Search PubMed⌕ Search

Biomedical subjects

W M Daggett

Publications and source records attributed to W M Daggett.

At least 19 recordsLinked to original sources
PubMed1992

Monitoring myocardial reperfusion injury with NADH fluorometry.

Using NADH fluorometry to monitor myocardial metabolism, the mechanism of reperfusion injury was investigated after the delivery of an experimental reperfusate. Using an isolated working heart preparation, rat hearts underwent 15 min of global ischemia at 37 degrees C. Following the ischemic insult, an oxygenated enriched reperfusion solution was given for 5 min. The hearts were then returned to a working state and aortic flow recorded to evaluate recovery. NADH levels were monitored throughout the experiment with a fluorometer and glycogen, AMP, ADP, and ATP were measured biochemically pre- and postischemia, after reperfusion and after recovery. In this study, reperfusion injury was best abated by an enriched reperfusate. Our results indicate the mechanism for this amelioration is not high-energy phosphate replenishment. Rather, as indicated by NADH fluorescence, the hearts attain an intermediate level of metabolism that permits glycogen to be restored and functional recovery to be improved.

Animals↗
PubMed1992

Relationship between septal perfusion, viability, and motion before and after coronary artery bypass surgery.

The etiology of abnormal interventricular septal motion occurring after open-heart surgery using cardiopulmonary bypass has not been clarified. Intraoperative ischemic septal injury has been proposed as one explanation for this finding. To examine this possibility, resting septal perfusion and viability were studied using rest and redistribution thallium-201 scintigraphy in 16 patients before and after coronary artery bypass surgery. The results were compared with septal motion on preoperative and postoperative resting gated blood pool scans. Preoperatively, septal thallium uptake was normal in 10 of 16 patients, and septal motion was normal in 14 of 16. Postoperatively, septal thallium uptake was normal in 11 of 16 patients, while septal motion was abnormal in all. Thus abnormal postoperative septal motion is usually associated with normal septal perfusion and viability on thallium scans and therefore is not the result of septal ischemic injury in a majority of patients.

Adult↗
PubMed1992

Intraoperative aortic dissection.

Intraoperative aortic dissection is a rare but potentially fatal complication of open heart operations. If the dissection is promptly recognized and repaired, however, the outcome may be significantly better. In this study, we reviewed the hospital records of patients with dissection of the aortic arch occurring as a complication of a cardiac operation at Massachusetts General Hospital and Mt. Auburn Hospital from January 1980 through June 1990. During this period, 14,877 surgical procedures with the use of cardiopulmonary bypass and aortic cannulation were performed, and 24 patients (0.16%) with iatrogenic aortic dissection were identified. Dissection was discovered intraoperatively in 20 patients and postoperatively after complications developed in 4. Of the 20 patients whose injuries were discovered intraoperatively and repaired, 4 (20%) died. Of the 4 whose injuries were discovered after operation, 2 (50%) died. The primary cause of death was ventricular dysfunction resulting from myocardial ischemia. Dissections originated at the aortic cannulation site in 10 patients, at the cross-clamp site in 8, at the site of the partial-occlusion clamp in 7, at the proximal anastomosis in 1 patient, and as a result of direct injury in 1. Three of these patients had simultaneous injuries at the aortic cannulation site and at the heel of the partial-occlusion clamp. Two techniques of repair were used: primary repair and patch or tube graft insertion. There were two deaths in the patients who underwent primary repair and four deaths in patients requiring graft replacement. Although it is uncommon, intraoperative aortic dissection can be a lethal complication of cardiac operations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Postinfarct ventricular septal defect repair: effect of coronary artery bypass grafting.

