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Biomedical subjects

R E Katholi

Publications and source records attributed to R E Katholi.

At least 19 recordsLinked to original sources
PubMed1992

Increased incidence of silent ischemia after acute myocardial infarction.

OBJECTIVE: To determine the incidence of angina pectoris during induced myocardial ischemia in patients who have had thrombolytic therapy for acute myocardial infarction in comparison with patients with angina pectoris. DESIGN: During percutaneous transluminal coronary angioplasty, both study groups had coronary artery occlusion by the balloon dilatation catheter for 5 minutes. SETTING: A tertiary, cardiology referral center. PATIENTS: Twenty-five patients with angina pectoris who were undergoing angioplasty were compared with 30 patients having angioplasty 2 days after thrombolytic therapy for acute myocardial infarction. OUTCOMES: Development of angina pectoris during balloon occlusion of the coronary artery was the primary end point; the ischemic response and muscle viability were assessed using both surface and intracoronary electrocardiograms and pulmonary artery wedge pressure. RESULTS: During balloon occlusion 16 (64%) of 25 patients in the angina pectoris group developed angina. In contrast, nine (30%) of 30 patients in the thrombolysis group had angina pectoris during balloon occlusion of the infarct artery (P less than .01). The electrocardiographic response to ischemia and changes in pulmonary wedge pressure were similar in the two study groups. CONCLUSION: After thrombolytic therapy for myocardial infarction, silent ischemia may be the rule rather than the exception.

Angina Pectoris↗
PubMed1992

Six-year survival after coronary thrombolysis and early revascularization for acute myocardial infarction.

Six-year follow-up was conducted in a consecutive series of 192 patients receiving thrombolytic therapy for acute myocardial infarction (AMI) with ST-segment elevation. Cardiac catheterization was performed within a day, and patients with an open infarct artery routinely had early revascularization: 99 (67%) underwent coronary bypass surgery and 18 (12%) coronary angioplasty. With this treatment strategy, 6-year cardiac mortality was 14.5%, 6% (12 patients) in hospital and 9% (16 patients) for survivors of hospitalization. Multivariate analysis showed that predictors of cardiac death among survivors of hospitalization were a closed infarct artery at catheterization (p less than 0.01), diabetes (p less than 0.01) and anterior myocardial infarction (p = 0.01). A subset of 146 patients underwent radionuclide angiography before hospital discharge; for them, predictors of mortality were a closed infarct artery at catheterization (p less than 0.01), anterior wall AMI (p = 0.02), and Killip class III to IV on admission (p less than 0.06). Left ventricular ejection fraction was not a significant predictor of mortality for this subset of patients.

Aged↗
PubMed1992

Axial heterogeneity of adenosine transport and metabolism in the rabbit proximal tubule.

Transport and metabolism of adenosine were studied in the S1, S2, and S3 segments of the rabbit proximal renal tubule. Isolated segments were perfused in vitro with uniformly labelled 14C-adenosine to measure the lumen-to-bath flux of adenosine. This flux rate was measured by the disappearance of 14C from the luminal fluid (JD) and simultaneously by the appearance of 14C in the bathing solution (JA), expressed as femtomoles per minute per millimeter of tubule length (fmol.min-1.mm-1). At a perfused concentration of 83.3 microM adenosine, when corrected for metabolism, the JDs for adenosine in the S1, S2, and S3 segments were 735, 212, and 273, respectively. JAs, corrected for metabolism, were 0, 0, and 4.8 fmol.min-1.mm-1 for the S1, S2, and S3 segments, indicating that very little or no 14C-adenosine moved across the basolateral membrane. To correct for metabolism of 14C-adenosine, the perfusion fluid, collected fluid, tubular extract, and bathing fluid, from three tubules of each segment type, were analyzed by high-performance liquid chromatography to identify 14C-adenosine and its 14C-metabolites. At 83.3 microM, all segments metabolized adenosine extensively. Consequently, adenosine-5'-monophosphate (AMP) and inosine were found in tubule cells of all segments. Inosine also appeared in the collected fluid, but AMP did not. In S1 and S2 segments, none of the 14C in the bathing solutions could be identified and no adenosine was found. Of the small amounts of 14C found in bathing solutions from S3 segments, about 27% appeared to be adenosine, the rest were inosine and hypoxanthine or unidentified metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1990

Determinants of hospital charges for coronary artery bypass surgery: the economic consequences of postoperative complications.

