressure or heart rate was found to be associated with ischemia. The threshold for rate-induced ischemia depended on the coexisting value of blood pressure and vice versa. Ischemia was absent if mean arterial pressure exceeded heart rate, that is, if the pressure-rate ratio exceeded one.

Animals↗
PubMed1985

Parasympathetic control of transmural coronary blood flow in dogs.

The transmural distribution of coronary blood flow was studied during vagal stimulation in closed-chest, morphine- and alpha-chloralose-anesthetized dogs. The left main coronary artery was cannulated and perfused at constant pressure. Bradycardia during vagal stimulation was prevented by atrioventricular heart block and ventricular pacing. Beta-adrenergic receptors were blocked with propranolol (1 mg/kg iv), and aortic pressure was stabilized by means of a pressure reservoir. Regional myocardial blood flow was measured with 9-micron radioactive microspheres during vagal stimulation and during intracoronary acetylcholine infusion. Vagal stimulation increased coronary blood flow uniformly across the left ventricular wall. In contrast, intracoronary acetylcholine infusion, at a rate selected to increase total flow to the same degree, vasodilated the subendocardium more than the subepicardium, increasing the inner/outer blood flow ratio. It is concluded that both vagal activation and acetylcholine produce coronary vasodilation that is independent of left ventricular preload, afterload, and heart rate. Acetylcholine vasodilation preferentially vasodilates the subendocardium, increasing the inner/outer flow ratio, but vagal stimulation produces uniform vasodilation across the left ventricular wall.

Acetylcholine↗
PubMed1984

A new system of infiltration anesthesia and sedation for plastic surgery.

This technique produces patient cooperation during the phase of local anesthetic injection by judicious use of intravenous ketamine. The addition of diazepam and a narcotic drug to low-dose ketamine may account for a low incidence of hallucinations and psychic sensations. The use of a dilute solution of lidocaine and a very low concentration of epinephrine allows large areas to be anesthetized. The ultralow concentration of epinephrine provides effective vasoconstriction. The result is good patient acceptance, a stable blood pressure and heart rate, and a low incidence of complications classically associated with local anesthetic toxicity.

Adult↗
PubMed1984

Detection of anesthesia machine faults.

One hundred ninety people attending an anesthesia meeting were given ten minutes to identify five faults intentionally created in a standard anesthesia machine. 7.3% of participants found no machine faults and 3.4% found all five faults. The average number of identified faults was 2.2. Professional background did not influence the scores, but fault detection ability was increased in practitioners with ten years or more of experience. Concealed faults that did not make the machine inoperable were most frequently missed. Greater emphasis should be placed on aggressive system checking in education programs and in daily clinical practice.

Anesthesiology↗
PubMed1983

Effect of coronary artery pressure on transmural distribution of adrenergic coronary vasoconstriction in the dog.

The transmural distribution of alpha-receptor coronary vasoconstriction was studied in 14 closed-chest, morphine- and chloralose-anesthesized dogs. The alpha-receptor-blocking agent, phenoxybenzamine (0.25 mg/kg), was infused into either the anterior or circumflex coronary artery while collection of coronary sinus blood minimized recirculation. The left main coronary artery was cannulated and perfused at constant pressure. Myocardial lactate extraction and blood flow (9 micron radioactive microspheres) were measured during adrenergic activation with intracoronary norepinephrine (2 micrograms/min) at coronary artery pressures of 100, 70, 50, and 38 mm Hg. Flow was 15-25% less in the control region (alpha-receptors intact) than in the alpha-receptor-blocked region, in all layers of the left ventricular wall, at coronary pressures of 100 and 70 mm Hg. When coronary pressure was 50 mm Hg, lactate production resulted (-4% extraction) and significant alpha-receptor vasoconstriction was observed in the outer layer, but was marginal (P = 0.043) in the inner layer, of the left ventricle. Flows were not different in control and alpha-receptor-blocked regions at a coronary pressure of 38 mm Hg (lactate extraction -49%). These data indicate a uniform transmural alpha-receptor vasoconstriction at normal coronary artery pressures that diminished as the heart was progressively underperfused.

Animals↗