Between June 1968 and April 1991, 75 patients who had undergone coronary angiography underwent repair of a postinfarction ventricular septal defect. Group 1 (n = 33) includes patients who had two- or three-vessel serious (> 75% narrowing) proximal coronary artery disease and underwent complete revascularization in addition to repair of the ventricular septal defect. Group 2 (n = 19) patients also had two- or three-vessel coronary artery disease but bypass grafting was not performed; only the ventricular defect was repaired. Group 3 (n = 23) patients had only single-vessel coronary artery disease that corresponded to the region of the infarct; they underwent ventricular septal defect repair only. Follow-up of hospital survivors was 96% complete at a mean of 86.2 months (range, 1 to 288 months). Hospital mortality after ventricular septal defect repair was 21.2% in the cohort with bypassed coronary artery disease (group 1), 26.3% in those with unbypassed disease (group 2), and 26.1% in those with only single-vessel coronary artery disease (group 3) (p = 0.88). With follow-up after 5 and 10 years, the actuarial survival was 72.2% +/- 8% and 47.8% +/- 10%, respectively, in the bypassed group, 29.2% +/- 11% and 0%, respectively, in the unbypassed group, and 52.2% +/- 10% and 36.5% +/- 11%, respectively, in the cohort with single-vessel disease. Bypassing associated coronary artery disease significantly increased long-term survival when compared with patients with unbypassed coronary artery disease (p = 0.0015).

Aged↗
PubMed1992

Blunt injuries of the thoracic aorta.

We managed 51 patients with thoracic aortic injuries caused by blunt trauma between 1977 and 1990. Forty-nine injuries were located in the upper descending aorta and one each in the ascending aorta and aortic arch. Three patients arrived moribund and underwent thoracotomy for resuscitation, and all died. The diagnosis was confirmed by aortography in 48. One patient died of aortic rupture, 1 died of hypoxemia, and 1 refused operation and died. Forty-four patients had aortic repair, 42 with graft insertion. Gott shunts were placed in 23 with 3 cases of paraplegia (13%). Simple cross-clamping was used in 19 with 1 case of paraplegia (5.2%). We found statistically significant differences between the cross-clamp times of patients without paraplegia compared with those in whom paraplegia developed in both the shunt and no-shunt groups. Logistic regression analysis showed that the only factor significantly associated with paraplegia was cross-clamp time. There were two postoperative deaths (4.4%). Seven patients had medical therapy initially and aortic repair was delayed to allow other injuries to stabilize. Before aortic repair, 18 patients had intraarterial pressure monitoring and 34 received beta-blockers or antihypertensive drugs. We conclude that aortic repair with graft insertion is usually successful in nonmoribund patients, simple cross-clamping is associated with a relatively low risk of paraplegia, the incidence of paraplegia is directly associated with the duration of cross-clamp time, and selected patients can be managed medically while awaiting aortic repair.

Adolescent↗
PubMed1992

Survival after repair of postinfarction ventricular septal defects in patients over the age of 70.

Ventricular septal defect (VSD) is an infrequent but extremely serious complication of myocardial infarction. Operative mortality rates tend to be higher in the elderly population; however, long-term follow-up has not been specifically studied. It is, therefore, important to assess not only the early but also the long-term results of VSD repair in patients over 70 years of age to determine its value for the elderly patient. Between June 1968 and May 1991, 86 patients who experienced a myocardial infarction underwent surgical repair of an infarct related VSD at the Massachusetts General Hospital (MGH). Group I (n = 57) includes those patients younger than 70 years, and group II (n = 29) represents those patients age 70 years and older. Follow-up of hospital survivors ranged from 1 month to 24 years and was compiled in April and May, 1991. Three patients were lost to follow-up (4%), and these were younger than 70 years of age. There were no differences in the values of the preoperative variables for the younger and older groups with respect to sex, concomitant procedures performed (bypass vs no bypass), use of an intra-aortic balloon pump (IABP), location of VSD, presence of shock, total hospital days, or days between infarction and operation. There was, however, a difference between the two groups relative to the era when surgery was performed. More patients over the age of 70 underwent surgery after 1978 than before 1978 (p = 0.0012). The majority of survivors are in New York Heart Association (NYHA) Class I or II, and there was no difference between the younger and older groups in functional class at the time of follow-up (83.3% vs 91.7% of survivors in Class I or II, respectively). Using the generalized Wilcoxon test to analyze these survival data, there was no apparent difference in long-term survival (p = 0.97) when comparing the two age groups. The mean follow-up period was 77.02 months for the younger group and 80.52 months for the older group. The fact that more older patients were repaired after we had significant experience in the surgical management of patients with VSDs probably accounted for our excellent results in the older age group. Our data reveal that patients over the age of 70 can expect excellent long-term survival, with over 90% of these survivors remaining in NYHA Functional Class I or II.