This is a prospective study of 500 consecutive patients having coronary artery bypass surgery; mean hospital charge from time of surgery to discharge was +11,900 +/- 12,700. Multiple regression analysis was performed using preoperative variables and postoperative complications. No preoperative clinical feature was a significant predictor of higher average charge. Sternal wound infection (p = 0.0001), respiratory failure (p = 0.0001) and left ventricular failure (p = 0.017) were associated with higher average hospital charge. The absence of any complication predicted a lower average charge, and postoperative death (4.4 +/- 4.5 days after surgery) was also associated with lower average charge. A cost equation was developed: hospital charge equalled $11,217 + $41,559 of sternal wound infection, + $28,756 for respiratory failure, + $5,186 for left ventricular failure, - $1,798 for no complication and - $6,019 for death. Recognition of the influence of complications on charges suggests that low average charges can only be achieved by surgical programs with a low complication rate.

Aged↗
PubMed1990

Recurrent bacterial endocarditis in a man with tetralogy of Fallot: earliest recurrence on record.

Enterococcal endocarditis occurred in a young man with tetralogy of Fallot who had just completed therapy for staphylococcal endocarditis. The patient had a transient reversal of flow through the ventricular septal defect during staphylococcal endocarditis with lung abscesses and had persistently elevated teichoic acid antibody titers during the second episode caused by enterococcus. Our review of the literature on recurrent infective endocarditis indicates that our case represents one of the shortest intervals of recurrence with a second organism.

Adult↗
PubMed1990

Control of artifacts in plasma adenosine determinations.

The literature concerning the role of adenosine (ADO) in physiology reveals no agreement about plasma ADO concentrations and suggests two main sources of error in these determinations: rapid ADO uptake by red blood cells or rapid ADO production from ADO nucleotides, which may be released by any cell lysis or platelet aggregation during plasma preparation. We therefore studied ADO concentrations in plasma from normal human forearm venous blood. ADO was determined by a high-performance liquid chromatographic procedure with a sensitivity of 3 nM (original plasma). Observed ADO concentrations ranged from 894 nM to 8.2 nM depending on the conditions of plasma preparation. In plasma prepared in plastic tubes from 4.5 ml of blood drawn into a plastic syringe containing 1.5 ml of an isotonic stopping solution (pH 7.4) containing heparin (60 units ml), dilazep (40 microM), EGTA (40 mM, EDTA (40 mM), erythro-9-(2-hydroxy-3-nonyl) adenine (40 microM), and alpha, beta-methylene adenosine-5'-diphosphate (525 nM), the plasma ADO concentration was 13.3 +/- 1.88 nM (SE) after correction for a simultaneous ADO recovery determination. The mean ADO recovery was 78% +/- 3.39. The mean plasma ADO concentration found by this method of collection and preparation is lower then reported by others. Proper collection methods are required to avoid artifacts when determining plasma ADO concentrations.

Adenosine↗
PubMed1988

Endogenous intrarenal adenosine preserves renal blood flow in one-kidney, one clip rats.

Intrarenal adenosine concentration is threefold greater in the one-kidney, one clip hypertensive rat compared with normotensive animals. Since exogenously administered adenosine may increase renal blood flow by direct vasodilation, inhibition of renin release, or prejunctional interruption of adrenergic neurotransmission, these studies examined whether endogenous intrarenal adenosine maintains renal blood flow distal to renal arterial stenosis. Administration of theophylline, which blocks the direct vasodilating effect of adenosine and antagonizes the inhibitory effect of adenosine on renin release and sympathetic neurotransmission, resulted in marked renal vasoconstriction in one-kidney, one clip hypertensive animals. This theophylline-induced renal vasoconstriction was markedly attenuated by angiotensin II blockade with saralasin and was unchanged by renal denervation or beta 1-adrenergic blockade with atenolol. These findings indicate that the marked renal vasoconstriction in one-kidney, one clip hypertension during theophylline administration is mainly mediated by angiotensin II, is to a lesser degree due to inhibition of adenosine-induced vasodilation, and is independent of sympathetic influences. These data suggest that endogenous interstitial adenosine preserves renal blood flow in one-kidney, one clip hypertension mainly by inhibiting renin release.

Adenosine↗
PubMed1987

Afferent renal nerves and hypertension.

Adenosine-sensitive nerve endings have been found in the renal pelvis which when stimulated increase sympathetic activity producing hypertension. When urinary adenosine concentration is lowered by intrarenal infusion of adenosine deaminase in one-kidney one-clip rats, peripheral sympathetic nervous system activity and arterial pressure decrease if the renal nerves are intact. These data suggest that a stimulus for afferent renal nerve activity in one-kidney, one-clip hypertension is intrarenal adenosine. This intrarenal adenosine hypertensive reflex was examined further observing the responses to renal pelvic xylocaine infusion, selective renal deafferentation, adrenal demedullation and spinal cord transection (T6). The intrarenal adenosine hypertensive reflex was interrupted by renal pelvic xylocaine infusion, renal deafferentation and adrenal demedullation in normotensive and one-kidney, one-clip hypertensive animals. The intrarenal adenosine hypertensive reflex persisted after spinal cord transection (T6). These data support the concept that adenosine-sensitive intact afferent renal nerves located in the renal pelvis enhance sympathoadrenal activity resulting in the maintenance of one-kidney, one-clip hypertension and that this intrarenal adenosine-hypertensive response may occur as a spinal-level reflex in the rat.