Adult↗
PubMed1992

Norepinephrine increases the economy of pressure development in isolated canine hearts.

To test for oxygen wasting by norepinephrine (NE) without relying on normalization by measures of performance such as the pressure-volume area, myocardial oxygen consumption (MVO2) was determined for isovolumic beats at five different left ventricular (LV) end-diastolic volumes (EDV) in nine isolated cross-perfused canine hearts in each of three states: a basal anesthetic state (B); after depression with halothane (H); and after adding NE to increase contractility back to the B state (H+NE). The end-diastolic and peak systolic pressure-volume lines were identical for B and H+NE. The R2 for a linear regression of MVO2 per beat for B vs. H+NE for beats originating at the same EDV and developing similar (within 10%) peak isovolumic pressures for all hearts was 0.85. The slope and intercept were 0.83 and 0.01, which are significantly less than one (P less than 0.001) and greater than zero (P less than 0.001), respectively. These data suggest that NE increases both the economy of pressure development as well as activation energy of an isovolumically contracting LV.

Animals↗
PubMed1992

Benefits of glucose and oxygen in multidose cold cardioplegia.

We tested the effects of glucose and oxygen in cardioplegic solutions on myocardial protection in the isolated perfused working rat heart. Recovery from 2 hours' hypothermic (8 degrees C) cardioplegic arrest was examined in 93 hearts. Cardioplegic solution, which was delivered every 15 minutes, was supplemented with glucose 28 mmol/L as a substrate or sucrose 28 mmol/L as a nonmetabolizable osmotic control; it was equilibrated with either 98% oxygen or 98% nitrogen, both with 2% carbon dioxide. Four combinations of hyperkalemic cardioplegic solution were studied: nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose. During hypothermic arrest, oxygenation of cardioplegic solution greatly reduced myocardial lactate production and prevented ischemic contracture as indicated by coronary vascular resistance. Glucose increased lactate production modestly but significantly only when the cardioplegic solution was nitrogenated. Although end-arrest myocardial adenosine triphosphate and creatine phosphate were greatly increased by oxygenation of cardioplegic solution (p less than 0.005), we could not detect improved preservation of these high-energy phosphates by glucose. Averaged over reperfusion, percent recovery of cardiac output for the nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose solutions was 32.3% +/- 6.1%, 45.9% +/- 4.6%, 44.5% +/- 4.6%, and 62.2% +/- 4.5%, respectively. Oxygenation of the glucose solution or addition of glucose to the oxygenated solution significantly improved recovery of cardiac output. The benefits of glucose and oxygen were additive, so that the oxygen-glucose cardioplegic solution provided the best functional recovery. We conclude that the addition of glucose to the fully oxygenated multidose cold cardioplegic solution improves functional recovery without increasing lactate production during arrest.

Adenine Nucleotides↗
PubMed1991

Oxygenated cardioplegia: the metabolic and functional effects of glucose and insulin.

Reports differ as to the efficacy of glucose and insulin as cardioplegic additives. Although deliberate oxygenation of crystalloid cardioplegic solutions improves myocardial protection, little is known about the protection afforded by glucose and insulin in such oxygenated solutions. In the isolated working rat heart, we studied the addition of oxygen, glucose, and insulin, separately and together, to a cardioplegic solution. The solution was equilibrated with O2 or N2, with glucose added as a substrate or sucrose as a nonmetabolizable osmotic control, with or without insulin. Hearts were arrested for 2 hours at 8 degrees C by multidose infusions. Oxygenation decreased lactate production and improved high-energy phosphate and glycogen preservation during arrest, prevented ischemic contracture, and improved functional recovery. The addition of glucose to the oxygenated solution increased the level of adenosine triphosphate at end-arrest from 10.5 +/- 0.5 to 13.9 +/- 0.6 nmol/mg dry weight and glycogen stores from 18.7 +/- 2.5 to 35.7 +/- 5.5 nmol/mg dry weight. The further addition of insulin did not better preserve these metabolites. Improvements in functional recovery due to glucose or insulin in the oxygenated solution attained statistical significance when both additives were included. Glucose increased lactate production significantly only when the solution was nitrogenated. Insulin added to the nitrogenated glucose-containing solution increased adenosine triphosphate and glycogen levels after 1 hour of arrest; and, although insulin did not prevent ischemic contracture from developing during the latter part of arrest with profound depletion of these metabolites, functional recovery was improved. The mechanism of improved functional recovery by insulin is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1991

Relation of myocardial protection to cardioplegic solution pH: modulation by calcium and magnesium.

The relationship between myocardial preservation and cardioplegic solution pH was assessed in isolated, perfused rat hearts. A base solution without calcium or magnesium and the same solution containing 0.2 mmol/L ionized calcium or 16 mmol/L magnesium or both ions were studied at several values of pH between 6.8 and 8.7. Hearts were arrested at 8 degrees C by multidose infusions of these bicarbonate-buffered solutions bubbled with oxygen and a varying percentage of carbon dioxide to control pH. Diastolic tone (left ventricular balloon) and adenosine triphosphate (ATP) depletion during arrest both increased as the cardioplegic solution became more alkaline. Calcium increased these effects of pH. Magnesium weakened the effect of pH on diastolic tone, maintained ATP at all pH levels, and inhibited the effects of calcium on the relationships of pH to diastolic tone and ATP. When data from all solutions were considered together, ATP depletion was shown to be linearly related to diastolic tone. Calcium depressed functional recovery (left ventricular developed pressure during reperfusion expressed as a percentage of its prearrest value) at all pH levels. With the other solutions, recovery was similar and best within a broad and relatively alkaline pH range. With the solution containing calcium and magnesium, at pH levels of 8.28 +/- 0.02, 7.87 +/- 0.03, 7.58 +/- 0.02, 7.41 +/- 0.01, 7.06 +/- 0.02, and 6.80 +/- 0.01, recovery at 5 minutes of reperfusion was 101.4% +/- 3.7%, 102.9% +/- 2.8%, 107.3% +/- 3.7%, 102.8% +/- 2.9%, 91.8% +/- 3.6%, and 94.3% +/- 3.5%, respectively. This effect of alkalinity was short-lived. Extreme alkalinity of the base, acalcemic solution produced the calcium paradox, as reported previously. Good preservation of ATP by the most acid solutions did not predict good functional recovery. Magnesium increased the persistence of frequent extrasystoles during early reperfusion, but the effect was attenuated by calcium. The data support the inclusion of magnesium in cardioplegic solutions, particularly when they contain calcium, show that cardioplegic solution pH can have major effects on the arrested heart, and suggest that a relatively alkaline pH may modestly benefit functional recovery.

Adenine Nucleotides↗
PubMed1991

Protection of the hypertrophied myocardium by crystalloid cardioplegia.

Patients with left ventricular hypertrophy (LVH) have a worse outcome after cardiac surgery than those without hypertrophy. We studied protection of hearts with LVH in an isolated rat heart model using multidose, cold, oxygenated cardioplegia. LVH was produced by banding the abdominal aorta in young rats. Six weeks after banding, this produced a 31% increase in the left ventricular dry weight/body weight ratio compared to two age-matched control groups comprising sham-operated and nonoperated animals. The recovery of cardiac output after arrest was higher in LVH (82 +/- 4% of prearrest) than in sham-operated (69 +/- 4%) or nonoperated (66 +/- 3%) control groups. The improved functional recovery in LVH occurred although there were no differences among the groups in myocardial adenosine triphosphate (ATP) and phosphocreatine (PCr) prior to arrest, at the end of arrest, or after reperfusion. Glycogen levels were also similar among the three groups prior to arrest and after reperfusion but were highest in LVH after arrest. Myocardial oxygen consumption (MVO2) and efficiency, expressed as cardiac output/MVO2, were similar among the groups prior to arrest. Myocardial efficiency after reperfusion declined in all groups but was best preserved in LVH. We also compared the sensitivity of hypertrophied and control hearts to the deleterious effects of calcium in cardioplegia. Calcium in the cardioplegia increased myocardial lactate production during arrest in a dose-related fashion and depressed myocardial levels of ATP, PCr, and glycogen at end arrest in all groups. Cardiac output recovery was also depressed by calcium but was still best in LVH. We conclude that the hypertrophied myocardium is well protected by standard cardioplegia and that calcium in cardioplegia does not preferentially depress recovery in LVH.