Adenosine↗
PubMed1985

Transient paradoxical renal vasoconstriction following cardiac operation. Treatment with volume depletion.

Following cardiac operation complicated by inferior myocardial injury, a patient developed normal cardiac output congestive heart failure associated with severe renal vasoconstriction, oliguria and azotemia. The patient's renal dysfunction responded to volume depletion with hemofiltration. These paradoxical renal responses to volume changes may be caused by transiently altered cardiac volume receptor thresholds or afferent signals resulting in cardiorenal dysfunction.

Constriction, Pathologic↗
PubMed1985

Renal nerves and hypertension: an update.

Increased efferent renal sympathetic nerve activity could facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the deoxycorticosterone acetate-salt-treated rat, which suggests that these responses result from, at least in part, loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in humans. The efferent renal sympathetic nerves play a diminishing role once hypertension is established in these models. Renal denervation in established one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not caused by changes in renin activity or sodium excretion but is associated with decreased sympathoadrenal activity. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. Interruption of afferent renal fibers also appears to be the mechanism by which renal denervation prevents or reverses the normal increase in arterial pressure seen after aortic baroreceptor deafferentation in the rat.

Adrenal Medulla↗
PubMed1984

Intrarenal adenosine produces hypertension by activating the sympathetic nervous system via the renal nerves in the dog.

Studies from our laboratory suggest that the afferent renal nerves from the clipped kidney enhance sympathetic nervous system activity in established one-kidney, one clip and two-kidney, one clip Goldblatt hypertension. Because adenosine is released during renal ischaemia and adenosine has been shown to increase the frequency of afferent renal nerve signals, we proposed the hypothesis that intrarenal adenosine might produce hypertension by activating the sympathetic nervous system via the afferent renal nerves. To examine this hypothesis, changes in arterial pressure and activity of the sympathetic nervous system were measured during renal artery infusion of adenosine before and after renal denervation in uninephrectomized sodium replete conscious dogs. Intrarenal adenosine infusion produced a 21 +/- 3 mmHg mean arterial pressure rise in association with an increase in plasma norepinephrine. Ganglionic blockade during intrarenal adenosine infusion resulted in a significantly greater decrease in arterial pressure compared to control responses. After renal denervation, intrarenal adenosine infusion resulted in no change in arterial pressure, plasma norepinephrine or arterial pressure response to ganglionic blockade. To further assess sympathetic activity changes, right renal norepinephrine secretion and multifibre efferent neural traffic were measured during left renal artery adenosine infusion in alpha-chloralose-anaesthetized dogs. Left renal artery adenosine infusion resulted in increased right renal vascular resistance in association with increased renal norepinephrine secretion and increased efferent neural activity. The data indicate that in the dog with intact renal nerves, intrarenal adenosine produces hypertension by activating the sympathetic nervous system.

Adenosine↗
PubMed1983

Neurohumoral mechanisms in acute aortic coarctation in conscious and anesthetized dogs.

To study the interactions of the renin-angiotensin system, sodium balance, and the sympathetic nervous system in the development of coarctation hypertension, an aortic gradient was created with a pneumatic cuff in 11 chronically instrumented conscious dogs. Significant hypertension associated with a significant rise in plasma renin activity and sodium retention occurred within 48 h. Competitive angiotensin II blockade caused a greater decrease in arterial pressure after coarctation than before coarctation. In contrast, plasma norepinephrine decreased significantly from control levels after coarctation, and alpha-adrenergic blockade with phentolamine caused less of a decrease in arterial pressure than before coarctation. This decrease in sympathetic activity was also accompanied by a decreased blood pressure response to pressor doses of angiotensin II and methoxamine after coarctation. To assess carotid baroreceptor influence on acute coarctation hypertension, aortic blood pressure responses to pressor agents were determined in 12 chlorolose-urethan-anesthetized dogs while carotid sinus pressure was independently varied. Maintaining carotid pressure at control levels after aortic constriction restored blood pressure responses to pressor agents to before-coarctation levels. These results suggest that 1) activation of the renin-angiotensin system and sodium retention contribute to the development of coarctation hypertension, and 2) there is a carotid sinus baroreceptor-mediated decrease in alpha-adrenergic activity with acute coarctation hypertension.