Animals↗
PubMed1991

The safety of intraaortic balloon pump catheter insertion through suprainguinal prosthetic vascular bypass grafts.

To determine the safety of intraaortic balloon pump catheter insertion for critical coronary ischemia through suprainguinal prosthetic bypass grafts, we examined our experience of 19 intraaortic balloon pumps placed through grafts in 17 patients by means of surgical exposure (8) or the percutaneous (11) approach. Fourteen intraaortic balloon pumps were placed through matured grafts at a time remote (2 to 13 years; mean, 7 years) from their vascular bypass surgery. Five were inserted through nonmatured grafts during the same hospitalization as their vascular reconstructive surgery (1 to 12 days; mean, 4 days). One patient, a day after an aortoiliac bypass, died during an urgent, surgical intraaortic balloon pump insertion for cardiogenic shock. All other patients had prompt reversal of their cardiac ischemia. Decreased limb perfusion developed during use of the intraaortic balloon pump in three patients, all of whom had their intraaortic balloon pump placed percutaneously through mature grafts. Two of these required surgical thrombectomy. Ten intraaortic balloon pump insertions in eight patients survived the hospitalization and were followed for a mean of 24 months (range, 2 weeks to 64 months). No localized groin or graft infections were identified. No bleeding complications or pseudoaneurysms occurred. Thus in patients with unstable, severe, cardiac disease, intraaortic balloon pumps can be safely placed through indwelling suprainguinal bypass grafts.

Aged↗
PubMed1990

Postinfarction ventricular septal defect repair: retrospective thoughts and historical perspectives.

Evolution of surgical techniques for repair of postinfarction ventricular septal rupture initially involved differentiation of these lesions from prior experience with surgical approaches to congenital ventricular septal defects, which were in the main not applicable. Second, understanding of the differing anatomical locations of postinfarction ventricular septal defects required innovation in terms of the location of the cardiotomy and type of repair necessary to achieve a successful result in any given patient. The gradual appreciation of different clinical courses pursued by patients after postinfarction ventricular septal rupture both in terms of location of the defect and the degree of right ventricular functional impairment has led to increased urgency relative to the timing of surgical repair. The incorporation of specific anatomical concepts of surgical repair and better understanding of the time course of physiological deterioration of patients can ultimately lead to an integrated approach aimed toward improved salvage of patients suffering this catastrophic complication of acute myocardial infarction.

Cardiac Surgical Procedures↗
PubMed1990

Late results with Carpentier-Edwards porcine bioprosthesis.

From 1977 to 1984, 429 patients underwent aortic valve replacement (AVR), and 339 underwent mitral valve replacement (MVR) with a Carpentier-Edwards bioprosthesis. Early mortality for AVR was 4.6% (isolated AVR, 1.9%) and for MVR was 5.3% (isolated MVR, 4.1%). Follow-up was 99.3% complete at a mean of 5.9 years. Actuarial event-free rates at 10 years for AVR and MVR were, respectively, 1) for structural valve deterioration, 91.4 +/- 3.2% versus 75.1 +/- 4.0% (p less than 0.01); 2) for nonstructural dysfunction, 100% versus 97.8 +/- 1.6% (p = NS); 3) for thromboembolism, 90.6 +/- 2.3% versus 87.3 +/- 2.6% (p = NS); 4) for anticoagulant-related bleeding, 95.3 +/- 1.1% versus 88.6 +/- 2.4% (p = 0.05); 5) for endocarditis, 87.8 +/- 5.7% versus 90.6 +/- 2.4% (p = NS); 6) for reoperation, 91.0 +/- 2.5% versus 74.4 +/- 3.7% (p less than 0.01); 7) for valve-related mortality, 76.1 +/- 6.9% versus 71.4 +/- 5.2% (p = 0.01); 8) for permanent physical impairment, 85.0 +/- 3.0% versus 71.5 +/- 3.6% (p less than 0.01); and 9) for combined operative mortality, valve-related mortality, and reoperation, 68.7 +/- 6.4% versus 51.5 +/- 4.9% (p = 0.01). No structural valve dysfunction was observed in any AVR patient whose valve was inserted after age 70. Age at operation was the only factor that predicted structural valve deterioration (p less than 0.01).

Actuarial Analysis↗
PubMed1989

Myocardial preservation related to magnesium content of hyperkalemic cardioplegic solutions at 8 degrees C.

This study investigates whether the addition of magnesium to a hyperkalemic cardioplegic solution containing 0.1 mM ionized calcium improves myocardial preservation, and whether there is an optimal magnesium concentration in this solution. Isolated perfused rat hearts were arrested for two hours by this cardioplegic solution, which was fully oxygenated and infused at 8 degrees C every 15 minutes to simulate clinical conditions. The cardioplegic solution contained either 0, 2, 4, 8, 16, or 32 mM magnesium. At end-arrest, the myocardial creatine phosphate concentration (nanomoles per milligram of dry weight) was 20.7 +/- 2.1, 22.9 +/- 1.7, 24.8 +/- 2.0, 31.3 +/- 1.4, 33.1 +/- 1.8, and 31.6 +/- 0.8, respectively, in hearts given cardioplegic solution containing these magnesium concentrations. Thus, the concentration of creatine phosphate was significantly higher at end-arrest when the cardioplegic solution contained 8, 16, or 32 mM than 0 or 2 mM magnesium (p less than 0.002) or 4 mM magnesium (p less than 0.02), and highest with 16 mM magnesium. Also, creatine phosphate was more sensitive to the magnesium concentration of the cardioplegic solution than was end-arrest adenosine triphosphate levels, which did not differ among the experimental groups. Aortic flow, expressed as a percentage of prearrest aortic flow, was 60.3 +/- 5.0, 70.2 +/- 5.5, 71.6 +/- 4.4, 71.8 +/- 4.8, 81.0 +/- 5.0, and 71.8 +/- 5.3, respectively. The addition of magnesium to the cardioplegic solution improved recovery of aortic flow (p less than 0.05, 16 mM versus 0 mM magnesium). We conclude from these data that with deep myocardial hypothermia and at an ionized calcium concentration of 0.1 mM, the addition of magnesium, over a broad concentration range, improved preservation of myocardial creatine phosphate and, at a concentration of 16 mM, improved aortic flow. The optimal magnesium concentration in the cardioplegic solution was 16 mM.

Adenine Nucleotides↗
PubMed1989

Pulmonary vascular responses to hypercalcemia and hypocalcemia in the dog.

The pulmonary artery responses in the isolated whole-blood perfused canine lung to ionized calcium ([Ca++]) were quantified over a range of hypercalcemia and hypocalcemia values ([Ca++] = 0.23-1.88 mM) under conditions of controlled pulmonary blood flow and constant mean aortic and left atrial pressures. Calcium chloride, administered as bolus doses in the clinical range (5-15 mg.kg-1) at initial normocalcemia and without interventions producing vasoconstriction did not influence mean pulmonary artery pressure at constant pulmonary blood flow. Stable hypercalcemia ([Ca++] = 1.88 +/- 0.05 mM) did not influence the slope of the pulmonary artery pressure-flow plot. Because normal pulmonary vasomotor tone is low and cannot readily be lowered further, the possible vasodilator action of hypocalcemia was assessed by its ability to decrease the slope of the mean pulmonary artery pressure-flow plot, which had been first increased by alveolar hypoxia (AHX) or infusion of the prostaglandin endoperoxide analog U46619 (PG). During AHX (n = 5), a graded reduction from normocalcemia ([Ca++] = 1.08 +/- 0.02 mM) to moderate hypocalcemia ([Ca++] = 0.8 and 0.5 mM) did not alter the pulmonary artery pressure-flow plot, but severe hypocalcemia ([Ca++] = 0.26 +/- 0.01 mM) decreased the slope by 13 +/- 0.9 mmHg.l-1.min-1. The comparison of severe hypocalcemia ([Ca++] = 0.23-0.27 mM) versus a high dose of nifedipine (bolus of 10 micrograms/kg followed by continuous infusion at 40 micrograms.kg-1.h-1) on pulmonary vascular tone increased by either AHX or PG infusion indicated that both hypocalcemia and nifedipine decreased the slope of the relationship between mean pulmonary artery pressure and flow (during AHX: -16.1 +/- 1.38 and -23.3 +/- 1.73 mmHg.l-1.min-1, both P = 0.0001 vs. AHX alone, and during PG: -17.05 +/- 1.95 and -8.4 +/- 1.78 mmHg.l-1.min-1, P = 0.0001 vs. PG alone). Two principal conclusions emerge. First, the pulmonary vessels are minimally sensitive to changes in ionized calcium throughout the clinical hypercalcemia and hypocalcemia ranges; extreme hypocalcemia is required to produce vasodilation, which was reversed with calcium infusion. Second, whereas the pulmonary vasodilator effects of extreme hypocalcemia were independent of the intervention inducing pulmonary vasoconstriction (AHX vs. PG), those of nifedipine were much more pronounced with AHX.