Angiotensin II↗
PubMed1983

Renal nerves in the pathogenesis of hypertension in experimental animals and humans.

Efferent renal innervation is composed of postganglionic sympathetic fibers to the renal arterioles, juxtaglomerular apparatus, and renal tubules. Increased efferent renal sympathetic nerve activity results in increased renal vascular resistance, renin release, and sodium retention. These responses from enhanced renal sympathetic activity contribute to normal cardiovascular homeostasis but could also facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the DOCA-salt-treated rat, suggesting that these responses are due, at least in part, to loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in man. Recent studies indicate that the kidney is a sensory organ with mechano-receptive and chemoreceptive afferent renal nerves involved in renorenal and cardiovascular regulation. Renal denervation in established one-kidney one-clip and two-kidney one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not due to change in renin activity or sodium excretion but is associated with decreased activity of the sympathetic nervous system. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. The role of the afferent renal nerves in renovascular hypertension in humans warrants further study.

Adenosine↗
PubMed1982

Decrease in peripheral sympathetic nervous system activity following renal denervation or unclipping in the one-kidney one-clip Goldblatt hypertensive rat.

Increased sympathetic nervous system activity has been demonstrated in established one-kidney one-clip hypertension in the rat. We have found that renal denervation in this model results in an attenuation of hypertension, unassociated with alterations in sodium or water balance or renin activity. To determine whether the depressor effect of renal denervation is associated with changes in peripheral sympathetic nervous system activity, sham operation (n = 12), renal denervation (n = 13), or unclipping (n = 13) was carried out 2 wk after the onset of one-kidney one-clip hypertension. Normotensive unine-phrectomized age- and sex-matched rats were used as controls (n = 14). Renal denervation resulted in a significant decrease in systolic blood pressure (201+/-7 to 151+/-6 mm Hg), while unclipping lowered systolic blood pressure to normotensive levels (130+/-6 mm Hg). 8 d after operation plasma norepinephrine and mean arterial pressure before and after ganglionic blockade with 30 mg/kg hexamethonium bromide were measured in conscious, unrestrained, resting animals, as indices of peripheral sympathetic nervous system activity. Plasma norepinephrine was significantly higher in hypertensive sham-operated rats (422+/-42 pg/ml) compared with normotensive controls (282+/-25 pg/ml) (P < 0.01). Both renal denervation and unclipping restored plasma norepinephrine to normal levels (273+/-22 and 294+/-24 pg/ml, respectively). Ganglionic blockade in hypertensive sham-operated animals resulted in a significantly greater decrease in mean arterial pressure than occurred in renal denervated, unclipped, or control rats. The data suggest that the depressor effect of renal denervation or unclipping in the one-kidney one-clip hypertensive rat is associated with a decrease in peripheral sympathetic nervous system activity.

Animals↗
PubMed1979

Mechanism of postarrhythmic renal vasoconstriction in the anesthetized dog.

The mechanism of postarrhythmic renal vasoconstriction was studied in 28 dogs anesthetized with pentobarbital sodium (30 mg/kg i.v.). Rapid atrial or ventricular pacing or induction of atrial fibrilation were used to produce at least 20% prompt decrease in cardiac output and mean arterial blood pressure. Return to control cardiac output and blood pressure occurred within 3 minutes after cessation of the arrhythmia, but renal blood flow remained significantly decreased (26%) with gradual recovery by 17.7 +/- 6.6 min. Infusion of phentolamine (0.25 mg/min) into the renal artery, intravenous hexamethonium (l mg/kg), adrenal demedullation, or cooling the cervical vagi prevented postarrhythmic renal vasoconstriction. In contrast, renal denervation, intravenous bretylium (10 mg/kg), intravenous atropine (0.5 mg/kg) or intrarenal SQ 20881 (0.20 mg/min) has no effect on postarrhythmic renal vasoconstriction. Intravenous propranolol (0.5 mg/kg) intensified postarrhythmic renal vasoconstriction. These data suggested that the postarrhythmic renal vasoconstrictive response required intact vagi and was due to alpha adrenergic stimulation by adrenal catecholamines. However, femoral arterial catecholamine levels were not elevated above control during postarrhythmic renal vasoconstriction. We therefore sought local vascular pathways by which catecholamines might reach the kidneys. An adrenorenal vascular network was found in each dog. Collection of catecholamines from these vessels during postarrhythmic renal vasoconstriction in six dogs revealed catecholamine concentrations threefold higher than simultaneously collected femoral arterial catecholamines levels. Because ligation of these vessels abolished postarrhythmic renal vasoconstriction in each dog, we conclude that postarrhythmic renal vasconstriction is due to adrenal catecholamines reaching the kidneys through an adreno-renal vascular network and that the response requires intact vagi.

Adrenal Glands↗