Animals↗
PubMed1989

The effects of calcium and magnesium in hyperkalemic cardioplegic solutions on myocardial preservation.

Sustained left ventricular pressure development during each infusion of a cold calcium-containing hyperkalemic cardioplegic solution has been observed in rat hearts. The present study was undertaken to relate such contraction (i.e., increase in resting pressure) to myocardial preservation and to the calcium and magnesium contents of a crystalloid hyperkalemic cardioplegic solution. Isolated perfused rat hearts with a left ventricular isovolumic balloon were arrested at 8 degrees C by the fully oxygenated cardioplegic solution infused every 15 minutes for 2 hours. Cardioplegic solutions containing ionized calcium in concentrations of 0, 0.1, or 1.2 mmol/L were each studied with (groups 2, 4, and 6) and without (groups 1, 3, and 5) the addition of magnesium (16 mmol/L). Hearts arrested by the cardioplegic solution with no calcium or magnesium (group 1) developed a pressure (averaged over the second to eighth infusion and expressed as percent prearrest left ventricular pressure) of 6.0% +/- 0.4% during cardioplegic infusions. This solution maintained end-arrest myocardial adenosine triphosphate (13.1 +/- 1.0 nmol/mg dry weight) and phosphocreatine (21.7 +/- 2.8 nmol/mg dry weight) contents near the prearrest contents and preserved left ventricular function at 95% +/- 3% of prearrest developed left ventricular pressure at 15 minutes of reperfusion at 37 degrees C. Calcium (groups 3 and 5) increased pressure development during cardioplegic infusions (10.4% +/- 0.5% and 15.1% +/- 0.9%), depleted adenosine triphosphate (7.2 +/- 1.0 and 7.4 +/- 0.9) and phosphocreatine (13.3 +/- 1.8 and 10.7 +/- 1.5), and depressed left ventricular functional recovery (71% +/- 1% and 73% +/- 3%). Magnesium alone (group 2) decreased pressure development during cardioplegic infusions (3.0% +/- 0.3%), maintained adenosine triphosphate (15.6 +/- 0.9), augmented phosphocreatine (38.3 +/- 1.2), and preserved left ventricular function (99% +/- 4%). Magnesium added to calcium (groups 4 and 6) prevented the calcium-induced increased pressure development during cardioplegic infusions (4.0% +/- 0.5% and 6.7% +/- 0.6%), maintained adenosine triphosphate (13.6 +/- 1.4 and 14.9 +/- 0.7), augmented phosphocreatine (31.3 +/- 1.6 and 32.2 +/- 2.4), and ameliorated the depression of functional recovery (82% +/- 2% and 86% +/- 2%). These data suggest that left ventricular pressure development during arrest contributed to calcium-induced energy depletion and impairment of functional recovery and that these deleterious effects were inhibited by magnesium. The inhibitory effects of magnesium on left ventricular pressure development were rapidly reversed on reperfusion. The data support the addition

Adenine Nucleotides↗